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作者用家兔急性心肌缺血及再灌注模型观察了降钙素基因相关肽（ＣＧＲＰ）对心外膜电图、心肌自由基代谢、心肌梗塞面积和心肌超微结构的影响．结果表明，心肌缺血和再灌注可导致心外膜电图出现特征性缺血改变，其ＳＴ段由０．６±０．４ｍＶ分别升高到１２．５±５．４和４．８±２．６ｍＶ（Ｐ均＜０．０１）；心律失常发生率分别为４０％和６２．５％；心肌组织ＳＯＤ活性由２３０±４０Ｕ／ｇ组织（ＭＣ）分别降低到１２０±５０及１１０±３０Ｕ／ｇＭＣ，而ＭＤＡ含量由３０±６ｎｍｏｌ／ｇＭＣ分别增加到８９±１６和１３８±１８ｎｍｏｌ／ｇＭＣ（Ｐ均＜０．０１）；缺血后心肌出现心肌梗塞，超微结构有明显损伤；静脉注射ＣＧＲＰ后，ＳＴ段恢复到２．７±２．１ｍＶ，心律失常消失，ＳＯＤ活性及ＭＤＡ含量分别升高到１８０±３０Ｕ／ｇＭＣ和降低到９７±１１ｎｍｏｌ／ｇＭＣ，心肌梗塞面积由缺血时９．８±１．２ｍｍ￣２降为５．３±０．６ｍｍ￣２（Ｐ均＜０．０１），超微结构损伤明显减轻，提示ＣＧＲＰ对缺血心肌有显著的保护作用；该作用为临床应用ＣＧＲＰ治疗急性心肌梗塞提供了可能的依据．
The effect of calcitonin gene-related peptide (CGRP) on epicardial electrocardiogram, myocardial free radical metabolism, myocardial infarct size and myocardial ultrastructure was observed in a rabbit model of acute myocardial ischemia and reperfusion. The results show that myocardial ischemia and reperfusion can lead to characteristic ischemia in epicardial electrocardiogram, the ST segment increased from 0.6 ± 0.4mV to 12.5 ± 5.4 and 4.8 ± 2.6mV (P <0.01). The incidence of arrhythmia was 40% and 62.5% respectively. The activity of SOD in myocardium was decreased from 230 ± 40U / g tissue (MC) to 120 ± 50 and 110 ± 30U / GMC, while the MDA content increased from 30 ± 6nmol / g to 89 ± 16 and 138 ± 18nmol / gMC respectively (P <0.01). Myocardial infarction was found in ischemic myocardium with obvious ultrastructure damage. Intravenous injection After CGRP, ST segment recovered to 2.7 ± 2.1mV, arrhythmia disappeared, SOD activity and MDA content increased to 180 ± 30U / gMC and decreased to 97 ± 11nmol / gMC respectively. The area of myocardial infarction was increased from 9 .8 ± 1.2mm ~ 2 down to 5.3 ± 0.6mm ~ 2 (P both <0.01). The ultrastructural damage was significantly reduced, suggesting that CGRP has a significant protective effect on ischemic myocardium. This effect provides a possible basis for the clinical application of CGRP in the treatment of acute myocardial infarction.