腺苷对心肌梗死再灌注无复流的保护作用及其对一氧化氮和内皮素影响的实验研究

目的:探讨腺苷对心肌梗死再灌注无复流的保护作用,以及这种保护作用与腺苷对一氧化氮(NO)和内皮素(ET)影响的关系。方法:制作离体兔心急性心肌梗死模型。30只兔心随机分为三组:A:假手术组,B:心肌梗死再灌注组,C:腺苷+心肌梗死再灌注组。分别取灌流开始5min和再灌流90min时冠脉流出液2ml,测定乳酸脱氢酶(LDH)、肌酸激酶(CK)、内皮素(ET)及一氧化氮(NO)含量。灌流结束时,测量无复流区域面积的百分比,并在光镜下观察心肌细胞的变化情况。结果:(1)A组灌流开始与结束时和B组、C组开始灌流时冠脉流出液中LDH、CK含量相比无显著性差异;(2)B组各项化验指标分别进行组内比较其结果有统计学差异。(3)灌流结束时,B组与C组相比NO的降低和ET的升高有统计学差异。(4)C组和B组比较无复流区域面积百分比明显缩小,有统计学差异。结论:腺苷对心肌梗死再灌注无复流具有明显的保护作用。腺苷升高NO和降低ET的作用可能是其发挥保护作用的原因之一。

Protective Effect of Adenosine on Myocardial Infarction Reperfusion No-Reflow Phenomenon and the Relationship between the Protective Effects and Nitric Oxide/ Endothelin in Isolated Rabbit Hearts

Objective: To study the protective effects of adenosine on myocardial infarction reperfusion no-reflow phenomenon, and the relationship between the protective effects and nitric oxide(NO)/endothelin(ET).Method: Isolated rabbit heart model with myocardial infarction and reperfusion was established. Thirty rabbits were randomly assigned to three groups: group A, served as control; group B, acute myocardial infarction reperfusion (AMIR); group C, treated with adenosine (20 μmol/L) before AMIR. The contents of lactate dehydrogenase (LDH), creatine kinase (CK),NO and ET in coronary effluent fluid were detected during the course of perfusion .Areas of no-reflow(%) and microcirculation of every rabbit heart were measured or observed.Results: The contents of LDH and CK in coronary effluent fluid were significantly lower in group C and group A than those in group B. The content of NO was evidently higher in group C than that in other groups.The consistence of ET was observedly lower in group C than that in group B; Areas of no-reflow(%) markedly decreased in group C than that of group B. Heart microcirculation injury was ameliorated.Conclusion: Adenosine is effective in the protection of myocardial infarction reperfusion no-reflow. Adenosine may restrict endothlin release and make nitric oxide hoist. One of the possible mechanisms that adenosine can safeguard myocardial infarction reperfusion no-reflow phenomenon may be the effect of adenosine on NO and ET.