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Effects of Hydrogen Sulphide on the Isolated Perfused Rat Heart

By Afthab Hussain, Helen Maddock, Hajar Al-Rajaibi and Ray J. Carson


This research was originally published in SQUMJ. Hussain, A., Maddock, H., Al-Rajaibi, H., Carson, R.J. Effects of Hydrogen Sulphide on the Isolated Perfused Rat Heart. SQU Med J 2011;11(2):236-244. © by Sultan Qaboos University Medical Journal \ud This is the original published version of the article. It is reproduced here with the publisher's permission. Hydrogen sulphide has been identified as a gas signalling molecule in the body, and has previously been shown to have vasorelaxant properties. The aim of the study was to investigate the effects of sodium hydrosulphide (NaHS), a hydrogen sulphide donor, on heart rate (HR), left ventricular developed pressure (LVDP) and coronary flow (CF) in the isolated perfused rat heart. Methods: A Langendorff isolated heart preparation was used to investigate the effect of a dose range of sodium hydrosulphide, in the presence and absence of inhibitors, on heart rate, left ventricular developed pressure and coronary flow. Results: Sodium hydrosulphide caused a significant decrease in heart rate at a concentration of 10-3 M (P <0.001). This decrease was partially inhibited by glibenclamide, a KATP channel blocker (P <0.05); L-NAME, a nitric oxide synthase inhibitor (P <0.001), and methylene blue (P <0.001), but not by H-89, a protein kinase A inhibitor. Sodium hydrosulphide significantly increased coronary flow at concentrations of 10-4 – 10-3M (P <0.05). This response was significantly increased in the presence of L-NAME (P <0.001) and methylene blue (P <0.001), whereas H-89 inhibited the increase in coronary flow due to sodium hydrosulphide (P <0.001). Sodium hydrosulphide significantly decreased LVDP at all concentrations (P <0.001). In the presence of glibenclamide and H-89, the time period of the decrease in LVDP due to sodium hydrosulphide was extended (P <0.001), whereas methylene blue and L-NAME caused a significant reduction in the response to sodium hydrosulphide (P <0.05, P <0.01 respectively). Conclusion: Sodium hydrosulphide reduced heart rate and LVDP, and increased coronary flow in the isolated perfused rat heart; however, the mechanisms of action could not be fully elucidated

Topics: Hydrogen sulphide, Heart, Langendorff, H2S gasotransmitter, Vasorelaxation
Publisher: Sultan Qaboos University
Year: 2011
OAI identifier:

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  4. (1989). Determination of sulphide in brain tissue by gas dialysis/ ion chromatography: post mortem studies and two case reports. doi
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  11. (2007). Hydrogen sulfide contributes to cardioprotection during ischemia-reperfusion injury by opening KATP channels. doi
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  16. (1997). Positive inotropic effect of exogenous and endogenous NO in hypertrophic rat hearts. doi
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  18. (1975). The effect of sulfhydryl reagents on the heart rate and coronary flow of the isolated perfused guinea-pig heart. Arch Int Pharmacodyn Ther
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