Gong Zi-Xi, Ran Ke, Chang Ye-Tian, Xu Jun-Mei
Department of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha 410011, China.
Zhejiang Da Xue Xue Bao Yi Xue Ban. 2009 Sep;38(5):521-4. doi: 10.3785/j.issn.1008-9292.2009.05.015.
To investigate the protective effects of morphine postconditioning on myocardial ischemia-reperfusion (I/R)injury and the potential mechanisms in rabbits.
Thirty-two New Zealand male white rabbits were randomly assigned into 4 groups: Group 1 (Sham), Group 2 (I/R), Group 3 (ischemic postconditioning), Group 4 (ischemia and morphine postconditioning). Group 1 was perfused for 160 min; Group 2 underwent 40 min ischemia and 120 min reperfusion; Group 3 underwent three cycles of 30 s reperfusion and 30 s left anterior descending coronary artery re-occlusion immediately after 40 min ischemia and before 120 min reperfusion; Group 4 was given morphine 1.0 mg/kg immediately after 40 min ischemia in 1 min and before 120 min reperfusion. Blood samples were taken from arterial line at 20 min before occlusion, 20 min after occlusion, 40 min after occlusion, 1 h after reperfusion and 2 h after reperfusion for determination of the plasma levels of cardiac troponin I (cTnI). At the end of the reperfusion, infarct size (IS) and area at risk were defined by Evans and TTC staining. Plasma SOD activity and MDA were determined at the end of reperfusion.
The levels of cTnI were significantly lower during reperfusion in the two postconditioning groups than those in I/R group. The plasma MDA content was significantly lower and SOD activity was significantly higher in the two postconditioning groups than those in I/R group, but there was no difference between two postconditioning groups. Morphine significantly reduced infarct size of the left ventricular area at risk as compared with I/R group (P<0.05).
Morphine postconditioning is as effective as ischemic postconditioning in the protection of myocardium against I/R injury in rabbits. Decrease in oxygen free radicals and increased antioxidant activity might be involved in its mechanism.
探讨吗啡后处理对兔心肌缺血再灌注损伤的保护作用及其潜在机制。
将32只新西兰雄性白兔随机分为4组：第1组（假手术组）、第2组（缺血再灌注组）、第3组（缺血后处理组）、第4组（缺血加吗啡后处理组）。第1组灌注160分钟；第2组经历40分钟缺血和120分钟再灌注；第3组在缺血40分钟后、再灌注120分钟前，进行3个周期的30秒再灌注和30秒左冠状动脉前降支重新闭塞；第4组在缺血40分钟后1分钟内、再灌注120分钟前立即给予吗啡1.0mg/kg。在闭塞前20分钟、闭塞后20分钟、闭塞后40分钟、再灌注1小时和再灌注2小时从动脉导管采集血样，测定血浆心肌肌钙蛋白I（cTnI）水平。再灌注结束时，通过伊文思蓝和TTC染色确定梗死面积（IS）和危险区面积。在再灌注结束时测定血浆超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量。
两个后处理组再灌注期间cTnI水平显著低于缺血再灌注组。两个后处理组血浆MDA含量显著低于缺血再灌注组，SOD活性显著高于缺血再灌注组，但两个后处理组之间无差异。与缺血再灌注组相比，吗啡显著减小了左心室危险区梗死面积（P<0.05）。
吗啡后处理在保护兔心肌免受缺血再灌注损伤方面与缺血后处理同样有效。氧自由基减少和抗氧化活性增加可能参与其机制。
