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1.
Arq. bras. cardiol ; 114(2): 295-303, Feb. 2020. tab, graf
Article in English | LILACS | ID: biblio-1088850

ABSTRACT

Abstract Background: Cigarette smoking is usually associated with hypertension and may modify vasoconstrictor response. Objective: The present study aimed to analyze and compare the interaction of passive cigarette smoking and hypertension on epinephrine and felypressin blood pressure effects after intravascular injection. Method: 45-day male Wistar rats had the main left renal artery partially constricted and the right kidney removed (1K1C model). Rats were placed in the chamber for exposition to passive cigarette smoking (10 cigarettes) during 10 min (6 days a week). Hypertensive rats received atenolol (90 mg/kg/day) by gavage for two weeks. Hypotensive and hypertensive response, response duration and heart rate were recorded from direct blood pressure values. The significance level was 5%. Results: Passive cigarette smoking increased maximal hypertensive response to epinephrine in normotensive and 1K1C-atenolol treated rats and to felypressin only in 1K1C-atenolol treated rats; it also reduced epinephrine hypotensive response. Epinephrine increased heart rate in normotensive and hypertensive passive smokers or non-smoker rats. Comparing the two vasoconstrictors, epinephrine showed greater hypertensive response in normotensive smokers, 1K1C-atenolol treated smokers and non-smokers. However, in normotensive-nonsmoker rats, felypressin showed a greater and longer hypertensive effect. Conclusions: Our results suggest that passive cigarette smoking may reduce epinephrine vasodilation and increase hypertensive response when compared to felypressin. Therefore, felypressin may be safe for hypertensive patients to avoid tachycardia and atenolol interaction, but for normotensive and non-smoker patients, epinephrine may be safer than felypressin.


Resumo Fundamento: O tabagismo geralmente está associado à hipertensão e pode modificar a resposta vasoconstritora. Objetivo: O presente estudo teve como objetivo analisar e comparar a interação do tabagismo passivo e hipertensão sobre os efeitos da epinefrina e felipressina na pressão arterial após injeção intravascular. Métodos: Ratos Wistar machos de 45 dias tiveram a artéria renal principal esquerda parcialmente obstruída e o rim direito removido (modelo 1K1C). Os ratos foram colocados na câmara para exposição ao tabagismo passivo (10 cigarros) durante 10 minutos (6 dias por semana). Ratos hipertensos receberam atenolol (90 mg/kg/dia) por gavagem durante duas semanas. A resposta hipotensora e hipertensiva, a duração da resposta e a frequência cardíaca foram registradas a partir da medida dos valores diretos da pressão arterial. O nível de significância foi de 5%. Resultados: O tabagismo passivo aumentou a resposta hipertensiva máxima à epinefrina em ratos normotensos e ratos 1K1C tratados com atenolol e à felipressina apenas em ratos 1K1C tratados com atenolol; também reduziu a resposta hipotensiva à epinefrina. A epinefrina aumentou a frequência cardíaca em ratos fumantes passivos ou não-fumantes, normotensos e hipertensos. Comparando os dois vasoconstritores, a epinefrina apresentou maior resposta hipertensiva em fumantes normotensos, ratos 1K1C fumantes e não fumantes tratados com atenolol. No entanto, em ratos normotensos e não fumantes, a felipressina apresentou um efeito hipertensivo maior e mais prolongado. Conclusões: Nossos resultados sugerem que o tabagismo passivo pode reduzir a vasodilatação da epinefrina e aumentar a resposta hipertensiva quando comparado à felipressina. Portanto, a felipressina pode ser segura para pacientes hipertensos, com o objetivo de evitar a interação entre taquicardia e atenolol, mas para pacientes normotensos e não-fumantes, a epinefrina pode ser mais segura que a felipressina.


Subject(s)
Animals , Male , Atenolol/pharmacology , Tobacco Smoke Pollution/adverse effects , Blood Pressure/drug effects , Epinephrine/pharmacology , Felypressin/pharmacology , Antihypertensive Agents/pharmacology , Time Factors , Vasoconstrictor Agents/pharmacology , Vasodilation/drug effects , Rats, Wistar , Dose-Response Relationship, Drug , Drug Interactions , Heart Rate/drug effects , Hypertension/drug therapy , Hypotension
6.
J. appl. oral sci ; 20(6): I-I, Nov.-Dec. 2012.
Article in English | LILACS-Express | LILACS | ID: lil-660627
10.
J. appl. oral sci ; 20(1)Jan.-Feb. 2012.
Article in English | LILACS-Express | LILACS | ID: lil-618145
13.
Rev. Fac. Odontol. Porto Alegre ; 51(2): 5-8, maio-ago. 2010. ilus
Article in English | LILACS, BBO | ID: lil-719557

ABSTRACT

Periodontitis is a chronic disease characterized by bone loss and inflammatory changes. We studied the effect of a homeopathic agent (Mercúrios Corrosivos 6 CH) and a non-steroidal anti-inflammatory drug (nimesulide) on the alveolar bone loss progression in experimentally induced periodontitis in rats. Sixty (60) Wistar rats were separated into group 1 (homeopathy), group 2 (nimesulide) and group 3 (saline solution). Silk ligatures were placed at the gingival margin level of the lower right first molar of all rats. Alveolar bone loss was evaluated by light microscopic analysis and analyzed using software Image J. The results were submitted to the analysis of variance (ANOVA) and Tukey’s posttest (p<0.05). The analysis revealed that there was a higher bone loss in diseased sites as compared with healthy sites. A significant reduction in the alveolar bone resorption was observed in group 2 (nimesulide) as compared with group 1 (homeopathy) 7 days after the induction of periodontitis. Our data provided evidence that homeopathy does not decrease alveolar bone loss as opposed to nimesulide in experimentally induced periodontitis.


Subject(s)
Animals , Rats , Alveolar Bone Loss , Homeopathy , Periodontitis , Sulfonamides/therapeutic use , Analysis of Variance , Rats, Wistar
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