失血性休克复苏时心肌损伤和一氧化氮的变化及灵芝多糖的干预作用  

Myocardial injury and changes of nitric oxide content in hemorrhagic shock / reperfusion and the effect of ganoderma lucidum polysaccharide on them

作　　者：杨红梅[1] 王黎[1] 陈洁[1] 裴瑞[1] 徐秋霞[1] 郭安齐[1] 桂兴芬[1] 

机构地区：[1]河南职工医学院,河南郑州450003

出　　处：《中国中西医结合急救杂志》2003年第5期304-306,共3页Chinese Journal of Integrated Traditional and Western Medicine in Intensive and Critical Care

摘　　要：目的 :探讨失血性休克和复苏再灌注过程中心肌损伤和一氧化氮 (NO)浓度的变化及灵芝多糖的干预作用。方法 :复制家兔失血性休克再灌注模型 ,随机分成假手术组、生理盐水再灌注组和质量分数为 1%的灵芝多糖再灌注组 ;观察 3组动物平均动脉血压 (MAP)、心功能、血浆 NO浓度及心肌 NO含量和一氧化氮合酶(NOS)活性的变化。结果 :两个再灌注组动物在失血性休克 4 0 m in时左心室舒张末压 (L VEDP)比休克前及假手术组略有升高 ,但差异不显著 (P均 >0 .0 5 ) ,左心室内压最大变化速率 (± dp/dt max)则明显降低 (P均 <0 .0 5 ) ,血浆 NO浓度则显著升高 (P均 <0 .0 5 )。生理盐水再灌注组动物再灌注 4 0 min时 ,心功能较休克 4 0 m in时进一步降低 (P<0 .0 5 ) ,血浆 NO浓度进一步升高 ,心肌 NOS活性和 NO含量明显高于假手术组 (P均 <0 .0 5 )。灵芝多糖组再灌注 4 0 min时较生理盐水再灌注组、心功能明显改善 ,血浆 NO浓度、心肌 NO含量和心肌 NOS活性均明显降低 (P均 <0 .0 5 )。结论 :失血性休克再灌注过程中心肌 NOS活性、血浆 NO浓度、心肌NO含量均升高 ,而心功能降低 ,提示 NO在失血性休克再灌注心肌损伤中起重要作用 ;而灵芝多糖可通过抑制 NOS活性、降低 NO浓度对失血性休克再灌注心肌损伤起保护作用。Objective: To investigate the myocardial injury and changes of nitric oxide(NO) content in hemorrhagic shock / reperfusion (HSR) rabbits and the effect of ganoderma lucidum polysaccharide(GLP) on them. Methods: Using the HSR model of rabbits, animals were divided into three groups: sham operation group, reperfusion with normal saline(NS) group, reperfusion with 1% GLP group. The mean artery pressure (MAP), ventricular function, NO content in serum and myocardium, the activity of NOS in myocardium were examined. Results: At 40 minutes after hemorrhagic shock, left ventricular enddiastolic pressure(LVEDP) were slightly increased in the two reperfusion groups, but the difference was not significant (all P >0.05). The maximum rate of intraventricular pressure rise (+dp/dtmax) and maximum rate of intraventricular pressure down (dp/dtmax) were reduced, and NO content in serum were increased significantly compared with those before shock and in sham operation group (all P <0.05). At 40 minutes after reperfusion, ventricular functions were reduced, NO content in serum and myocardium, the activity of NOS in myocardium were all increased significantly in reperfusion with NS group compared with those in sham operation group (all P <0.05). At the same time, the cardiac function was improved, NO concentration in serum and myocardium, the activity of NOS in myocardium were significantly decreased in reperfusion with 1% GLP group than those in reperfusion with NS group (all P <0.05).Conclusion: In HSR process , the activity of NOS, the NO content in serum and myocardium are all increased, the cardiac function is decreased. The myocardial injury in HSR is related with changes of NO content. GLP has protective effect on myocardial injury in HSR .Its mechanism would be inhibiting the activity of NOS and reduced NO content in myocardium .

关 键 词：失血性休克 复苏 心肌损伤 一氧化氮 灵芝多糖 一氧化氮合酶 缺血再灌注 

分 类 号：R285.5[医药卫生—中药学]