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J Appl Physiol (October 12, 2006). doi:10.1152/japplphysiol.00096.2006
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Submitted on January 25, 2006
Accepted on September 25, 2006

Hydrogen sulfide and its cardioprotective effects in myocardial ischemia in experimental rats

Yi Zhun Zhu1*, Zhong Jing Wang2, Peiying Ho2, Yoke Yun Loke2, Yi-Chun Zhu3, Xiao Wei Huang4, Shan Hong Huang5, Chee Sin Tan2, Matt Whiteman6, Jia Lu2, and Philip K Moore2

1 Dept. of Pharmacology, National University of Singapore, Singapore, Singapore; Dept. of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China
2 Dept. of Pharmacology, National University of Singapore, Singapore, Singapore
3 Dept. of Physiology and Pathophysiology, Fudan University, Shanghai, China
4 Physiology and Pathophysiology, Fudan University, Shanghai, China
5 Dept. of Biochemistry, National University of Singapore, Singapore, Singapore
6 Dept. of Biochemistry, National University if Singapore, Singapore, Singapore

* To whom correspondence should be addressed. E-mail: phczhuyz{at}nus.edu.sg.

The role of hydrogen sulfide (H2S) in myocardial infarction (MI) has not been previously studied. We therefore investigated the effect of H2S in a rat model of MI. Animals were randomly divided into 3 groups (n=80) and received either vehicle, 14 µmol/kg of NaHS or 50mg/kg propargylglycine (PAG) everyday for 1 week before surgery and the treatment continued for a further 2 days after MI when the animals were sacrificed. The mortality was 35% in vehicle-, 40% in PAG- and 27.5% in NaHS-treated (p<0.05 vs vehicle) groups, respectively. Infarct size was 52.9±3.5% in vehicle-, 62.9±7.6% in PAG- and 43.4±2.8% in NaHS-treated (p<0.05 vs vehicle) groups. Plasma H2S concentration was significantly increased after MI (59.2±7.16 µM) compared to the baseline concentration (i.e. 38.2±2.07 µM before MI, p<0.05). Elevated plasma H2S after MI was abolished by treatment of PAG (39.2±5.02 µM). We further showed for the first time cystathionine-gamma-lyase (CSE, an enzyme responsible for endogenous H2S formation) was detected in the myocardium of the infarct area using immunohistochemical staining. In the hypoxic vascular smooth muscle cells, we found cell death was increased under the stimuli of hypoxia but the increased cell death was attenuated by the pre-treatment of NaHS (71 ±1.2% cell viability in hypoxic vehicle vs 95 ± 2.3% in non-hypoxic control, p<0.05). In conclusion, endogenous H2S was cardioprotective in the rat model of MI. PAG reduced endogenous H2S production after MI by inhibiting CSE. The results suggest that H2S might provide a novel approach to the treatment of myocardial infarction.




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