Background and purpose: Sodium sulphide (Na(2)S) disassociates to sodium (Na(+)) hydrosulphide, anion (HS(-)) and hydrogen sulphide (H(2)S) in aqueous solutions. Here we have established and characterized a method to detect H(2)S gas in the exhaled breath of rats.
Experimental approach: Male rats were anaesthetized with ketamine and xylazine, instrumented with intravenous (i.v.) jugular vein catheters, and a tube inserted into the trachea was connected to a pneumotach connected to a H(2)S gas detector. Sodium sulphide, cysteine or the natural polysulphide compound diallyl disulphide were infused intravenously while the airway was monitored for exhaled H(2)S real time.
Key results: Exhaled sulphide concentration was calculated to be in the range of 0.4-11 ppm in response to i.v. infusion rates ranging between 0.3 and 1.1 mg x kg(-1) x min(-1). When nitric oxide synthesis was inhibited with N(omega)-nitro-L-arginine methyl ester the amount of H(2)S exhaled during i.v. infusions of sodium sulphide was significantly increased compared with that obtained with the vehicle control. An increase in circulating nitric oxide using DETA NONOate [3,3-bis(aminoethyl)-1-hydroxy-2-oxo-1-triazene] did not alter the levels of exhaled H(2)S during an i.v. infusion of sodium sulphide. An i.v. bolus of L-cysteine, 1 g.kg(-1), and an i.v. infusion of the garlic derived natural compound diallyl disulphide, 1.8 mg x kg(-1) x min(-1), also caused exhalation of H(2)S gas.
Conclusions and implications: This method has shown that significant amounts of H(2)S are exhaled in rats during sodium sulphide infusions, and the amount exhaled can be modulated by various pharmacological interventions.