【摘要】 目的　探讨一氧化氮 ( NO)在止血带休克发病学中的意义。 2方法　本实验采用了 Rosenthal法复制大鼠止血带休克( tourniquet shock,To S)模型 [1 ] ,观察一氧化氮合酶 ( NOS)抑制剂氨基胍 ( AG)及一氧化氮 ( NO)合成前体物质 L -精氨酸 ( L -Arg)对To S的影响。 3结果　 To S时 ,平均动脉压 ( MAP)进行性降低 ,局部骨骼肌组织 NOS活性增强 ,血浆 NO含量增高 ;给予 AG后虽能增强动物血压松带后血压早期的回升 ,但晚期血压迅速下降 ,骨骼肌组织 W/D比值、组织髓过氧化物酶 ( MPO)的含量、血浆乳酸脱氢酶 ( L DH)、组织蛋白酶 D( CD)活性增高。而给予 L-Arg能减轻 To S晚期血压降低 ,并能减轻组织及血浆的上述损伤变化。 4结论　To S时内源性一氧化氮升高对机体具有适应保护意义更多还原

【Abstract】 To study the pathogenetic significance of nitric oxide(NO) in rat tourniquet shock.Methods Referring to Rosenthal method,the model rats of tourniquet shock(ToS) were made.The effects of aminoguanidine(AG),which inhibits nitric oxide sythase(NOS),and L arginine(L Arg),which is the substrate in process of nitric oxide sythesis,on these rats were observed.Results The mean arteria pressure(MAP) descended progressively and activity of NOS skeletal muscle and value of plasma NO were both increased in ToS rats.Although it accelerated MAP rising after releasing in early period,and lowered MAP quickly in later period after given AG.A more serious injuries,including increased values of skeletal muscle W/D and myeloperxidase(MPO) and increased activities of plasma lactate dehydrogenase(LDH) and cathepsin D(CD) were found in group AG.L Arg could significantly alleviate descending of MAP in loter period and tissue and plasma injury changes above.Conclusions The increase of engogenous NO in ToS rats is helpful in compensated protection for body.更多还原