Effects of Hydrogen Sulphide on the Isolated Perfused Rat Heart

• Main Authors: Afthab Hussain, Helen Maddock, Hajar Al-Rajaibi, Ray J Carson
• Format: Article
• Language: English
• Published: Sultan Qaboos University 2011-08-01
• Series: Sultan Qaboos University Medical Journal
• Subjects: hydrogen sulphide; heart; langendorff; h2s gasotransmitter; vasorelaxation
• Online Access: https://journals.squ.edu.om/index.php/squmj/article/view/1577
• ISSN: 2075-051X; 2075-0528

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.