Objectives: To explore the changes of hydrogen sulfide (H(2)S) in vascular tissues of rats with septic shock and endotoxin shock and its possible pathophysiological implication.
Methods: Rat models of septic shock induced by cecal ligation and puncture and of endotoxic shock induced by injection of endotoxin were used in this study. The authors measured hymodynamic variations, metabolic data, H(2)S and nitric oxide (NO) contents of different arteries in rats with septic shock and endotoxic shock.
Results: The results showed that hemodynamic parameters including the heart rate (HR), the mean arterial pressure (BP), and the +dP/dt max decreased markedly, while the left ventricular end-diastolic pressure (LVEDP) increased significantly and the rats developed hypoglycemia and lactic acidosis. Arterial H(2)S contents were significantly increased (P<0.01) in both septic and endotoxic shock (P<0.01). Endogenous H(2)S and NO contents all negatively correlated with BP, cardiac function and the degree of hypoglycemia (P<0.01).
Conclusions: The results of our study demonstrated that endogenous vascular H(2)S increased in rats with septic shock and endotoxic shock. It was suggested that endogenous H(2)S was involved in physiological and pathophysiological process during shock.