感染性和内毒素性休克大鼠动脉组织中硫化氢的变化

探讨内源性硫化氢 (H2 S)在感染性和内毒素性休克大鼠血管组织中的含量变化及意义。用盲肠结扎穿孔法制备大鼠感染性休克模型和静脉注射内毒素法制备内毒素休克大鼠模型 ,观察大鼠血液动力学、代谢变化及测定内源性硫化氢含量和一氧化氮含量 ,并计算其相关性。感染性及内毒素性休克大鼠的血液动力学参数均明显低于对照组 ,而左室舒张末压明显高于对照组 (P <0 0 1) ,血糖明显低于对照组 (P <0 0 1) ,血乳酸水平明显高于对照组(P <0 0 1)。感染性和内毒素性休克大鼠动脉组织中H2 S含量明显高于对照组 ,(均P <0 0 1)。休克大鼠血管H2 S含量与血压、心功能及低血糖的程度呈高度负相关 (均P <0 0 1)。以上结果说明内源性H2 S可能参与休克过程中的病理生理调节

Changes in arterial hydrogen sulfide (H2S) content during septic shock and endotoxin shock in rats

The aim of the study was to explore the changes of H 2S in vascular tissues of rats with septic shock and endotoxin shock. A rat model of septic shock induced by cecal ligation and puncture and a model of endotoxic shock induced by injection endotoxin were developed to study the changes of endogenous H 2S in vascular tissues of rats during shock. Also, we measured hymodynamic variations, metabolic data, H 2S and nitric oxide (NO) contents of arteries. Hemodynamic parameters including heart rate (HR), mean arterial pressure ( BP), and the +dP/dt max decreased significantly while the left ventricular end diastolic pressure (LVEDP) increased significantly.The rats had hypoglycemia and severe lactic acidosis. H 2S contents in arteries were significantly increased in rats with septic shock and endotoxic shock. Endogenous vascular H 2S contents were negatively correlated with BP, cardiac function and the degree of hypoglycemia ( P <0.01). Endogenous vascular H 2S increased in rats with septic shock and endotoxic shock. It was suggested that H 2S play a role in physiological and pathophysiological process during the shock.