Experimental Study Of Myocardial Injury After Cardiopulmonary Resuscitation In Rats

Objective: To review the myocardial cell injury and apoptosis after Cardiopulmonary resuscitation in rats, and investigate the possible mechanism; to observe the protective effects of growth hormone on myocardial injury in rats after Cardiopulmonary resuscitation.Methods: Cardiac arrest was induced by asphyxiation and ice-cold 0.5M KCL and resuscitation efforts were begun five minutes after arrest. Male Sprague Dawley rats were randomly divided into 6 groups: sham control group; after Cardiopulmonary resuscitation rats were allowed to reperfuse spontaneously for 3 hours, 6 hours, 12 hours, 24 hours and growth hormone treatment for 24 hours. Creatine kinase-MB and tumor necrosis factor a in blood were measured after Cardiopulmonary resuscitation. The myocardial cells in left ventricle were assessed by terminal deoxynucleotidyl transf erase-mediated dutp-FITC nick endlabeling (TUNEL) and transmission electron microscope (TEM). Bcl-2,Bax and NF-кB protein expression were studied using immunocytochemistry at 3 hour, 6 hour, 12 hour, and 24 hour after resuscitation.Result: CK-MB levels in 3 hour group began to rise and reached the top value in 24 hour group. After Cardiopulmonary resuscitation TNF-alpha levels in serum increased markedly compared to the sham control group. TUNEL-positive myocardial cells could be found at 3 hour post-resuscitation in the left ventricle. There were 4.70% TUNEL-positive cells at 24 hour. Bcl-2 immunoreactivity was continuous to increase, but Bax protein expression was higher than Bcl-2; Bcl-2/Bax ratio was imbalance. Nuclear NF-кB protein expression was early observed at 6 hour, there were 8.40% NF-кB-positive cells at 24 hour. Compared to the routine treatment 24 hour group, growth hormone treatment group showed a significant reduction of plasma CK-MB and TNF-alpha level; the TUNEL-positive cells markedly decreased, but an increase in myocardial Bcl-2 expression.Conclusion: Myocardial injury happened in rats after Cardiopulmonary resuscitation. Myocardial cells apoptosis may be principal manifestation of myocardial injury afterCPR. The results of this study demonstrate that Bcl-2/Bax ratio imbalance and NF-кB expression have an important role in myocardial programmed cell death. Growthhormone can inhibit myocardial apoptosis via promoting the expression of Bcl-2, thusprotect the myocardium in rats after resuscitation.