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Cardioprotective effects of hydrogen sulfide and nitric oxide and their interactions during the process of myocardial ischemia in rats

Chang-Qing Chen#, Hong Xin#, Yi-Chun Zhu, Yi-Zhun Zhu*

  1. 1. Department of Pharmacology, School of Pharmacy and Institute of Biomedical Sciences, Fudan University, Shanghai 200032, China
    2. Department of Physiology and Pathophysiology, Fudan University, Shanghai 200032, China
  • Received:2008-12-25 Revised:2009-02-10 Online:2009-03-15 Published:2009-03-15
  • Contact: Yi-Zhun Zhu*

Abstract: The relationship between hydrogen sulfide (H2S) and nitric oxide (NO) in myocardial infarction (MI) has not been previously reported. In the current investigation, we sought to determine the roles of both H2S and NO in MI in rats. Animals were randomly divided into 5 groups and treated with L-NG-nitro arginine methyl ester (L-NAME), sildenafil, saline, propargylglycine (PAG) and L-cysteine, respectively, for 1 week prior to performing MI surgery or sham operation. The mortality rates were lower in sildenafil and L-cysteine treated rats in the MI group. The infarct area was significantly reduced in sildenafil and L-cysteine treated rats. Moreover, plasma H2S measurements revealed that the level in the sildenafil treated group was lower than in the L-NAME treated MI group, which was consistent with an observed decrease in cystathionine gamma-lyase (CSE) enzyme activity. CSE protein expression level in the L-NAME treated MI group was significantly higher than in sildenafil treated MI group. eNOS protein content in the L-cysteine treated MI group was lower than in the PAG treated MI group and eNOS gene expression is significantly decreased in the L-cysteine treated rats. We demonstrated that endogenous H2S and NO are cardioprotective in the rat model of MI. Indeed, both the H2S-CSE and NO-NOS system appear to have a mutual down-regulation effect in MI process in our experimental rat model.

Key words: Hydrogen sulfide, Hydrogen sulfide, Nitric oxide, Nitric oxide, Cystathionine gamma-lyase, Cystathionine gamma-lyase, Myocardial infarction, Myocardial infarction

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