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1.
Braz. j. med. biol. res ; 53(3): e8761, 2020. tab, graf
Article in English | LILACS | ID: biblio-1089339

ABSTRACT

Nitric oxide (NO) inhibition by high-dose NG-nitro-L-arginine methyl ester (L-NAME) is associated with several detrimental effects on the cardiovascular system. However, low-dose L-NAME increases NO synthesis, which in turn induces physiological cardiovascular benefits, probably by activating a protective negative feedback mechanism. Aerobic exercise, likewise, improves several cardiovascular functions in healthy hearts, but its effects are not known when chronically associated with low-dose L-NAME. Thus, we tested whether the association between low-dose L-NAME administration and chronic aerobic exercise promotes beneficial effects to the cardiovascular system, evaluating the cardiac remodeling process. Male Wistar rats were randomly assigned to control (C), L-NAME (L), chronic aerobic exercise (Ex), and chronic aerobic exercise associated to L-NAME (ExL). Aerobic training was performed with progressive intensity for 12 weeks; L-NAME (1.5 mg·kg-1·day-1) was administered by orogastric gavage. Low-dose L-NAME alone did not change systolic blood pressure (SBP), but ExL significantly increased SBP at week 8 with normalization after 12 weeks. Furthermore, ExL promoted the elevation of left ventricle (LV) end-diastolic pressure without the presence of cardiac hypertrophy and fibrosis. Time to 50% shortening and relaxation were reduced in ExL, suggesting a cardiomyocyte contractile improvement. In addition, the time to 50% Ca2+ peak was increased without alterations in Ca2+ amplitude and time to 50% Ca2+ decay. In conclusion, the association of chronic aerobic exercise and low-dose L-NAME prevented cardiac pathological remodeling and induced cardiomyocyte contractile function improvement; however, it did not alter myocyte affinity and sensitivity to intracellular Ca2+ handling.


Subject(s)
Animals , Male , Physical Conditioning, Animal/physiology , Calcium/analysis , Nitric Oxide Synthase/drug effects , NG-Nitroarginine Methyl Ester/pharmacology , Enzyme Inhibitors/pharmacology , Myocardial Contraction/drug effects , Body Weight/physiology , Rats, Wistar , Ventricular Pressure/drug effects , Nitric Oxide Synthase/metabolism , NG-Nitroarginine Methyl Ester/administration & dosage , Models, Animal , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/physiology , Enzyme Inhibitors/administration & dosage , Adiposity , Hemodynamics , Motor Activity/physiology , Myocardium/pathology
2.
Braz. j. med. biol. res ; 52(4): e7626, 2019. graf
Article in English | LILACS | ID: biblio-1001516

ABSTRACT

Reactive oxygen species (ROS) are highly reactive chemical species that may cause irreversible tissue damage, and play a critical role in cardiovascular diseases. Hydrogen sulfide (H2S) is a gasotransmitter that acts as a ROS scavenger with cardio-protective effects. In this study, we investigated the cytoprotective effect of H2S against H2O2-induced apoptosis in cardiomyocytes. H9c2 rat cardiomyoblasts were treated with H2S (100 μM) 24 h before challenging with H2O2 (100 μM). Apoptosis was then assessed by annexin V and PI, and mitochondrial membrane potential was measured using a fluorescent probe, JC-1. Our results revealed that H2S improved cell viability, reduced the apoptotic rate, and preserved mitochondrial membrane potential. An increased Bcl-2 to Bax ratio was also seen in myocytes treated with H2S after H2O2-induced stress. Our findings indicated a therapeutic potential for H2S in preventing myocyte death following ischemia/reperfusion.


Subject(s)
Animals , Rats , Apoptosis/drug effects , Myoblasts, Cardiac/drug effects , Hydrogen Peroxide , Antioxidants/pharmacology , Reference Values , Sulfides/pharmacology , Cell Survival/drug effects , Cells, Cultured , Blotting, Western , Reproducibility of Results , Reactive Oxygen Species/metabolism , Apoptosis/physiology , Oxidative Stress/drug effects , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/metabolism , Myoblasts, Cardiac/metabolism , Membrane Potential, Mitochondrial , Flow Cytometry/methods , Hydrogen Sulfide/pharmacology
3.
Braz. j. med. biol. res ; 52(3): e7994, 2019. graf
Article in English | LILACS | ID: biblio-984040

ABSTRACT

Myocardial infarction (MI) is a common presentation for ischemic heart disease, which is a leading cause of death. Emodin is a Chinese herbal anthraquinone used in several diseases. However, the effect of emodin in hypoxia-induced injury in cardiomyocytes has not been clearly elucidated. Our study aimed to clarify the functions of emodin in hypoxia-induced injury in rat cardiomyocytes H9c2 and explore the underlying mechanism. The effects of emodin on cell viability and apoptosis were analyzed by the Cell counting kit-8 assay and flow cytometry assay, respectively. The cell proliferation- and cell apoptosis-related proteins were detected by western blot. qRT-PCR was used to determine the relative expression of miR-138. Cell transfection was performed to alter miR-138 and MLK3 expression. miR-138 target was performed by dual luciferase activity assay. Sirt1/AKT and Wnt/β-catenin pathways-related factors phosphorylation were analyzed by western blot. Emodin inhibited hypoxia-induced injury in H9c2 cells by promoting cell viability and reducing cell apoptosis. miR-138 was down-regulated by hypoxia treatment but up-regulated by emodin. Up-regulation of miR-138 alleviated hypoxia-induced cell injury. Down-regulation of miR-138 attenuated the growth-promoting effect of emodin on hypoxia-induced injury, whereas up-regulation of miR-138 enhanced the growth-promoting effects of emodin. The underlying mechanism might be by inactivating Sirt1/AKT and Wnt/β-catenin pathways. MLK3 was negatively regulated by miR-138 expression and inactivated Sirt1/AKT and Wnt/β-catenin pathways. Emodin alleviated hypoxia-induced injury in H9c2 cells via up-regulation of miR-138 modulated by MLK3, as well as by activating Sirt1/AKT and Wnt/β-catenin pathways.


Subject(s)
Animals , Rats , Cell Hypoxia/drug effects , Cell Survival/drug effects , Emodin/therapeutic use , Myocytes, Cardiac/pathology , Cell Proliferation/drug effects , Hypoxia/complications , Signal Transduction , Up-Regulation , Cell Line , Myocytes, Cardiac/drug effects , MicroRNAs
4.
Braz. j. med. biol. res ; 52(12): e8834, 2019. graf
Article in English | LILACS | ID: biblio-1055472

ABSTRACT

Polydatin (PD), a monocrystalline polyphenolic drug mainly found in the roots of Polygonum cuspidatum, has various pharmacological activities. Long non-coding RNAs (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) was found to participate in the suppression of multiple cancers. Here, we proposed to study the effect of PD on myocardial infarction (MI) by inducing DGCR5. CCK-8 assay was performed to detect the viability of H9c2 cells. Flow cytometry was utilized to test apoptosis of H9c2 cells. These results determined the optimal concentration and effect time of hypoxia as well as PD. Si-DGCR5 was transfected into cells and the expression level was determined by qRT-PCR. Western blot was utilized to evaluate the expression of apoptosis-related proteins, Bcl-2, Bax, and cleaved-caspase-3, as well as autophagy-associated proteins including Beclin-1, p62, and LC3-II/LC3-I. As a result, PD efficiently attenuated hypoxia-induced apoptosis and autophagy in H9c2 cells. The expression of DGCR5 was down-regulated by hypoxia and up-regulated by PD. Besides, knocking-down the expression of DGCR5 inhibited the protection of PD in H9c2 cells. In addition, PD up-regulated the accumulation of DGCR5, DGCR5 decreased the expression of Bcl-2 and p62, raised the expression of Bax and cleaved-caspase-3, and the proportion of LC3-II/LC3-I. PD stimulated the PI3K/AKT/mTOR and MEK/ERK signaling pathways via up-regulating the expression of DGCR5. Our data demonstrated that PD reduced cell apoptosis and autophagy induced by hypoxia in cardiomyocytes. Moreover, PD activated PI3K/AKT/mTOR and MEK/ERK signaling pathways by up-regulating the expression of DGCR5.


Subject(s)
Animals , Rats , Stilbenes/pharmacology , Cell Hypoxia/drug effects , Apoptosis/drug effects , Myocytes, Cardiac/drug effects , Cell Proliferation/drug effects , RNA, Long Noncoding/drug effects , Glucosides/pharmacology , Signal Transduction , Up-Regulation/drug effects , Cell Line , Cytoprotection , Myocytes, Cardiac/metabolism , Myocytes, Cardiac/pathology
5.
Braz. j. med. biol. res ; 52(7): e8732, 2019. tab, graf
Article in English | LILACS | ID: biblio-1011598

ABSTRACT

Inflammation plays an important role in the development of cardiovascular diseases (CVDs), suggesting that the immune system is a target of therapeutic interventions used for treating CVDs. This study evaluated mechanisms underlying inflammatory response and cardiomyocyte hypertrophy associated with bacterial lipopolysaccharide (LPS)- or heat shock protein 60 (HSP60)-induced Toll-like receptor (TLR) stimulation and the effect of a small interfering RNA (siRNA) against Ca2+/calmodulin-dependent kinase II delta B (CaMKIIδB) on these outcomes. Our results showed that treatment with HSP60 or LPS (TLR agonists) induced cardiomyocyte hypertrophy and complement system C3 and factor B gene expression. In vitro silencing of CaMKIIδB prevented complement gene transcription and cardiomyocyte hypertrophy associated with TLR 2/4 activation but did not prevent the increase in interleukin-6 and tumor necrosis factor-alfa gene expression in primary cultured cardiomyocytes. Moreover, CaMKIIδB silencing attenuated nuclear factor-kappa B expression. These findings supported the hypothesis that CaMKIIδB acts as a link between inflammation and cardiac hypertrophy. Furthermore, the present study is the first to show that extracellular HSP60 activated complement gene expression through CaMKIIδB. Our results indicated that a stress stimulus induced by LPS or HSP60 treatment promoted cardiomyocyte hypertrophy and initiated an inflammatory response through the complement system. However, CaMKIIδB silencing prevented the cardiomyocyte hypertrophy independent of inflammatory response induced by LPS or HSP60 treatment.


Subject(s)
Animals , Rats , Myocytes, Cardiac/pathology , Toll-Like Receptors/metabolism , Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism , Signal Transduction/physiology , Gene Expression , Lipopolysaccharides/pharmacology , NF-kappa B/metabolism , Rats, Wistar , Chaperonin 60/pharmacology , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/metabolism , RNA, Small Interfering , Inflammation/metabolism
6.
Rev. bras. anestesiol ; 68(6): 591-596, Nov.-Dec. 2018. tab, graf
Article in English | LILACS | ID: biblio-977407

ABSTRACT

Abstract Introduction: Hepatic ischemia-reperfusion injury is a common pathophysiological process in liver surgery. Whether Propofol can reduce myocardial ischemia-reperfusion injury induced by hepatic ischemia-reperfusion injury in rats, together with related mechanisms, still needs further studies. Objective: To investigate if propofol would protect the myocardial cells from apoptosis with hepatic ischemia-reperfusion injury. Methods: Male Sprague-Dawley rats (n = 18) were randomly allocated into three groups: Sham Group (Group S, n = 6), Hepatic Ischemia-reperfusion Injury Group (Group IR, n = 6) and Propofol Group (Group P, n = 6). Group S was only subjected to laparotomy. Group IR was attained by ischemia for 30 min and reperfusion for 4 h. Group P was subjected identical insult as in Group IR with the administration of propofol started 10 min before ischemia with 120 mg.kg−1, following by continuous infusion at 20 mg.kg−1.h−1. Cell apoptosis was examined by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay. Endoplasmic reticulum Ca2+-ATPase2 (SERCA2) and cysteine-containing aspartic acid cleaved-caspase3 (cleaved-caspase3) were assayed by western blot and Altimeter polymerase chain reaction. Results: Apoptosis rate was increased, with mRNA and protein of SERCA2 down-regulated and cleaved-caspase3 up-regulated in Group IR compared with Group S (p < 0.01). Apoptosis rate was decreased, with mRNA and protein of SERCA2 up-regulated and cleaved-caspase3 down-regulated in Group P compared with Group IR (p < 0.01). Conclusions: Propofol can reduce hepatic ischemia-reperfusion injury-induced myocardial cell apoptosis, meanwhile, can up-regulate mRNA and protein of SERCA2 in rats.


Resumo Introdução: A lesão hepática por isquemia-reperfusão é um processo fisiopatológico comum em cirurgias hepáticas. Mais estudos ainda são necessários para avaliar se o propofol pode reduzir a lesão de isquemia-reperfusão miocárdica induzida pela lesão de isquemia-reperfusão hepática em ratos, juntamente com os mecanismos que estão relacionados. Objetivo: Investigar se propofol protege as células do miocárdio da apoptose com a lesão hepática por isquemia-reperfusão. Métodos: Ratos machos da raça Sprague-Dawley (n = 18) foram alocados aleatoriamente em três grupos: Grupo Sham (Grupo S, n = 6), Grupo Lesão Hepática por Isquemia-reperfusão (Grupo IR, n = 6) e Grupo Propofol (Grupo P, n = 6). O Grupo S foi submetido apenas à laparotomia. O grupo IR foi submetido à isquemia por 30 min e reperfusão por 4 h. O grupo P foi submetido à mesma isquemia do grupo IR, com a administração de 120 mg.kg-1 de propofol iniciada 10min antes da isquemia, seguida de infusão contínua a 20 mg.kg-1.h-1. A apoptose celular foi examinada por meio do ensaio de marcação de terminações dUTP pela deoxinucleotidil transferase. Retículo endoplasmático Ca2+-ATPase2 (SERCA2) e caspase-3 do ácido aspártico contendo cisteína (caspase-3 clivada) foram avaliados com o ensaio western blot e reação em cadeia da polimerase. Resultados: A taxa de apoptose foi maior com mRNA e proteína de SERCA2 regulados para baixo e caspase-3 clivada suprarregulada no Grupo IR, em comparação com o Grupo S (p < 0,01). A taxa de apoptose foi menor com mRNA e proteína de SERCA2 suprarregulada e caspase-3 clivada sub-regulada no Grupo P, em comparação com o Grupo IR (p < 0,01). Conclusões: O propofol pode reduzir a apoptose de células miocárdicas induzida por lesão hepática por isquemia-reperfusão. Entretanto, pode suprarregular o mRNA e a proteína de SERCA2 em ratos.


Subject(s)
Animals , Male , Rats , Reperfusion Injury/prevention & control , Propofol/administration & dosage , Apoptosis/drug effects , Anesthetics, Intravenous/administration & dosage , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/physiology , Sarcoplasmic Reticulum Calcium-Transporting ATPases/biosynthesis , Sarcoplasmic Reticulum Calcium-Transporting ATPases/drug effects , Liver/blood supply , Random Allocation , Propofol/pharmacology , Rats, Sprague-Dawley , Anesthetics, Intravenous/pharmacology
7.
Arq. bras. cardiol ; 111(2): 162-169, Aug. 2018. graf
Article in English | LILACS | ID: biblio-950215

ABSTRACT

Abstract Background: Pioglitazone has been widely used as an insulin-sensitizing agent for improving glycemic control in patients with type 2 diabetes mellitus. However, cardiovascular risk and protective effects of pioglitazone remain controversial. Objectives: In this study, we investigated whether pioglitazone affects cardiomyocyte apoptosis and hypertrophy by regulating the VEGFR-2 signaling pathway. Methods: Cardiomyocytes were enzymatically isolated from 1- to 3-day-old Sprague-Dawley rat ventricles. Effects of pioglitazone and the VEGFR-2-selective inhibitor apatinib on cardiomyocyte apoptotic rate was determined using flow cytometry, and hypertrophy was evaluated using [3H]-leucine incorporation. The protein expressions of unphosphorylated and phosphorylated VEGFR-2, Akt, P53, and mTOR were determined by Western-Blotting. Analysis of variance (ANOVA) was used to assess the differences between groups. Results: Pioglitazone and VEGFR-2-selective inhibitor apatinib reduced rat cardiomyocyte viability and cardiomyocyte hypertrophy induced by angiotensin II in vitro. Furthermore, in the same in vitro model, pioglitazone and apatinib significantly increased the expression of Bax and phosphorylated P53 and decreased the expression of phosphorylated VEGFR-2, Akt, and mTOR, which promote cardiomyocyte hypertrophy. Conclusions: These findings indicate that pioglitazone induces cardiomyocyte apoptosis and inhibits cardiomyocyte hypertrophy by modulating the VEGFR-2 signaling pathway.


Resumo Fundamento: A pioglitazona tem sido amplamente utilizada como droga sensibilizadora da insulina para melhorar o controle glicêmico em pacientes com diabetes mellitus tipo 2. No entanto, o risco cardiovascular bem como os efeitos protetores da pioglitazona ainda são controversos. Objetivos: Neste estudo, investigamos se os efeitos da pioglitazona sobre a apoptose e a hipertrofia de cardiomiócitos ocorrem via regulação da via de sinalização do VEGFR-2. Métodos: os cardiomiócitos foram isolados enzimaticamente dos ventrículos de ratos Sprague-Dawley de 1-3 anos de vida. Os efeitos da pioglitazona e do inibidor seletivo de VEGFR-2 apatinib sobre a taxa de apoptose dos cardiomiócitos foram avaliados por citometria de fluxo, e a hipertrofia avaliada por incorporação de leucina-[3H]. As expressões de VEGFR-2, Akt, P53, e mTOR fosforiladas e não fosforiladas foram determinadas por Western Blotting. Análise de variância (ANOVA) foi usada para avaliar diferenças entre os grupos. Resultados: a pioglitazona e o apatinib reduziram a viabilidade e a hipertrofia de cardiomiócitos induzida por angiotensina II in vitro. Além disso, no mesmo modelo in vitro, a pioglitazona e o apatinib aumentaram significativamente a expressão de Bax e P53 fosforilada, e diminuiu a expressão de VEGFR-2, Akt, e mTOR, que promove hipertrofia de cardiomiócitos. Conclusões: Esses resultados indicam que a pioglitazona induz a apoptose e inibe a hipertrofia de cardiomiócitos pela modulação da via de sinalização de VEGFR-2.


Subject(s)
Animals , Rats , Apoptosis/drug effects , Vascular Endothelial Growth Factor Receptor-2/drug effects , Thiazolidinediones/pharmacology , Hypoglycemic Agents/pharmacology , Signal Transduction/drug effects , Rats, Sprague-Dawley , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/pathology , Pioglitazone , Hypertrophy/chemically induced , Hypertrophy/pathology , Animals, Newborn
8.
Arq. bras. cardiol ; 110(1): 44-51, Jan. 2018. graf
Article in English | LILACS | ID: biblio-887998

ABSTRACT

Resumo Background: Melatonin is a neuroendocrine hormone synthesized primarily by the pineal gland that is indicated to effectively prevent myocardial reperfusion injury. It is unclear whether melatonin protects cardiac function from reperfusion injury by modulating intracellular calcium homeostasis. Objective: Demonstrate that melatonin protect against myocardial reperfusion injury through modulating IP3R and SERCA2a to maintain calcium homeostasis via activation of ERK1 in cardiomyocytes. Methods: In vitro experiments were performed using H9C2 cells undergoing simulative hypoxia/reoxygenation (H/R) induction. Expression level of ERK1, IP3R and SERCA2a were assessed by Western Blots. Cardiomyocytes apoptosis was detected by TUNEL. Phalloidin-staining was used to assess alteration of actin filament organization of cardiomyocytes. Fura-2 /AM was used to measure intracellular Ca2+ concentration. Performing in vivo experiments, myocardial expression of IP3R and SERCA2a were detected by immunofluorescence staining using myocardial ischemia/ reperfusion (I/R) model in rats. Results: In vitro results showed that melatonin induces ERK1 activation in cardiomyocytes against H/R which was inhibited by PD98059 (ERK1 inhibitor). The results showed melatonin inhibit apoptosis of cardiomyocytes and improve actin filament organization in cardiomyocytes against H/R, because both could be reversed by PD98059. Melatonin was showed to reduce calcium overload, further to inhibit IP3R expression and promote SERCA2a expression via ERK1 pathway in cardiomyocytes against H/R. Melatonin induced lower IP3R and higher SERCA2a expression in myocardium that were reversed by PD98059. Conclusion: melatonin-induced cardioprotection against reperfusion injury is at least partly through modulation of IP3R and SERCA2a to maintain intracellular calcium homeostasis via activation of ERK1.


Resumo Fundamento: A melatonina é um hormônio neuroendócrino sintetizado principalmente pela glândula pineal que é indicado para prevenir efetivamente a lesão de reperfusão miocárdica. Não está claro se a melatonina protege a função cardíaca da lesão de reperfusão através da modulação da homeostase do cálcio intracelular. Objetivo: Demonstrar que a melatonina protege contra a lesão de reperfusão miocárdica através da modulação de IP3R e SERCA para manter a homeostase de cálcio por meio da ativação de ERK1 em cardiomiócitos. Métodos: Foram realizados experimentos in vitro usando células H9C2 submetidas a indução de hipoxia / reoxigenação simulada (H/R). O nível de expressão de ERK1, IP3R e SERCA foi avaliado por Western Blots. A apoptose de cardiomiócitos foi detectada por TUNEL. A coloração de faloidina foi utilizada para avaliar a alteração da organização de filamentos de actina dos cardiomiócitos. Fura-2 / AM foi utilizado para medir a concentração intracelular de Ca2+. Realizando experiências in vivo, a expressão miocárdica de IP3R e SERCA foi detectada por coloração com imunofluorescência usando modelo de isquemia miocárdica / reperfusão (I/R) em ratos. Resultados: resultados in vitro mostraram que a melatonina induz a ativação de ERK1 em cardiomiócitos contra H/R que foi inibida por PD98059 (inibidor de ERK1). Os resultados mostraram que a melatonina inibe a apoptose dos cardiomiócitos e melhora a organização do filamento de actina em cardiomiócitos contra H/R, pois ambas poderiam ser revertidas pela PD98059. A melatonina mostrou reduzir a sobrecarga de cálcio, além de inibir a expressão de IP3R e promover a expressão de SERCA através da via ERK1 em cardiomiócitos contra H/R. A melatonina induziu menor IP3R e maior expressão de SERCA no miocárdio que foram revertidas pela PD98059. Conclusão: a cardioproteção induzida pela melatonina contra lesão de reperfusão é pelo menos parcialmente através da modulação de IP3R e SERCA para manter a homeostase de cálcio intracelular via ativação de ERK1.


Subject(s)
Animals , Male , Rats , Myocardial Reperfusion Injury/metabolism , Myocardial Reperfusion Injury/prevention & control , MAP Kinase Signaling System/drug effects , Myocytes, Cardiac/drug effects , Sarcoplasmic Reticulum Calcium-Transporting ATPases/drug effects , Inositol 1,4,5-Trisphosphate Receptors/drug effects , Melatonin/pharmacology , Myocardial Reperfusion Injury/pathology , Rats, Sprague-Dawley , Myocytes, Cardiac/pathology , Disease Models, Animal , Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism , Inositol 1,4,5-Trisphosphate Receptors/metabolism
9.
Yonsei Medical Journal ; : 279-286, 2018.
Article in English | WPRIM | ID: wpr-713092

ABSTRACT

PURPOSE: The mechanisms underlying repolarization abnormalities during pregnancy are not fully understood. Although maternal serotonin (5-hydroxytryptamine, 5-HT) production is an important determinant for normal fetal development in mice, its role in mothers remains unclear. We evaluated the role of serotonin in ventricular repolarization in mice hearts via 5Htr3 receptor (Htr3a) and investigated the mechanism of QT-prolongation during pregnancy. MATERIALS AND METHODS: We measured current amplitudes and the expression levels of voltage-gated K⁺ (Kv) channels in freshly-isolated left ventricular myocytes from wild-type non-pregnant (WT-NP), late-pregnant (WT-LP), and non-pregnant Htr3a homozygous knockout mice (Htr3a(−/−)-NP). RESULTS: During pregnancy, serotonin and tryptophan hydroxylase 1, a rate-limiting enzyme for the synthesis of serotonin, were markedly increased in hearts and serum. Serotonin increased Kv current densities concomitant with the shortening of the QT interval in WT-NP mice, but not in WT-LP and Htr3a(−/−)-NP mice. Ondansetron, an Htr3 antagonist, decreased Kv currents in WT-LP mice, but not in WT-NP mice. Kv4.3 directly interacted with Htr3a, and this binding was facilitated by serotonin. Serotonin increased the trafficking of Kv4.3 channels to the cellular membrane in WT-NP. CONCLUSION: Serotonin increases repolarizing currents by augmenting Kv currents. Elevated serotonin levels during pregnancy counterbalance pregnancy-related QT prolongation by facilitating Htr3-mediated Kv currents.


Subject(s)
Action Potentials/drug effects , Animals , Cell Membrane/drug effects , Disease Models, Animal , Electrocardiography , Female , HSC70 Heat-Shock Proteins/metabolism , HSP90 Heat-Shock Proteins/metabolism , Heart Ventricles/drug effects , Mice, Inbred C57BL , Mice, Knockout , Myocytes, Cardiac/drug effects , Potassium Channels/metabolism , Pregnancy , Rabbits , Rats, Sprague-Dawley , Receptors, Serotonin, 5-HT3/metabolism , Serotonin/metabolism , Serotonin 5-HT3 Receptor Agonists/pharmacology
10.
Braz. j. med. biol. res ; 50(2): e5286, 2017. tab, graf
Article in English | LILACS | ID: biblio-839258

ABSTRACT

We aimed to study the effect of fentanyl (Fen) preconditioning on cardiomyocyte apoptosis induced by ischemia-reperfusion (I/R) in rats. A total of 120 Sprague Dawley male rats (age: 3 months) were randomly divided into: sham operation group (S group), I/R group, normal saline I/R group (NS group), and fentanyl low, middle, and high dose groups (Fen1: 2 μg/kg; Fen2: 4 μg/kg; Fen3: 6 μg/kg). Heart rate (HR), mean arterial pressure (MAP), left ventricular developed pressure (LVDP), ±dp/dtmax, malondialdehyde (MDA), superoxide dismutase (SOD) activity, creatine phosphokinase-MB (CK-MB), and cardiac troponin-I (cTnI) were measured. Myocardial ischemic (MI) area, total apoptotic myocardial cells, and protein and mRNA expressions of B-cell lymphoma 2 (Bcl-2) and Bax were detected. HR and MAP were higher, while LVDP and ±dp/dtmax were close to the base value in the Fen groups compared to those in the I/R group. Decreased MDA concentration and CK-MB value and increased SOD activity were found in the Fen groups compared to the I/R group, while cTnI concentration was significantly lower in the Fen1 and Fen2 groups (all P<0.05). Myocardial damage was less in the Fen groups compared to the I/R group and the MI areas and apoptotic indexes were significantly lower in the Fen1 and Fen2 groups (all P<0.05). Furthermore, significantly increased protein and mRNA expressions of Bcl-2, and decreased protein and mRNA expressions of Bax were found in the Fen groups compared to the I/R group (all P<0.05). Fentanyl preconditioning may suppress cardiomyocyte apoptosis induced by I/R in rats by regulating Bcl-2 and Bax.


Subject(s)
Animals , Male , Rats , Apoptosis/drug effects , Fentanyl/therapeutic use , Myocardial Reperfusion Injury/prevention & control , Myocytes, Cardiac/drug effects , Protective Agents/therapeutic use , Myocardial Reperfusion Injury/pathology , Myocytes, Cardiac/pathology , Rats, Sprague-Dawley
11.
Braz. j. med. biol. res ; 50(6): e5868, 2017. tab, graf
Article in English | LILACS | ID: biblio-839308

ABSTRACT

We aimed to investigate the effect of etanercept, a tumor necrosis factor-α (TNF-α) inhibitor, on rat cardiomyocyte hypertrophy and its underlying mechanism. Primary neonatal rat cardiomyocytes were isolated from Sprague-Dawley rats. The model of rat cardiomyocyte hypertrophy was induced by endothelin, and then treated with different concentrations of etanercept (1, 10, and 50 μM). After treatment, cell counts, viability and cell apoptosis were evaluated. The mRNA levels of myocardial hypertrophy marker genes, including atrial natriuretic factor (ANF), matrix metalloproteinase (MMP)-9 and MMP-13, were detected by qRT-PCR, and the expressions of apoptosis-related proteins (Bcl-2 and Bax) were measured by western blotting. The protein levels of transforming growth factor-β1 (TGF-β1), interleukin (IL)-1β, IL-6, leukemia inhibitory factor (LIF) and cardiotrophin-1 (CT-1) were determined using enzyme linked immunosorbent assay (ELISA) kits. In the present study, TNF-α level in cardiomyocytes with hypertrophy was significantly enhanced (P<0.05). Compared to the model group, cell number and viability were significantly increased and ratio of apoptotic cells was reduced by etanercept (P<0.05, P<0.01, or P<0.001). In addition, etanercept remarkably reduced the mRNA levels of ANF, MMP-9 and MMP-13, inhibited the expression of Bax, and increased the expression of Bcl-2 compared to the model group (P<0.05). ELISA results further showed that etanercept lowered the levels of IL-1β, IL-6, LIF and CT-1 but not TGF-β1 compared to the model group (P<0.05). Etanercept may protect rat cardiomyocytes from hypertrophy by inhibiting inflammatory cytokines secretion and cell apoptosis.


Subject(s)
Animals , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Cardiomegaly/metabolism , Etanercept/pharmacology , Myocytes, Cardiac/drug effects , Protective Agents/pharmacology , Animals, Newborn , Apoptosis/drug effects , Atrial Natriuretic Factor/metabolism , Cardiomegaly/chemically induced , Cell Proliferation/drug effects , Cell Survival/drug effects , Cells, Cultured , Cytokines/drug effects , Disease Models, Animal , Inflammation/metabolism , Matrix Metalloproteinase 13/metabolism , Matrix Metalloproteinase 9/metabolism , Myocytes, Cardiac/metabolism , Rats, Sprague-Dawley , Tumor Necrosis Factor-alpha/metabolism
12.
Braz. j. med. biol. res ; 50(12): e6733, 2017. graf
Article in English | LILACS | ID: biblio-888967

ABSTRACT

Myostatin is a novel negative regulator of skeletal muscle mass. Myostatin expression is also found in heart in a much less extent, but it can be upregulated in pathological conditions, such as heart failure. Myostatin may be involved in inhibiting protein synthesis and/or increasing protein degradation in skeletal and cardiac muscles. Herein, we used cell cultures and isolated muscles from rats to determine protein degradation and synthesis. Muscles incubated with myostatin exhibited an increase in proteolysis with an increase of Atrogin-1, MuRF1 and LC3 genes. Extensor digitorum longus muscles and C2C12 myotubes exhibited a reduction in protein turnover. Cardiomyocytes showed an increase in proteolysis by activating autophagy and the ubiquitin proteasome system, and a decrease in protein synthesis by decreasing P70S6K. The effect of myostatin on protein metabolism is related to fiber type composition, which may be associated to the extent of atrophy mediated effect of myostatin on muscle.


Subject(s)
Animals , Male , Muscle Fibers, Skeletal/drug effects , Muscle Fibers, Skeletal/metabolism , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/metabolism , Myostatin/pharmacology , Muscle Proteins/drug effects , Muscle Proteins/metabolism , Phosphorylation/drug effects , Phosphorylation/physiology , Time Factors , Tyrosine/drug effects , Tyrosine/metabolism , Gene Expression , Cells, Cultured , Blotting, Western , Reproducibility of Results , Rats, Wistar , Real-Time Polymerase Chain Reaction , Proteolysis/drug effects
13.
Braz. j. med. biol. res ; 50(8): e6204, 2017. tab, graf
Article in English | LILACS | ID: biblio-888983

ABSTRACT

Oxidative stress plays an important role in the development of diabetic cardiomyopathy. In the present study, we determined whether the effect of astragalus polysaccharides (APS) on diabetic cardiomyopathy was associated with its impact on oxidative stress. Streptozotocin (STZ)-induced diabetic mice and heterozygous superoxide dismutase (SOD2+/-) knockout mice were administered APS. The hemodynamics, cardiac ultrastructure, and the apoptosis, necrosis and proliferation of cardiomyocytes were assessed to evaluate the effect of APS on diabetic and oxidative cardiomyopathy. Furthermore, H2O2 formation, oxidative stress/damage, and SOD activity in cardiomyocytes were evaluated to determine the effects of APS on cardiac oxidative stress. APS therapy improved hemodynamics and myocardial ultrastructure with reduced apoptosis/necrosis, and enhanced proliferation in cardiomyocytes from both STZ-induced diabetic mice and heterozygous SOD2+/- knockout mice. In addition, APS therapy reduced H2O2 formation and oxidative stress/damage, and enhanced SOD activity in both groups of mice. Our findings suggest that APS had benefits in diabetic cardiomyopathy, which may be partly associated with its impact on cardiac oxidative stress.


Subject(s)
Animals , Male , Mice , Polysaccharides/therapeutic use , Superoxide Dismutase/genetics , Plant Extracts/therapeutic use , Astragalus Plant/chemistry , Diabetes Mellitus, Experimental/drug therapy , Diabetic Cardiomyopathies/drug therapy , Apoptosis/drug effects , Streptozocin , Mice, Knockout , Oxidative Stress/drug effects , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/ultrastructure , Microscopy, Electron, Transmission , Cell Proliferation/drug effects , Diabetes Mellitus, Experimental/pathology , Diabetic Cardiomyopathies/pathology , Mice, Inbred C57BL
14.
Acta cir. bras ; 31(4): 271-277, Apr. 2016. tab, graf
Article in English | LILACS | ID: lil-781332

ABSTRACT

PURPOSE: T o investigate the possible protective effect of thymoquinone (TQ) in cisplatin (CP) induced myocardial injury. METHODS: A total of 28 adult male Wistar-Albino rats were randomly and equally divided into four groups as follows: Group 1 (control), Group 2 (CP at 15 mg/kg dose), Group 3 (TQ 40 mg/kg/day for two days prior to CP injection and on third day, CP at 15 mg/kg dose was intraperitoneally administered and TQ treatment continued until fifth day) and Group 4 (TQ at 40mg/kg/day dose for five days). RESULTS: There was a significant increment in CP group in terms of congestion, edema and pycnotic nuclei in myocardial fibers, comparing with other groups. TQ group exhibited significant increase in expression of antiapoptotic protein Bcl-2, comparing with CP group (p<0.05). In only CP administered group, expression of antiapoptotic protein Bcl-2 was lowest comparing with other groups. CONCLUSION: Established data indicate that cisplatin is cardiotoxic and thymoquinone may be useful in treating CP-induced cardiac injury.


Subject(s)
Animals , Male , Benzoquinones/pharmacology , Cisplatin/toxicity , Cardiomyopathies/chemically induced , Cardiomyopathies/prevention & control , Antineoplastic Agents/toxicity , Antioxidants/pharmacology , Reference Values , Time Factors , Immunohistochemistry , Random Allocation , Reproducibility of Results , Benzoquinones/therapeutic use , Treatment Outcome , Rats, Wistar , Apoptosis/drug effects , Oxidative Stress/drug effects , Proto-Oncogene Proteins c-bcl-2/analysis , Proto-Oncogene Proteins c-bcl-2/drug effects , Myocytes, Cardiac/drug effects , Cardiotoxicity/etiology , Cardiotoxicity/pathology , Cardiotoxicity/prevention & control , Heart/drug effects , Cardiomyopathies/pathology , Myocardium/pathology , Antioxidants/therapeutic use
15.
Acta cir. bras ; 31(3): 190-197, Mar. 2016. tab, graf
Article in English | LILACS | ID: lil-777097

ABSTRACT

ABSTRACT PURPOSE: To investigate the effects of Borage oil on cardiac remodeling after myocardial infarction (MI). METHODS: Male Wistar rats underwent ligation of the left coronary artery and divided into three groups: MI (control), BO-18 (18 mg/kg of borage oil) and BO-180 (180 mg/kg of borage oil). After seven days, heart was arrested in diastole and processed for histological evaluation of: MI size, LV dilation, myocyte hypertrophy, inflammatory infiltration and fibrosis in MI region and in remote region. The relative weight of the lung was used as a marker of heart failure. The MI size was comparable among groups. RESULTS: Compared to control, BO treated groups showed lower weight of heart and lungs, reduced LV dilation and myocyte hypertrophy. Hemodynamic measurements were comparable. The treatment attenuated the inflammatory infiltration and fibrosis in remote myocardium. CONCLUSION: Borage oil attenuates progression of cardiac remodeling after myocardial infarction and congestive heart failure.


Subject(s)
Animals , Male , Plant Oils/pharmacology , gamma-Linolenic Acid/pharmacology , Ventricular Remodeling/drug effects , Heart Ventricles/pathology , Anti-Inflammatory Agents/pharmacology , Myocardial Infarction/pathology , Organ Size , Fibrosis , Rats, Wistar , Models, Animal , Myocytes, Cardiac/drug effects , Heart Failure/pathology , Lung/pathology
16.
Arq. bras. cardiol ; 106(1): 18-25, Jan. 2016. tab, graf
Article in Portuguese | LILACS | ID: lil-771049

ABSTRACT

Abstract Background: Although the beneficial effects of resistance training (RT) on the cardiovascular system are well established, few studies have investigated the effects of the chronic growth hormone (GH) administration on cardiac remodeling during an RT program. Objective: To evaluate the effects of GH on the morphological features of cardiac remodeling and Ca2+ transport gene expression in rats submitted to RT. Methods: Male Wistar rats were divided into 4 groups (n = 7 per group): control (CT), GH, RT and RT with GH (RTGH). The dose of GH was 0.2 IU/kg every other day for 30 days. The RT model used was the vertical jump in water (4 sets of 10 jumps, 3 bouts/wk) for 30 consecutive days. After the experimental period, the following variables were analyzed: final body weight (FBW), left ventricular weight (LVW), LVW/FBW ratio, cardiomyocyte cross-sectional area (CSA), collagen fraction, creatine kinase muscle-brain fraction (CK-MB) and gene expressions of SERCA2a, phospholamban (PLB) and ryanodine (RyR). Results: There was no significant (p > 0.05) difference among groups for FBW, LVW, LVW/FBW ratio, cardiomyocyte CSA, and SERCA2a, PLB and RyR gene expressions. The RT group showed a significant (p < 0.05) increase in collagen fraction compared to the other groups. Additionally, the trained groups (RT and RTGH) had greater CK-MB levels compared to the untrained groups (CT and GH). Conclusion: GH may attenuate the negative effects of RT on cardiac remodeling by counteracting the increased collagen synthesis, without affecting the gene expression that regulates cardiac Ca2+ transport.


Resumo Fundamento: Apesar de os efeitos benéficos do treinamento resistido (TR) sobre o sistema cardiovascular estarem bem estabelecidos, poucos estudos têm investigado os efeitos crônicos da administração de hormônio do crescimento (GH) sobre a remodelação cardíaca durante um programa de TR. Objetivo: avaliar os efeitos do GH sobre a remodelação cardíaca em suas características morfológicas e na expressão dos genes do trânsito de Ca2+ em ratos submetidos ao TR. Métodos: Ratos Wistar machos foram divididos em 4 grupos (n = 7 por grupo): controle (CT), GH, TR e TR com GH (TRGH). A dose de GH foi de 0,2 UI/kg, a cada dois dias, por 30 dias. O modelo de TR utilizado foi o salto vertical em água (4 séries de 10 saltos, 3 vezes/semana) durante 30 dias consecutivos. Após o período experimental, as seguintes variáveis foram analisadas: peso corporal final (PCF), peso do ventrículo esquerdo (PVE), razão PVE/PCF, área seccional de cardiomiócitos (ASC), fração de colágeno, creatina quinase fração músculo-cérebro (CK-MB) e expressão gênica de SERCA2a, fosfolambam (PLB) e rianodina (RyR). Resultados: Não houve diferença significativa (p > 0,05) entre os grupos para PCF, PVE, razão PVE/PCF, ASC, e expressão gênica de SERCA2a, PLB e RyR. O grupo TR mostrou um significativo aumento (p < 0,05) da fração de colágeno em comparação aos outros. Além disso, os grupos treinados (TR e TRGH) apresentaram maiores níveis de CK-MB em comparação aos não treinados (CT e GH). Conclusão: Esses resultados indicam que o GH pode atenuar os efeitos negativos do TR na remodelação cardíaca por contrabalançar o aumento da síntese de colágeno, sem afetar a expressão de genes que regulam o trânsito de Ca2+ cardíaco.


Subject(s)
Animals , Male , Growth Hormone/pharmacology , Resistance Training/methods , Ventricular Remodeling/drug effects , Body Weight , Calcium-Binding Proteins/analysis , Calcium/metabolism , Collagen/analysis , Collagen/drug effects , Creatine Kinase, BB Form/blood , Creatine Kinase, BB Form/drug effects , Gene Expression , Heart Ventricles/drug effects , Myocytes, Cardiac/drug effects , Organ Size , Polymerase Chain Reaction , Rats, Wistar , Ryanodine/analysis , Sarcoplasmic Reticulum Calcium-Transporting ATPases/analysis , Sarcoplasmic Reticulum Calcium-Transporting ATPases/drug effects , Time Factors , Ventricular Remodeling/genetics
17.
Article in English | WPRIM | ID: wpr-110767

ABSTRACT

The protective effect of aspirin during exposure to heat stress in broiler chickens was investigated. We assayed pathological damage, expression and distribution of Hsp90 protein and hsp90 mRNA expression in chicken heart tissues after oral administration of aspirin following exposure to high temperature for varying times. Heat stress induced increases in plasma aspartate aminotransferase, creatine kinase and lactate dehydrogenase activities while causing severe heart damage, which was characterized by granular and vacuolar degeneration, nuclear shrinkage and even myocardium fragmentation in cardiac muscle fibers. After aspirin administration, myocardial cells showed fewer pathological lesions than broilers treated with heat alone. A high positive Hsp90 signal was always detected in the nuclei of myocardial cells from broilers treated with aspirin, while in myocardial cells treated with heat alone, Hsp90 in the nuclei decreased, as did that in the cytoplasm. Aspirin induced rapid and significant synthesis of Hsp90 before and at the initial phase of heat stress, and significant expression of hsp90 mRNA was stimulated throughout the experiment when compared with cells exposed to heat stress alone. Thus, specific pre-induction of Hsp90 in cardiovascular tissue was useful for resisting heat stress damage because it produced stable damage-related enzymes and fewer pathologic changes.


Subject(s)
Animals , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Aspirin/pharmacology , Cell Nucleus/genetics , Chickens , Gene Expression Regulation/drug effects , HSP90 Heat-Shock Proteins/genetics , Hot Temperature , Myocytes, Cardiac/drug effects , Stress, Physiological/drug effects
18.
Braz. j. med. biol. res ; 49(6): e5273, 2016. tab, graf
Article in English | LILACS | ID: biblio-951687

ABSTRACT

The present study tested the hypotheses that i) transforming growth factor beta 1 (TGF-β1) enhances differentiation of rat bone marrow mesenchymal stem cells (MSCs) towards the cardiomyogenic phenotype and ii) intramyocardial implantation of the TGF-β1-treated MSCs improves cardiac function in heart failure rats. MSCs were treated with different concentrations of TGF-β1 for 72 h, and then morphological characteristics, surface antigens and mRNA expression of several transcription factors were assessed. Intramyocardial implantation of these TGF-β1-treated MSCs to infarcted heart was also investigated. MSCs were initially spindle-shaped with irregular processes. On day 28 after TGF-β1 treatment, MSCs showed fusiform shape, orientating parallel with one another, and were connected with adjoining cells forming myotube-like structures. Immunofluorescence revealed the expression of cardiomyocyte-specific proteins, α-sarcomeric actin and troponin T, in these cells. The mRNA expression of GATA4 and Nkx2.5 genes was slightly increased on day 7, enhanced on day 14 and decreased on day 28 while α-MHC gene was not expressed on day 7, but expressed slightly on day 14 and enhanced on day 28. Transmission electron microscopy showed that the induced cells had myofilaments, z line-like substances, desmosomes, and gap junctions, in contrast with control cells. Furthermore, intramyocardial implantation of TGF-β1-treated MSCs to infarcted heart reduced scar area and increased the number of muscle cells. This structure regeneration was concomitant with the improvement of cardiac function, evidenced by decreased left ventricular end-diastolic pressure, increased left ventricular systolic pressure and increased maximal positive pressure development rate. Taken together, these results indicate that intramyocardial implantation of differentiated MSCs enhanced by TGF-β1 improved cardiac function in heart failure rats.


Subject(s)
Animals , Male , Bone Marrow Transplantation/methods , Mesenchymal Stem Cell Transplantation/methods , Mesenchymal Stem Cells/drug effects , Heart Failure/surgery , Time Factors , RNA, Messenger/analysis , Cell Differentiation , Polymerase Chain Reaction , Reproducibility of Results , Treatment Outcome , Myosin Heavy Chains/analysis , Myocytes, Cardiac/drug effects , Microscopy, Electron, Transmission , GATA4 Transcription Factor/analysis , Homeobox Protein Nkx-2.5/analysis
19.
Arch. endocrinol. metab. (Online) ; 59(2): 141-147, 04/2015. tab, graf
Article in English | LILACS | ID: lil-746464

ABSTRACT

Objective Investigate the effect of GC-1 on tolerance to exercise in rats with experimental hypothyroidism. Materials and methods Hypothyroidism was induced with methimazole sodium and perchlorate treatment. Six groups with eight animals were studied: control group (C), hypothyroid group without treatment (HYPO); hypothyroidism treated with physiological doses of tetraiodothyronine (T4) or 10 times higher (10×T4); hypothyroidism treated with equal molar doses of GC-1 (GC-1) or 10 times higher (10×GC-1). After eight weeks, each animal underwent an exercise tolerance test by measuring the time (seconds), in which the rats were swimming with a load attached to their tails without being submerging for more than 10 sec. After the test, the animals were killed, and blood samples were collected for biochemical analysis, and the heart and soleus muscle were removed for weighing and morphometric analysis of the cardiomyocyte. Results Hypothyroidism significantly reduced tolerance to exercise and, treatment with GC-1 1× or T4 in physiological doses recover tolerance test to normal parameters. However, high doses of T4 also decreased tolerance to physical exercise. Conversely, ten times higher doses of GC-1 did not impair tolerance to exercise. Interestingly, hypothyroidism, treated or not with T4 in a physiological range, GC-1 or even high doses of GC-1 (10X) did not change cardiomyocyte diameters and relative weight of the soleus muscle. In contrast, higher doses of T4 significantly increased cardiomyocyte diameter and induced atrophy of the soleus muscle. Conclusion Unlike T4, GC-1 in high doses did not modify tolerance to physical exercise in the rats with hypothyroidism. .


Subject(s)
Animals , Acetates/pharmacology , Exercise Tolerance/drug effects , Hypothyroidism/drug therapy , Phenols/pharmacology , Thyroid Hormone Receptors beta/agonists , Exercise Tolerance/physiology , Hypothyroidism/blood , Hypothyroidism/chemically induced , Hypothyroidism/physiopathology , Methimazole , Muscle, Skeletal/drug effects , Myocytes, Cardiac/drug effects , Perchlorates , Rats, Wistar , Sodium Compounds , Swimming , Thyrotropin/blood , Thyroxine/administration & dosage , Thyroxine/blood , Triiodothyronine/blood
20.
Cad. saúde pública ; 31(3): 586-596, 03/2015. tab
Article in Portuguese | LILACS | ID: lil-744827

ABSTRACT

O objetivo deste estudo foi identificar fatores associados à utilização dos serviços odontológicos, públicos (básicos e especializados) e privados. Foi realizado inquérito populacional de base domiciliar em dois municípios da Bahia, Brasil. Informantes-chave forneceram dados socioeconômicos e de utilização dos serviços odontológicos (desfecho). A organização do serviço público odontológico local foi classificada em pior/melhor. Realizou-se regressão logística politômica uni e múltipla. Do total de 1.290 indivíduos, 38,76% usaram o serviço privado, 33,80% atenção básica e 17,29% atenção básica e o Centro de Especialidades Odontológicas (CEO). Um perfil de vulnerabilidade social foi associado ao uso do serviço público, quando comparado ao privado. Menor escolaridade (OR = 1,47; IC95%: 1,03-2,10) e pior organização do serviço (OR = 1,74; IC95%: 1,22-2,48) foram associados ao menor uso da rede de serviços atenção básica e CEO em comparação ao uso exclusivo da atenção básica. A desigualdade na utilização dos serviços odontológicos foi observada mesmo quando comparados grupos mais homogêneos, como os usuários dos serviços públicos.


The aim of this study was to identify factors associated with the use of primary and specialized public dental health services and private services. A population-based household survey was conducted in two cities of Bahia State, Brazil. Key informants provided data on socioeconomic variables and use of dental health services. Organization of the local public dental health service was ranked as worse versus better. Univariate and multivariate polytomous logistic regression was performed. Of the total of 1,290 individuals, 38.76% used private services, 33.80% used public primary care, and 17.29% used both primary care and the Center for Dental Specialties. Less use of both primary care and specialized public services was associated with lower education (OR = 1.47; 95%CI: 1.03-2.10) and worse organization of services (OR = 1.74; 95%CI: 1.22-2.48), when compared to the exclusive use of primary care. The study showed inequality in the use of dental services, even when comparing more homogeneous groups, namely users of public services.


El objetivo de este estudio fue identificar los factores asociados al uso de los servicios odontológicos (primarios y especializados) públicos y privados. Se realizó una encuesta poblacional en dos ciudades de Bahía, Brasil. Los informantes clave contestaron cuestiones socioeconómicas y de utilización de los servicios odontológicos (resultado). La organización de los servicios odontológicos públicos locales fue clasificada en peor/mejor. Se realizó regresión simple y múltiple con variable politómica. Del total de 1.290 personas, un 38,76% utilizaron el servicio privado, un 33,80% la atención primaria y un 17,29% atención primaria y el Centro de Especialidades Dentales (CED). Una menor escolaridad (OR = 1,47; IC95%: 1.03-2.10) y una peor organización de servicio (OR = 1,74; IC95%: 1,22-2,48) se asociaron con un menor uso de la red de servicios de atención primaria y CED, en comparación con el uso exclusivo de la atención primaria. La desigualdad en el uso de los servicios dentales se observó incluso cuando se comparan grupos más homogéneos, como usuarios de servicios públicos.


Subject(s)
Animals , Rabbits , Action Potentials/physiology , Membrane Potentials/physiology , Myocytes, Cardiac/physiology , Potassium/metabolism , Tacrolimus Binding Proteins/metabolism , Ventricular Function, Left/drug effects , Action Potentials/drug effects , Cells, Cultured , Membrane Potentials/drug effects , Myocytes, Cardiac/drug effects , Up-Regulation/physiology
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