| PrefaceThe mechanism of myocardial ischemia-reperfusion injury ( MIRI) is complicated. It is shown in some investigations that apoptosis occur-rences during myocardial ischemia-reperfusion in rabbit , rat and the human being. C-fos gene is related to MIRI, which expresses in the myocardial ischemia area at the earlier period, and related to the is-chemia prolonging time. Esmolo is a selective adrenergic beta-Antago-nists , which can reduce the oxygen and energy consumption of myo-cardium by clinical investigation, and it shows the protective effects. In the experimental study it was found that continuous coronary perfu-sion with warm esmolol-enriched blood avoided myocardial ischemia and minimized myocardial edema, thus completely preserving cardiac performance. Some clinical data showed the alternative technique to be superior to standard crystalloid cardioplegia in terms of both func-tional and structural myocardial protection. The concept of beta-bloc-ker-induced cardiac surgical conditions is a useful alternative for myo-cardial protection during coronary artery surgery and may be particu-larly beneficial for severely compromised hearts. In this study, by ob-serving the morphological feature of myocardial cell and the expression of apoptosis-related c-fos gene during global ischemia reperfusion in i-solated Langendorff perfused rat heart, we investigate the effects of es-molol in order to provide rational basis for clinical application.Material and MethodsThe global myocardial ischemia-reperfusion was induced with Langendorff system. Forty Wistar rats were randomly divided into 5 groups; group N as control, this group was continuously perfused with pure K-H perfusate for 95min ; group C as ischemia-reperfusion con-trol, this group was perfused with pure K-H perfusate for the first 35min then halted for 30min, lasdy reperfused with K-H perfusate for 30min; group EH,EM,and EL, these groups were first perfused with K-H perfusate for 15min, then treated with esmolol 100μg ?ml<sub>-120 μg ?ml\4μ,g ?ml-1'K-H perfusate respectively prior to ischemia for 20min, halted for 30min, lasdy reperfused with K-H perfusate for 30min. The isolated rat hearts were perfused in condition of constant temperature (37 ?.2?C) and pressure (90cmH20, lcmH20 =0. 098 kPa) , and then the left ventricular myocardiums were extracted for use. We observed the ultrastructure changes of cardiomyocytes un-der transmission electron microscopy. We detected the expression of c-fos protein by immunochemical staining. The expression of c-fos protein were quantified using computer image analysis system. Results are expressed as the mean ?SD. Statistical analyses were carried out by Excel, PERA (protein expression relative area of c-fos gene) data were compared using the T-test. A P value of <0.05 was considered statistically significant.Results1. The morphological ultrastructure changes of rat myocardial cell Under transmission electron microscopy, we observed that themorphological ultrastructure was normal on the whole in group N; ap-optotic body was found in group C; the apoptotic earlier period ap-pearances were shown in group EH,EM and EL.2. The protein expression of c-fos gene in rat myocardial cell Compared with the values of group N, protein expression relativearea of c-fos gene(PERA) were increased significantly in group C, EH,EM,EL( P<0. 01). But decreased significantly in group EHU EM,EL, compared with those of group C ( P <0.05) . The PERAs in group EM,EL were significantly higher than those in group EH(P <0. 05) , and those in group EL were no significantly difference from those in group EM (P<0.05).Discussion1. Although a large portion of the cell loss during cardiac ische-mia and reperfusion occurs through necrosis, there is presently increas-ing interest in the possibility that myocardial cell death may also occur through apoptosis. Unlike necrosis, apoptosisproceeds through a ge-netically programmed series of biochemical and morphological steps de-signed to avoid...
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