| Continuous myocardial ischemia Lead to necrosis, The most effective way of preventing and relieving it caused by ischemia is to make the blocked blood vessel recanalized. However, theories that have been discovered and clinical experience had proved that reperfusion not only can't improve myocardial function but make it worse, which bring about arrhythmia cordis and enlarge area of myocardium infarction. It is called ischemia-reperfusion injury. Reperfusion itself can bring about histionic injury which is difficult to distinguish from ischemic injuries. At present, the mechanism of ischemia-reperfusion injury has much controversy, SO. I want to investigate the histopathological change of the two injuries and relationship between them and myocardial apoptosis by making the model of ischemia-reperfusion injury, in order to probe into the function of apoptosis in the mechanism of myocardial ischemia and ischemia-reperfusion injury, and to provide a new theory and basis for clinical prevention and therapy of myocardial ischemia and reperfusion. 18 male healthy rabbits were experimented. The rabbits were divided into 3 groups at random, with 6 in each group. One of these groups are used as control group and the others experimental group I-II. Animals in experimental groups were anesthetized, and the left ventricle branches of left coronary arteries were ligatured. The ligations were confirmed by naked eyes, and electrocardiogram showed the ischemias were obvious, and then the models of myocardial ischemia were set up. On the basis of them, as the scheduled time of ischemia reached, the blocked blood vessel was recanalized to set up model of myocardial ischemia-reperfusion. The process was done as designed. After the experiments, their hearts were removed out. Samples were separately grouped into central ischemic region (CIR). And normal blood supply region (NBSR). Each segment was redivided into 3 parts to be used as samples for light microscopy, electron microscopy and TdT-mediated dUTP nick end labeling (TUNEL). Under light microscope, the myocardium in NBSR and control group shows normal myocardial structure. In group I the CIR assumes obvious myocardial necrosis. The muscle appears to be unclear fibers, disappeared strains, dissolved cytoplasm and cytoblast. The CIR of experimental group II assume focal necrosis of little areas. There are also atrophied cytoblast, concentrated chromosomes in apoptosis. By TUNEL, there is no TUNEL positive stain cell in NBSR of grouts I~II and control group, SO neither the CIR in I. In group II, a great quantity TUNEL positive cells was observed in the CIR. The statistics data show the average apotosis rate of CIR cardiomyocytes in experimental Group II was 21.10%. Under electronic microscope, the myocardium in NBSR of control group and groups I~II assumes normal microscopic structure. CIR of group I assumes confused musculature, liquidized myoplasm, abnormal and dissolved cytoblast, swollen mitochondrion and break-up and vacuolated brests. Group II assumes early apoptosis as swollen mitochondrion and partially break-up brests, slightly abnormal cytoblast, chromatin edged, and also assume typical characteristics of apoptosis as cytoplasm, little nucleous, abnormal cytoblast, chromatin condensed and edged, appeared contraction band, etc. Our results show that, the ischemic injures of heart are to be as primarily the necrosis, and no myocardial apoptosis cells were seen. The myocardium injures and the postponed necrosis during ischemic-reperfusion are caused primarily by apoptosis. This offers new thinking for the further study of therapy and prognosis of myocardium infarct. This offers new reference basis for the inspection of injury degree and evaluationg the therapy effect. |
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