ABSTRACT
Hydrogen sulphide has been identified as a gas signaling 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 and 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. 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. 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 K [ATP] channel blocker [P <0.05]; L-NAME, a nitric oxide synthase inhibitor [P <0.01], 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]. 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