降钙素基因相关肽对缺血及再灌注心肌的保护作用

Protective effect of calcitonin gene-related peptide on ischemic and reperfused myocardium

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．

In the present study, we observed the effect of calcitonin gene-related peptide(CGRP)on epicar- dial electrogram, myocardial free radical metabolism,myocardial infarction scale and myocardial supermi-crostructures following myocardial ischemia and reperfusion. The results showed that after myocardial is-chemia and reperfusion,the characteristic ischemic change occurred in epicardial electrogram with a high inci-dence of arrhythmia. Its ST segment was elevated from 0.6±0.4 mV to 12.5±5. 4 and 4.8±2. 6 mV(P< 0.01)and the arrhythmic incidences were 4%and 62.5%respectively; Cardial SOD activity was decreased from 230±40 U/g MC to 120±50 and 110±30 U/g MC, but the content of MDA was increased from 30±6nmol/g MC to 89±16 and 138±18 nmol/g MC(P<0.01);Myocardial infarction was observed following ischemia with the supermicrostructures obviously injured. After intravenous injection of CGRP,the previousabnormal changes were alleviated significantly (P<0.01),suggesting that CGRP has obvious protective ef-fect on ischemic and reperfused myocardium. This also ushers in a possibility of clinical use of CGRP for the treatment of AMI.