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1.
Acta Physiologica Sinica ; (6): 878-884, 2021.
Article in Chinese | WPRIM | ID: wpr-921291

ABSTRACT

The aim of the present study was to investigate the protective effect of propofol on the experimental myocardial infarction in rats. The myocardial infarction model was established by ligating the anterior descending branch of left coronary artery in rats. Model rats were treated with propofol. Cardiac function was evaluated by echocardiography. Cardiac hemodynamic changes were detected by multiconductor biorecorder. Pathological changes in the infarcted myocardia were detected by HE staining. The expression levels of cardiac hypertrophy marker genes and fibrosis marker proteins were analyzed by real-time quantitative PCR and Western blot. The results showed that, compared with the sham surgery group, the model group exhibited larger infarct size (> 40%), impaired heart function, and significantly increased left ventricular end-diastolic pressure (LVEDP). Propofol reduced cardiac function impairment and decreased LVEDP in the model group. Propofol significantly reduced lung weight/body weight ratio, heart weight/body weight ratio, left ventricular weight/body weight ratio and left atrial weight/body weight ratio in the model group. Furthermore, after myocardial infarction, the administration of propofol significantly improved the diastolic strain rate, down-regulated the mRNA expression levels of myocardial hypertrophy markers, atrial natriuretic peptide and β-myosin heavy chain, and reversed the up-regulation of matrix metalloproteinase 2 (MMP2), MMP9 and tissue inhibitor of metalloproteinase-2 (TIMP-2) induced by myocardial infarction. These results suggest propofol can reduce adverse ventricular remodeling, cardiac dysfunction, myocardial hypertrophy and fibrosis after myocardial infarction, and has protective effect against the experimental myocardial infarction induced by coronary artery ligation in rats.


Subject(s)
Animals , Cardiotonic Agents/pharmacology , Matrix Metalloproteinase 2 , Matrix Metalloproteinase 9 , Myocardial Infarction/drug therapy , Myocardium , Propofol/pharmacology , Rats , Tissue Inhibitor of Metalloproteinase-2/genetics , Ventricular Remodeling
2.
Article in English | WPRIM | ID: wpr-881036

ABSTRACT

Cardiovascular disease is the main cause of mortality and morbidity in the world, especially in developing countries. Drug therapy is one of the main ways to treat cardiovascular diseases. Among them, great progress has been made in the treatment of cardiovascular diseases with traditional Chinese medicine. In terms of experimental research, the mechanism of traditional Chinese medicine in the treatment of cardiovascular diseases has been thoroughly discussed in vitro and in vivo. In terms of clinical treatment, traditional Chinese medicine with flavonoids, saponins and alkaloids as the main effective components has a definite effect on the treatment of cardiovascular diseases such as arrhythmia, myocardial ischemia, angina pectoris and myocardial infarction, with high safety and good application prospects. With the further research on the effective ingredients, mechanism and adverse reactions of traditional Chinese medicine, it will be beneficial to the effectiveness of traditional Chinese medicine, reduce side effects and promote the modernization of traditional Chinese medicine. Calycosin and its derivatives, the main bioactive flavonoids in Astragalus membranaceus have multiple biological effects, such as antioxidant, pro-angiogenesis, anti-tumour, and anti-inflammatory effects. Based on the above biological effects, calycosin has been shown to have good potential for cardiovascular protection. The potent antioxidant effect of calycosin may play an important role in the cardiovascular protective potential. For injured cardiac myocytes, calycosin and its derivatives can alleviate the cell damage mainly marked by the release of myocardial enzymes and reduce the death level of cardiac myocytes mainly characterized by apoptosis through various mechanisms. For vascular endothelial cells, calycosin also has multiple effects and multiple mechanisms, such as promoting vascular endothelial cell proliferation, exerting vasodilating effect and directly affecting the synthesis function of endothelial cells. The present review will address the bioactivity of calycosin in cardiovascular diseases such as protective effects on cardiac myocytes and vascular endothelial cells and elucidate main mechanism of calycosin and its derivatives to exert the above biological effects.


Subject(s)
Apoptosis/drug effects , Cardiotonic Agents/pharmacology , Cardiovascular Diseases/drug therapy , Cell Proliferation/drug effects , Drugs, Chinese Herbal/pharmacology , Humans , Isoflavones/pharmacology , Medicine, Chinese Traditional , Muscle Cells/drug effects
3.
Acta cir. bras ; 34(11): e201901104, Nov. 2019. graf
Article in English | LILACS | ID: biblio-1054677

ABSTRACT

Abstract Purpose: Myocardial ischemia/reperfusion (Ml/R) injury is a leading cause of damage in cardiac tissues, with high rates of mortality and disability. Biochanin A (BCA) is a main constituent of Trifolium pratense L. This study was intended to explore the effect of BCA on Ml/R injury and explore the potential mechanism. Methods: In vivo MI/R injury was established by transient coronary ligation in Sprague-Dawley rats. Triphenyltetrazolium chloride staining (TTC) was used to measure myocardial infarct size. ELISA assay was employed to evaluate the levels of myocardial enzyme and inflammatory cytokines. Western blot assay was conducted to detect related protein levels in myocardial tissues. Results: BCA significantly ameliorated myocardial infarction area, reduced the release of myocardial enzyme levels including aspartate transaminase (AST), creatine kinase (CK-MB) and lactic dehydrogenase (LDH). It also decreased the production of inflammatory cytokines (IL-1β, IL-18, IL-6 and TNF-α) in serum of Ml/R rats. Further mechanism studies demonstrated that BCA inhibited inflammatory reaction through blocking TLR4/NF-kB/NLRP3 signaling pathway. Conclusion: The present study is the first evidence demonstrating that BCA attenuated Ml/R injury through suppressing TLR4/NF-kB/NLRP3 signaling pathway-mediated anti-inflammation pathway.


Subject(s)
Animals , Male , Cardiotonic Agents/pharmacology , Myocardial Reperfusion Injury/prevention & control , NF-kappa B/drug effects , Genistein/pharmacology , Toll-Like Receptor 4/drug effects , NLR Family, Pyrin Domain-Containing 3 Protein/drug effects , Aspartate Aminotransferases/blood , Reference Values , Myocardial Reperfusion Injury/metabolism , Signal Transduction/drug effects , Blotting, Western , Reproducibility of Results , Cytokines/blood , NF-kappa B/metabolism , Rats, Sprague-Dawley , Creatine Kinase/blood , Lactate Dehydrogenases/blood , Toll-Like Receptor 4/metabolism , Anti-Inflammatory Agents/pharmacology
4.
Acta cir. bras ; 34(11): e201901106, Nov. 2019. tab, graf
Article in English | LILACS | ID: biblio-1054683

ABSTRACT

Abstract Purpose: To investigate whether GDF11 ameliorates myocardial ischemia reperfusion (MIR) injury in diabetic rats and explore the underlying mechanisms. Methods: Diabetic and non-diabetic rats subjected to MIR (30 min of coronary artery occlusion followed by 120 min of reperfusion) with/without GDF11 pretreatment. Cardiac function, myocardial infarct size, creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), superoxide dismutase (SOD) 15-F2tisoprostane, autophagosome, LC3II/I ratio and Belcin-1 level were determined to reflect myocardial injury, oxidative stress and autophagy, respectively. In in vitro study, H9c2 cells cultured in high glucose (HG, 30mM) suffered hypoxia reoxygenation (HR) with/without GDF11, hydrogen peroxide (H2O2) and autophagy inhibitor 3-methyladenine (3-MA) treatment, cell injury; oxidative stress and autophagy were assessed. Results: Pretreatment with GDF11 significantly improved cardiac morphology and function in diabetes, concomitant with decreased arrhythmia severity, infarct size, CK-MB, LDH and 15-F2tisoprostane release, increased SOD activity and autophagy level. In addition, GDF11 notably reduced HR injury in H9c2 cells with HG exposure, accompanied by oxidative stress reduction and autophagy up-regulation. However, those effects were completely reversed by H2O2 and 3-MA. Conclusion: GDF11 can provide protection against MIR injury in diabetic rats, and is implicated in antioxidant stress and autophagy up-regulation.


Subject(s)
Animals , Male , Autophagy/drug effects , Myocardial Reperfusion Injury/metabolism , Myocardial Reperfusion Injury/drug therapy , Oxidative Stress/drug effects , Diabetes Mellitus, Type 1/metabolism , Growth Differentiation Factors/pharmacology , Reference Values , Superoxide Dismutase/analysis , Cardiotonic Agents/pharmacology , Myocardial Reperfusion Injury/pathology , Up-Regulation/drug effects , Cell Line , Blotting, Western , Reproducibility of Results , Rats, Sprague-Dawley , Streptozocin , Microscopy, Electron, Transmission , Diabetes Mellitus, Experimental/metabolism , Hemodynamics/drug effects , Antioxidants/pharmacology
5.
Acta cir. bras ; 34(5): e201900505, 2019. graf
Article in English | LILACS | ID: biblio-1010872

ABSTRACT

Abstract Purpose: To evaluate the cardioprotective response of the pharmacological modulation of β-adrenergic receptors (β-AR) in animal model of cardiac ischemia and reperfusion (CIR), in spontaneously hypertensive (SHR) and normotensive (NWR) rats. Methods: CIR was induced by the occlusion of left anterior descendent coronary artery (10 min) and reperfusion (75 min). The SHR was treated with β-AR antagonist atenolol (AT, 10 mg/kg, IV) 5 min before CIR, and NWR were treated with β-AR agonist isoproterenol (ISO, 0.5 mg/kg, IV) 5 min before CIR. Results: The treatment with AT increased the incidence of VA, AVB and LET in SHR, suggesting that spontaneous cardioprotection in hypertensive animals was abolished by blockade of β-AR. In contrast, the treatment with ISO significantly reduced the incidence of ventricular arrhythmia, atrioventricular blockade and lethality in NWR (30%, 20% and 20%, respectively), suggesting that the activation of β-AR stimulate cardioprotection in normotensive animals. Serum CK-MB were higher in SHR/CIR and NWR/CIR compared to respective SHAM group (not altered by treatment with AT or ISO). Conclusion: The pharmacological modulation of β-AR could be a new cardioprotective strategy for the therapy of myocardial dysfunctions induced by CIR related to cardiac surgery and cardiovascular diseases.


Subject(s)
Animals , Male , Atenolol/pharmacology , Cardiotonic Agents/pharmacology , Myocardial Reperfusion Injury/drug therapy , Receptors, Adrenergic, beta/drug effects , Adrenergic beta-Agonists/pharmacology , Adrenergic beta-1 Receptor Antagonists/pharmacology , Isoproterenol/pharmacology , Rats, Inbred SHR , Time Factors , Blood Pressure/drug effects , Biomarkers/blood , Myocardial Reperfusion Injury/physiopathology , Myocardial Reperfusion Injury/blood , Reproducibility of Results , Treatment Outcome , Creatine Kinase, MB Form/blood , Heart Function Tests
6.
Rev. Assoc. Med. Bras. (1992) ; 64(8): 745-754, Aug. 2018. tab, graf
Article in English | LILACS | ID: biblio-976841

ABSTRACT

SUMMARY OBJECTIVES This study aimed at assessing the role of beta-blockers on preventing anthracycline-induced cardiotoxicity in adults. METHODS A systematic review was performed on electronic databases, including relevant studies that analysed beta-blockers as cardioprotective agents before the use of anthracyclines by adult oncologic patients. RESULTS After application of eligibility and selection criteria, eight articles were considered as high quality, complying with the proposed theme; all eight clinical trials, four of them placebo-controlled, with a total number of 655 patients included. From this sample, 281 (42.9%) used beta-blocker as intervention, and carvedilol was the most frequent (167 patients - 25.5%). Six studies were considered positive regarding the cardioprotection role played by beta-blockers, although only four demonstrated significant difference on left ventricle ejection fraction after chemotherapy on groups that used beta-blockers compared to control groups. Carvedilol and nebivolol, but not metoprolol, had positive results regarding cardioprotection. Other beta-blockers were not analysed in the selected studies. CONCLUSIONS Despite the potential cardioprotective effect of beta-blockers, as demonstrated in small and unicentric clinical trials, its routine use on prevention of anthracycline-associated cardiotoxicity demands greater scientific evidence.


RESUMO OBJETIVO Este estudo teve como objetivo analisar o papel dos betabloqueadores na prevenção da cardiotoxicidade induzida pelas antraciclinas em adultos. MÉTODOS Foi realizada uma revisão sistemática em bases de dados eletrônicos, incluindo os estudos relevantes que analisaram fármacos betabloqueadores como agentes cardioprotetores antes do início do uso de antraciclinas por pacientes oncológicos adultos. RESULTADOS Após aplicação dos critérios de elegibilidade e seleção, foram obtidos oito artigos considerados de boa qualidade, que se adequavam à temática proposta, sendo todos ensaios clínicos, quatro placebo-controlados, totalizando 655 pacientes incluídos. Destes, 281 (42,9%) fizeram uso de algum betabloqueador como intervenção, sendo o carvedilol o mais utilizado (167 pacientes - 25,5%). Seis estudos foram considerados positivos quanto à cardioproteção exercida pelos betabloqueadores, porém apenas quatro demonstraram diferença na fração de ejeção do ventrículo esquerdo após a quimioterapia nos grupos que usaram betabloqueadores em relação aos grupos controle. O carvedilol e o nebivolol, mas não o metoprolol, tiveram resultados positivos quanto à cardioproteção. Outros betabloqueadores não foram avaliados nos estudos incluídos. CONCLUSÕES Apesar de haver um potencial efeito cardioprotetor dos betabloqueadores, conforme demonstrado em ensaios clínicos pequenos e unicêntricos, sua utilização rotineira na prevenção da cardiotoxicidade associada às antraciclinas requer maiores comprovações científicas.


Subject(s)
Humans , Adult , Cardiotonic Agents/pharmacology , Adrenergic beta-Antagonists/pharmacology , Anthracyclines/adverse effects , Heart Diseases/chemically induced , Heart Diseases/prevention & control , Stroke Volume , Cardiotonic Agents/therapeutic use , Reproducibility of Results , Adrenergic beta-Antagonists/therapeutic use , Cardiotoxicity/prevention & control , Carvedilol/therapeutic use , Carvedilol/pharmacology
7.
Rev. bras. cir. cardiovasc ; 33(3): 258-264, May-June 2018. tab, graf
Article in English | LILACS | ID: biblio-958409

ABSTRACT

Abstract Objective: The injury-reducing effect of acetaminophen, an effective analgesic and antipyretic on ischemia-reperfusion continues to attract great attention. This study analyzed the protective effect of acetaminophen on myocardial injury induced by ischemia-reperfusion in an experimental animal model from lower extremity ischemia-reperfusion. Methods: Twenty-four Sprague-Dawley female rats were randomized into three groups (n=8) as (i) control group (only laparotomy), (ii) aortic ischemia-reperfusion group (60 min of ischemia and 120 min of reperfusion) and (iii) ischemia-reperfusion + acetaminophen group (15 mg/kg/h intravenous acetaminophen infusion starting 15 minutes before the end of the ischemic period and lasting till the end of the reperfusion period). Sternotomy was performed in all groups at the end of the reperfusion period and the heart was removed for histopathological examination. The removed hearts were histopathologically investigated for myocytolysis, polymorphonuclear leukocyte (PMNL) infiltration, myofibrillar edema and focal hemorrhage. Results: The results of histopathological examination showed that acetaminophen was detected to particularly diminish focal hemorrhage and myofibrillar edema in the ischemia-reperfusion + acetaminophen group (P<0.001, P=0.011), while there were no effects on myocytolysis and PMNL infiltration between the groups (P=1.000, P=0.124). Conclusion: Acetaminophen is considered to have cardioprotective effect in rats, by reducing myocardial injury induced by abdominal aortic ischemia-reperfusion.


Subject(s)
Humans , Animals , Female , Cardiotonic Agents/pharmacology , Myocardial Reperfusion Injury/prevention & control , Lower Extremity/blood supply , Acetaminophen/pharmacology , Aorta, Abdominal/pathology , Reference Values , Time Factors , Myocardial Reperfusion Injury/pathology , Random Allocation , Rats, Sprague-Dawley , Constriction , Disease Models, Animal , Edema, Cardiac/pathology , Ischemia/prevention & control , Ischemia/blood , Myofibrils/pathology
8.
Acta cir. bras ; 33(6): 524-532, June 2018. graf
Article in English | LILACS | ID: biblio-949352

ABSTRACT

Abstract Purpose: To evaluate in vivo animal model of cardiac ischemia/reperfusion the cardioprotective activity of pancreatic lipase inhibitor of the orlistat. Methods: Adult male Wistar rats were anesthetized, placed on mechanical ventilation and underwent surgery to induce cardiac I/R by obstructing left descending coronary artery followed by reperfusion to evaluation of ventricular arrhythmias (VA), atrioventricular block (AVB) and lethality (LET) with pancreatic lipase inhibitor orlistat (ORL). At the end of reperfusion, blood samples were collected for determination of triglycerides (TG), very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), high-density lipoprotein (HDL), lactate dehydrogenase (LDH), creatine kinase (CK), and creatine kinase-MB (CK-MB). Results: Treatment with ORL has been able to decrease the incidence of VA, AVB and LET. Besides that, treatment with ORL reduced serum concentrations of CK and LDL, but did not alter the levels of serum concentration of TG, VLDL and HDL. Conclusion: The reduction of ventricular arrhythmias, atrioventricular block, and lethality and serum levels of creatine kinase produced by treatment with orlistat in animal model of cardiac isquemia/reperfusion injury suggest that ORL could be used as an efficient cardioprotective therapeutic strategy to attenuate myocardial damage related to acute myocardial infarction.


Subject(s)
Animals , Male , Cardiotonic Agents/pharmacology , Myocardial Reperfusion Injury/prevention & control , Lactones/pharmacology , Myocardial Infarction/prevention & control , Arrhythmias, Cardiac/prevention & control , Triglycerides/blood , Myocardial Reperfusion Injury/blood , Random Allocation , Reproducibility of Results , Risk Factors , Treatment Outcome , Rats, Wistar , Creatine Kinase/blood , Electrocardiography , Atrioventricular Block/prevention & control , L-Lactate Dehydrogenase/blood , Lipoproteins, HDL/blood , Lipoproteins, LDL/blood , Lipoproteins, VLDL/blood , Myocardial Infarction/blood
9.
Acta cir. bras ; 33(2): 117-124, Feb. 2018. tab, graf
Article in English | LILACS | ID: biblio-886260

ABSTRACT

Abstract Purpose: To observe the efficacy of phosphocreatine pre-administration (PCr-PA) on X-linked inhibitor of apoptosis protein (XIAP), the second mitochondia-derived activator of caspase (Smac) and apoptosis in the ischemic penumbra of rats with focal cerebral ischemia-reperfusion injury (CIRI). Methods: A total of 60 healthy male Sprague Dawley (SD) rats were randomly divided into three groups (n=20): group A (the sham operation group), group B <intraperitoneally injected with 20 mg/kg (10 mg/ml) of saline before preparing the ischemia-reperfusion (IR) model>, and group C <intraperitoneally injected with 20 mg/kg (10 mg/ml) of PCr immediately before preparing the IR model>. After 24 h for reperfusion, the neurological function was evaluated and the tissue was sampled to detect expression of XIAP, Smac and caspase-3 positive cells in the ischemic penumbra so as to observe the apoptosis. Results: Compared with group B, neurological deficit scores, numbers of apoptotic cells, expression of Smac,caspase-9 and the numbers of Caspase-3 positive cells were decreased while expression of XIAP were increased in the ischemic penumbra of group C. Conclusions: Phosphocreatine pre-administration may elicit neuroprotective effects in the brain by increasing expression of X-linked inhibitor of apoptosis protein, reducing expression of second mitochondia-derived activator of caspase, and inhibiting the apoptosis in the ischemic penumbra.


Subject(s)
Humans , Animals , Male , Rats , Phosphocreatine/pharmacology , Cardiotonic Agents/pharmacology , Reperfusion Injury/metabolism , Brain Ischemia/metabolism , Mitochondrial Proteins/metabolism , Intracellular Signaling Peptides and Proteins/metabolism , X-Linked Inhibitor of Apoptosis Protein/metabolism , Random Allocation , Brain Ischemia/prevention & control , Rats, Sprague-Dawley , Apoptosis/drug effects , Neuroprotective Agents/pharmacology , Disease Models, Animal , Drug Evaluation, Preclinical , Apoptosis Regulatory Proteins , Caspase 3/metabolism
10.
Biol. Res ; 51: 34, 2018. tab, graf
Article in English | LILACS | ID: biblio-983938

ABSTRACT

BACKGROUND AND AIMS: Atherosclerotic cardiovascular disease is highly prevalent and its underlying pathogenesis involves dyslipidemia including pro-atherogenic high density lipoprotein (HDL) remodeling. Vitamins C and E have been proposed as atheroprotective agents for cardiovascular disease management. However, their effects and benefits on high density lipoprotein function and remodeling are unknown. In this study, we evaluated the role of vitamin C and E on non HDL lipoproteins as well as HDL function and remodeling, along with their effects on inflammation/ oxidation biomarkers and atherosclerosis in atherogenic diet-fed SR-B1 KO/ApoER61h/h mice. METHODS AND RESULTS: Mice were pre-treated for 5 weeks before and during atherogenic diet feeding with vitamin C and E added to water and diet, respectively. Compared to a control group, combined vitamin C and E administration reduced serum total cholesterol and triglyceride levels by decreasing apo B-48-containing lipoproteins, remodeled HDL particles by reducing phospholipid as well as increasing PON1 and apo D content, and diminished PLTP activity and levels. Vitamin supplementation improved HDL antioxidant function and lowered serum TNF-α levels. Vitamin C and E combination attenuated atherogenesis and increased lifespan in atherogenic diet-fed SR-B1 KO/ApoER61h/h mice. CONCLUSIONS: Vitamin C and E administration showed significant lipid metabolism regulating effects, including HDL remodeling and decreased levels of apoB-containing lipoproteins, in mice. In addition, this vitamin supplementation generated a cardioprotective effect in a murine model of severe and lethal atherosclerotic ischemic heart disease.


Subject(s)
Animals , Male , Female , Ascorbic Acid/pharmacology , Vitamin E/pharmacology , Myocardial Ischemia/prevention & control , Apolipoprotein B-48/drug effects , Hyperlipidemias/prevention & control , Lipoproteins, HDL/drug effects , Antioxidants/pharmacology , Reference Values , Coronary Artery Disease/prevention & control , Coronary Artery Disease/blood , Enzyme-Linked Immunosorbent Assay , Cardiotonic Agents/pharmacology , Immunoblotting , Reproducibility of Results , Cytokines/blood , Treatment Outcome , Myocardial Ischemia/blood , Dietary Supplements , Phospholipid Transfer Proteins/blood , Diet, Atherogenic , Scavenger Receptors, Class B/drug effects , Scavenger Receptors, Class B/blood , Lipid Metabolism/drug effects , Apolipoprotein B-48/blood , Hyperlipidemias/blood , Lipoproteins, HDL/blood , Mice, Inbred C57BL
11.
Rev. bras. ter. intensiva ; 29(4): 490-498, out.-dez. 2017. graf
Article in Portuguese | LILACS | ID: biblio-899547

ABSTRACT

RESUMO A dobutamina é o inotrópico mais comumente utilizado em pacientes com choque séptico, com o objetivo de aumentar o débito cardíaco e corrigir a hipoperfusão. Embora alguns ensaios clínicos tenham demonstrado que a dobutamina pode melhorar a hemodinâmica sistêmica e regional, outras pesquisas identificaram que seus efeitos são heterogêneos e imprevisíveis. Nesta revisão, analisamos as propriedades farmacodinâmicas da dobutamina e seus efeitos fisiológicos. Nosso objetivo foi demonstrar que os efeitos da dobutamina podem diferir entre voluntários saudáveis, estudos experimentais e insuficiência cardíaca clínica, em modelos de estudo em animais e em pacientes com choque séptico. Discutimos as evidências que suportam a afirmativa de que a dobutamina utilizada no tratamento do choque séptico frequentemente se comporta como fármaco cronotrópico e vasodilatador, sem evidências de ação inotrópica. Como seus efeitos colaterais são muito comuns e os benefícios terapêuticos não são claros, sugerimos que ela deve ser utilizada com cautela no choque séptico. Antes de uma decisão terapêutica definitiva, a eficácia e a tolerabilidade da dobutamina devem ser avaliadas por um tempo curto com monitoramento estrito de seus efeitos positivos e efeitos colaterais negativos.


ABSTRACT Dobutamine is the inotrope most commonly used in septic shock patients to increase cardiac output and correct hypoperfusion. Although some experimental and clinical studies have shown that dobutamine can improve systemic and regional hemodynamics, other research has found that its effects are heterogenous and unpredictable. In this review, we analyze the pharmacodynamic properties of dobutamine and its physiologic effects. Our goal is to show that the effects of dobutamine might differ between healthy subjects, in experimental and clinical cardiac failure, in animal models and in patients with septic shock. We discuss evidence supporting the claim that dobutamine, in septic shock, frequently behaves as a chronotropic and vasodilatory drug, without evidence of inotropic action. Since the side effects are very common, and the therapeutic benefits are unclear, we suggest that dobutamine should be used cautiously in septic shock. Before a definitive therapeutic decision, the efficacy and tolerance of dobutamine should be assessed during a brief time with close monitoring of its positive and negative side effects.


Subject(s)
Humans , Animals , Shock, Septic/drug therapy , Cardiotonic Agents/pharmacology , Dobutamine/pharmacology , Shock, Septic/physiopathology , Cardiac Output/drug effects , Cardiotonic Agents/adverse effects , Drug Monitoring/methods , Dobutamine/adverse effects , Hemodynamics/drug effects
12.
Acta cir. bras ; 31(7): 456-462, tab, graf
Article in English | LILACS | ID: lil-787264

ABSTRACT

ABSTRACT PURPOSE: To investigate the protective effect of β-myrcene (MYR) on oxidative and histological damage in mice heart tissue caused global cerebral ischemia/reperfusion (IR) in C57BL/J6 mice. METHODS: Animals(n=40) were randomly divided into four groups: (1)control, (2)IR, (3)MYR and (4)MYR+IR. The control group was received 0.1% carboxymethyl cellulose as a vehicle following a medial incision without carotid occlusion. In the IR group, the bilateral carotid arteries were clipped for 15min, and treated with the vehicle intraperitoneally(ip) for 10 days. MYR (200mg/kg) was received dissolved in 0.1%CMC for 10 days. In the MYR+IR group, the IR model was applied exactly as in the IR group, and then they were treated with MYR 10 days. RESULTS: The cerebral IR caused oxidative damage (increase TBARS, decrease antioxidant parameters). Treatment of MYR was increased in GSH,GPx,CAT,SOD activity while TBARS level was decreased. In addition, degenerative changes in I/R group heart tissue were ameliorated by MYR administration. CONCLUSİON: The administration of β-myrcene protects oxidative and histological damage in the heart tissue after global ischemia-reperfusion and may be useful safe alternative treatment for cardiac tissue after ischemic stroke.


Subject(s)
Animals , Male , Cardiotonic Agents/pharmacology , Reperfusion Injury/complications , Brain Ischemia/complications , Monoterpenes/pharmacology , Heart/drug effects , Antioxidants/pharmacology , Superoxide Dismutase/metabolism , Catalase/metabolism , Random Allocation , Thiobarbituric Acid Reactive Substances/metabolism , Oxidative Stress/drug effects , Models, Animal , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Mice, Inbred C57BL , Myocardium/metabolism , Myocardium/pathology
13.
Arq. bras. cardiol ; 106(5): 396-403, May 2016. tab, graf
Article in English | LILACS | ID: lil-784172

ABSTRACT

Abstract Background: Tobacco smoke exposure is an important risk factor for cardiac remodeling. Under this condition, inflammation, oxidative stress, energy metabolism abnormalities, apoptosis, and hypertrophy are present. Pentoxifylline has anti‑inflammatory, anti-apoptotic, anti-thrombotic and anti-proliferative properties. Objective: The present study tested the hypothesis that pentoxifylline would attenuate cardiac remodeling induced by smoking. Methods: Wistar rats were distributed in four groups: Control (C), Pentoxifylline (PX), Tobacco Smoke (TS), and PX-TS. After two months, echocardiography, invasive blood pressure measurement, biochemical, and histological studies were performed. The groups were compared by two-way ANOVA with a significance level of 5%. Results: TS increased left atrium diameter and area, which was attenuated by PX. In the isolated heart study, TS lowered the positive derivate (+dp/dt), and this was attenuated by PX. The antioxidants enzyme superoxide dismutase and glutathione peroxidase were decreased in the TS group; PX recovered these activities. TS increased lactate dehydrogenase (LDH) and decreased 3-hydroxyacyl Coenzyme A dehydrogenases (OH-DHA) and citrate synthase (CS). PX attenuated LDH, 3-OH-DHA and CS alterations in TS-PX group. TS increased IL-10, ICAM-1, and caspase-3. PX did not influence these variables. Conclusion: TS induced cardiac remodeling, associated with increased inflammation, oxidative stress, apoptosis, and changed energy metabolism. PX attenuated cardiac remodeling by reducing oxidative stress and improving cardiac bioenergetics, but did not act upon cardiac cytokines and apoptosis.


Resumo Fundamento: Exposição à fumaça de cigarros é um fator significativo de risco para a remodelação cardíaca. Nesta condição, estão presentes inflamação, estresse oxidativo, anormalidades do metabolismo energético, apoptose e hipertrofia. A pentoxifilina tem propriedades anti-inflamatórias, anti-apoptóticas, anti-trombóticas e anti-proliferativas. Objetivo: O presente estudo testou a hipótese de que a pentoxifilina atenuaria a remodelação cardíaca induzida pelo fumo. Métodos: Ratos Wistar foram distribuídos em quatro grupos: Controle (C), Pentoxifilina (PX), Fumaça de Cigarro (FC), e PX-FC. Depois de dois meses, foram feitos ecocardiografia, medição de pressão arterial invasiva e estudos bioquímicos e histológicos. Os grupos foram comparados por ANOVA de duas vias com nível de significância de 5%. Resultados: FC aumentou o diâmetro e a área do átrio esquerdo, o que foi atenuado pela PX. No estudo de coração isolado, FC diminuiu a derivada positiva (+dp/dt), o que foi atenuado por PX. Os antioxidantes enzima superóxido-dismutase e glutationa peroxidase foram reduzidos no grupo FC; PX recuperou essas atividades. FC aumentou o lactato desidrogenase (LDH) e reduziu as desidrogenases 3-hidroxiacil Coenzima A (OH-DHA) e citrato sintase (CS). PX atenuou alterações de LDH, 3-OH-DHA e CS no grupo PX-FC. FC aumentou IL-10, ICAM-1 e caspase-3. PX não teve influência nestas variáveis. Conclusão: FC induziu remodelação cardíaca, associada a um aumento de inflamação, estresse oxidativo, apoptose e metabolismo energético alterado. PX atenuou remodelação cardíaca, reduzindo estresse oxidativo e melhorando bioenergética cardíaca, mas não agiu nas citocinas cardíacas nem na apoptose.


Subject(s)
Animals , Male , Rats , Pentoxifylline/pharmacology , Tobacco Smoke Pollution/adverse effects , Cardiotonic Agents/pharmacology , Oxidative Stress/drug effects , Ventricular Remodeling/drug effects , Heart Ventricles/drug effects , Ventricular Function , Rats, Wistar , Disease Models, Animal
14.
Arq. bras. cardiol ; 103(4): 308-314, 10/2014. tab
Article in English | LILACS | ID: lil-725316

ABSTRACT

Background: Ivabradine is a novel specific heart rate (HR)-lowering agent that improves event-free survival in patients with heart failure (HF). Objectives: We aimed to evaluate the effect of ivabradine on time domain indices of heart rate variability (HRV) in patients with HF. Methods: Forty-eight patients with compensated HF of nonischemic origin were included. Ivabradine treatment was initiated according to the latest HF guidelines. For HRV analysis, 24-h Holter recording was obtained from each patient before and after 8 weeks of treatment with ivabradine. Results: The mean RR interval, standard deviation of all normal to normal RR intervals (SDNN), the standard deviation of 5-min mean RR intervals (SDANN), the mean of the standard deviation of all normal-to-normal RR intervals for all 5-min segments (SDNN index), the percentage of successive normal RR intervals exceeding 50 ms (pNN50), and the square root of the mean of the squares of the differences between successive normal to normal RR intervals (RMSSD) were low at baseline before treatment with ivabradine. After 8 weeks of treatment with ivabradine, the mean HR (83.6 ± 8.0 and 64.6 ± 5.8, p < 0.0001), mean RR interval (713 ± 74 and 943 ± 101 ms, p < 0.0001), SDNN (56.2 ± 15.7 and 87.9 ± 19.4 ms, p < 0.0001), SDANN (49.5 ± 14.7 and 76.4 ± 19.5 ms, p < 0.0001), SDNN index (24.7 ± 8.8 and 38.3 ± 13.1 ms, p < 0.0001), pNN50 (2.4 ± 1.6 and 3.2 ± 2.2 %, p < 0.0001), and RMSSD (13.5 ± 4.6 and 17.8 ± 5.4 ms, p < 0.0001) substantially improved, which sustained during both when awake and while asleep. Conclusion: Our findings suggest that treatment with ivabradine improves HRV in nonischemic patients with HF. .


Fundamento: A ivabradina é um novo agente redutor específico da frequência cardíaca (FC) que melhora a sobrevida livre de eventos de pacientes com insuficiência cardíaca (IC). Objetivo: Avaliar o efeito da ivabradina nos índices temporais da variabilidade da frequência cardíaca (VFC) em pacientes com IC. Métodos: Quarenta e oito pacientes com IC compensada de etiologia não-isquêmica foram incluídos no estudo. O tratamento com ivabradina foi iniciado de acordo com as recomendações mais recentes para a IC. O Holter de 24 horas foi utilizado para analisar os índices da VFC em cada paciente antes e após 8 semanas de tratamento com ivabradina. Resultados: Todos os índices da VFC, o intervalo RR médio, o desvio padrão de todos os intervalos RR normais (DPNN), o desvio padrão de intervalos RR médios de 5 minutos (DPNNM), a média do desvio padrão de todos os intervalos RR normais para todos os segmentos de 5 minutos (índice DPNN), porcentagem de intervalos RR normais sucessivos superiores a 50 milissegundos (pNN50), e a raiz quadrada da média dos quadrados das diferenças entre intervalos RR sucessivos (RMQQD) apresentaram redução no ínicio do estudo, antes do tratamento com ivabradina. Após 8 semanas de tratamento com ivabradina, as médias das FC (83,6 ± 8,0 e 64,6 ± 5,8, p < 0,0001) e todos os índices da VFC, médias dos intervalos RR (713 ± 74 e 943 ± 101 ms, p < 0,0001), DPNN (56,2 ± 15,7 e 87,9 ± 19,4 ms, p < 0,0001), DPNNM (49,5 ± 14,7 e 76,4 ± 19,5 ms, p < 0,0001), índice DPNN (24,7 ± 8,8 e 38,3 ± 13,1 ms, p < 0,0001), pNN50 (2,4 ± 1,6 e 3,2 ± 2,2%, p < 0,0001) e RMQQD (13,5 ± 4,6 e 17,8 ± 5,4 ms , p < 0,0001), foram substancialmente melhorados, e permaneceram nestas ...


Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Benzazepines/therapeutic use , Cardiomyopathy, Dilated/drug therapy , Cardiotonic Agents/therapeutic use , Heart Rate/drug effects , Benzazepines/pharmacology , Cardiomyopathy, Dilated/physiopathology , Cardiotonic Agents/pharmacology , Electrocardiography, Ambulatory , Heart Failure/drug therapy , Heart Failure/physiopathology , Heart Rate/physiology , Statistics, Nonparametric , Time Factors , Treatment Outcome
15.
Article in English | IMSEAR | ID: sea-162149

ABSTRACT

Chocolate is made from the seeds of a tropical rainforest tree called “Theobroma cacao”. When compared with other food sources based on oxygen radical absorbance capacity (ORAC) measurement, dark chocolate is a major source of flavonols with highest antioxidant levels. Some of the health benefits of cocoa consumption include antioxidant properties such as polyphenolic compounds, among others are monomeric flavanols, epicatechin, catechin and oligomeric procyanidins. Both experimental and observational studies have suggested that chocolate consumption has a positive influence on human health, with antioxidant, antihypertensive, anti-inflammatory, anti-atherogenic, and antithrombotic effects as well as influence on insulin sensitivity, vascular endothelial function, and bioavailability of nitric oxide. In addition, dark chocolate consumption may alter lipid effects, by lowering total and low density lipoproteins and increasing high density lipoprotein cholesterol levels. The antioxidants found in chocolate have been shown to inhibit plasma lipid oxidation probably by scavenging free radical species. There are some experimental studies to prove that flavonoids could prevent LDL oxidation in vitro by scavenging radical species or sequestering metal ions. Dark chocolate (DC) has beneficial effects in the prevention of cardiovascular diseases (CVD) due to its antiinflammatory and antioxidant properties. Polyphenols rich dark chocolate showed progress in insulin sensitivity and decreased blood pressure in healthy subjects. Dark Chocolate has a dual effect on platelets by decreasing platelet aggregation and also it reduces platelet adhesion. Chocolate extends its great beneficial effect from being by and large a palatable pleasant and hence sustainable therapeutic option. Thus, dark chocolate may be suggested as a potential delicacy and one of the agents for the prevention and control of cardiometabolic syndrome.


Subject(s)
Antihypertensive Agents , Antioxidants/therapeutic use , Cacao/chemistry , Cacao/classification , Cacao/pharmacology , Cacao/physiology , Cardiotonic Agents/pharmacology , Flavonols/therapeutic use , Humans , Metabolic Syndrome/prevention & control , Metabolic Syndrome/therapy , Nitric Oxide/therapeutic use , Polyphenols/therapeutic use
16.
Pakistan Journal of Pharmaceutical Sciences. 2014; 27 (1): 1-9
in English | IMEMR | ID: emr-142973

ABSTRACT

Recently, it is suggested to use POLE [palm oil leaf extract] as a nutraceutical health product in food industry due to its newly discovered content of polyphenols and antioxidant vitamins. In the experiment, the antioxidant and anti-lipid-peroxidation activities of the extract were confirmed using; DPPH [1-diphenyl-2-picryl-hydrazil] radical scavenging activity, ferric ion induced lipid peroxidation inhibition, reducing power and hydrogen peroxide scavenging activity assays. The cardio-protective activity was studied in vivo using a model of metabolic syndrome induced by high fat diet. Lipid profile, obesity indices, renal tubular handling of water and electrolytes, blood pressure and arterial stiffness were measured at the end of the treatment period. Sprague Dawley rats weighing 150-200 g were divided into six groups, viz; group C; was treated as a negative control and fed with standard rodents chow, group H; was treated as a positive control and fed with an experimental diet enriched with saturated free fatty acids for 8 weeks, groups HP0.5, HP1 and HP2 which were fed with 0.5,1 and 2 g/kg [body weight] /day of POLE orally during the last 24 days of the high fat diet feeding period and group P; fed with highest dose of POLE. Results revealed that POLE possesses a cardio-protective effect which is ascribed to its content of polyphenols.


Subject(s)
Animals , Male , Antioxidants/pharmacology , Plant Leaves , Plant Extracts/pharmacology , Metabolic Syndrome/drug therapy , Rats, Sprague-Dawley , Cardiotonic Agents/pharmacology , Fatty Acids/administration & dosage , Kidney Tubules/physiopathology , Polyphenols
17.
Indian J Exp Biol ; 2013 Sept; 51(9): 694-701
Article in English | IMSEAR | ID: sea-149372

ABSTRACT

Normal rats pre-treated with P. kurroa (200 mg/kg) alone did not showed significant change, however, isoproterenol (ISP) administration resulted in hemodynamic and left ventricular dysfunction, oxidative stress, and lipid peroxidation. Such cardiac dysfunction was significantly prevented by P. kurroa root extract pre-treatment. Pre-treatment significantly attenuated the ISP-induced oxidative stress by restoring myocardial superoxide dismutase, catalase, and glutathione peroxidase enzymes except reduced glutathione content. P. kurroa pre-treatment markedly attenuated the ISP-induced rise in lipid peroxidation, thereby prevented leakage of myocyte creatine kinase-MB and lactate dehydrogenase enzymes. The results suggest that P. kurroa root extract possesses significant cardioprotective effect, which may be attributed to its antioxidant, anti-peroxidative, and myocardial preservative properties.


Subject(s)
Animals , Cardiotonic Agents/pharmacology , Male , Plant Extracts/pharmacology , Plant Roots/chemistry , Plantago/chemistry , Rats , Rats, Wistar
18.
Indian J Exp Biol ; 2013 Aug; 51(8): 653-660
Article in English | IMSEAR | ID: sea-149368

ABSTRACT

Isoproterenol injection (100 mg/kg; sc) produced changes in ECG pattern including ST-segment elevation and suppressed R-amplitude. The methanolic extract of M. vulgare at doses of 10, 20, and 40 mg/kg significantly amended the ECG changes. A severe myocardial necrosis and edematous along with a sharp reduction in the arterial blood pressure, left ventricular contractility (LVdP/dtmax or min), but a marked increase in the left ventricular end-diastolic pressure (LVEDP) were seen in the isoproterenol group. All parameters were significantly improved by the extract treatment. The extract (10 mg/kg) strongly increased LVdP/dtmax. Similarly, treatment with 40 mg/kg of M. vulgare lowered the elevated LVEDP and the heart to body weight ratio. In addition to in vitro antioxidant activity, the extract suppressed markedly the elevation of malondialdehyde levels both in serum and in myocardium. The results demonstrate that M. vulgare protects myocardium against isoproterenol-induced acute myocardial infarction and suggest that the effects could be related to antioxidant activities.


Subject(s)
Animals , Antioxidants/pharmacology , Cardiotonic Agents/pharmacology , Electrocardiography , Heart/drug effects , Heart/physiopathology , Isoproterenol/toxicity , Lipid Peroxidation/drug effects , Male , Malondialdehyde/metabolism , Marrubium/chemistry , Methanol/chemistry , Myocardial Infarction/chemically induced , Myocardial Infarction/drug therapy , Myocardial Infarction/pathology , Oxidative Stress/drug effects , Rats , Rats, Wistar
20.
Ann Card Anaesth ; 2013 Apr; 16(2): 94-99
Article in English | IMSEAR | ID: sea-147235

ABSTRACT

Aims and Objective: We tested the hypothesis that use of levosimendan would be associated with better perioperative hemodynamics and cardiac function during off-pump coronary artery bypass grafting (OPCAB) in patients with good left ventricular function. Materials and Methods: Thirty patients scheduled for OPCAB were randomized in a double-blind manner to receive either levosimendan 0.1 μg/kg/min or placebo after induction of general anesthesia. The hemodynamic variables were measured after induction of anesthesia, at 6 minute after application of tissue stabilizer for the anastomoses of left anterior descending artery, diagonal artery, left circumflex artery, and right coronary artery and at 6, 12, 18, and 24 hours after completion of surgery. Results: Compared with placebo group, cardiac index (CI) was significantly higher and systemic vascular resistance index (SVRI) was significantly lower at 6, 12, 18, and 24 hour after surgery in levosimendan group. Norepinephrine was infused in 60% of the patients in the levosimendan group compared to 6.7% in the control group ( P < 0.05). Lactate and mixed venous oxygen saturation were not significantly different between groups. Conclusions: Levosimendan significantly increased CI and decreased SVRI after OPCAB but it did not show any outcome benefit in terms of duration of ventilation and intensive care unit stay.


Subject(s)
Calcium/metabolism , Cardiotonic Agents/pharmacology , Coronary Artery Bypass, Off-Pump , Double-Blind Method , Female , Hemodynamics/drug effects , Humans , Hydrazones/pharmacology , Male , Pyridazines/pharmacology
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