الفهرس 
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Abstract
Hydrogen sulfide (H2S) is an endogenous gaseous messenger suggested to regulate cardiovascular functions. This study evaluates the possible protective effect of H2S in aconitine and barium chloride (BaCl2) models of dysrhythmia in rats in addition to cardiovascular dysfunction induced by cecal ligation and puncture (CLP) in rats. Model I: Cardiac dysrhythmias :The effects of sodium hydrosulphide (NaHS, i.v.) on electrocardiograph (ECG) patterns, biochemical cardiac markers (creatine kinase-MB isozyme and cardiac troponin I), cardiac histopathology and aconitine (30 µg/kg, i.v.) and BaCl2 (15 mg/kg, i.v.) -induced dysrhythmia were studied in rats. NaHS significantly decreased heart rate at doses of 3, 4, and 6, but not 0.8 and 1.2 mg/kg. Aconitine caused 100% ventricular tachycardia (VT), 80% ventricular fibrillation (VF), and 60% mortality after 26±5 sec. NaHS (0.8 mg/kg, i.v.) pretreatment significantly decreased the VT, VF and mortality to 62.5, 25, and 0% respectively and delayed the occurrence of VT by 349±2 sec. Similarly, BaCl2 caused 75% VF and 37.5% mortality after 18 ± 8 sec. NaHS (0.8 mg/kg i.v.) pretreatment significantly decreased VF to 50% without affecting mortality rate. Moreover, NaHS (0.8 mg/kg, i.p., daily for 3 days) had no significant effects on ECG patterns, cardiac biomarkers or histopathology. Our results indicate that H2S has a protective role against dysrhythmia without affecting ECG patterns, cardiac biomarkers or histopathology. Model II: CLP induced Sepsis: After 24 h of induction of CLP, CLP induced elevations in HR, mortality, serum CK-MB, cTnI, CRP and LDH in addition to impaired aortic contraction to KCl and phenylephrine and relaxation to acetylcholine without affecting sodium nitroprusside responses. Moreover, CLP increased cardiac and aortic MDA, and decreased SOD, without affecting GSH and caused a marked subserosal and interstitial inflammation in endocardium. NaHS, but not the irreversible inhibitor of H2S synthesis DL Propargyl glycine (PAG), protected against CLP induced changes in HR, mortality, cardiac and inflammatory biomarkers, oxidative stress and myocardium histopathological changes without affecting vascular dysfunction. Our results confirm that H2S can attenuate CLP-induced cardiac, but not vascular, dysfunction possibly through its anti-inflammatory and anti-oxidant effects.