Title of article :
Effects of Hydrogen Sulphide on the Isolated Perfused Rat Heart
Author/Authors :
Hussain, Afthab Coventry University - Faculty of Health Life Sciences - Biomolecular Sciences, UK , Maddock, Helen Coventry University - Faculty of Health Life Sciences - Biomolecular Sciences, UK , Al-Rajaibi, Hajar Sultan Qaboos University Hospital - Department of Physiology, Oman , Carson, Ray J University of Leicester - Leicester Medical School - Dept of Medical Social Care Education, UK
From page :
236
To page :
243
Abstract :
Objectives: 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.
Keywords :
Hydrogen sulphide , Heart , Langendorff , H2S gasotransmitter , Vasorelaxation
Journal title :
Sultan Qaboos University Medical Journal (SQUMJ)
Journal title :
Sultan Qaboos University Medical Journal (SQUMJ)
Record number :
2690596
Link To Document :
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