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研究心脏缺血预适应（ＰＣ）对溶血性磷脂酰胆碱（ＬＰＣ）损伤心肌作用的影响，并探讨降钙素基因相关肽（ＣＧＲＰ）在ＰＣ中的作用．离体大鼠心脏Ｌａｎｇｅｎｄｏｒｆ法灌流，记录心率，冠脉流量，左室压和左室压最大上升速率（＋ｄｐ／ｄｔｍａｘ），并测定灌流液中肌酸磷酸激酶（ＣＰＫ）含量．结果显示，ＬＰＣ能降低各项心功能指标，并使ＣＰＫ释放增加；ＰＣ（缺血５ｍｉｎ，再灌５ｍｉｎ，重复３次）能减轻ＬＰＣ的损伤作用；ＰＣ的心肌保护作用可被选择性ＣＧＲＰ受体拮抗剂ＣＧＲＰ８－３７所取消；预先给予ＣＧＲＰ或辣椒素能产生与ＰＣ相同的心肌保护作用．对照组，ＬＰＣ，ＰＣ＋ＬＰＣ，ＣＧＲＰ８－３７，ＣＧＲＰ８－３７＋ＰＣ＋ＬＰＣ，ＣＧＲＰ＋ＬＰＣ，ＣＧＲＰ８－３７＋ＣＧＲＰ＋ＬＰＣ，辣椒素＋ＬＰＣ组ＣＰＫ释放量分别为０．２６±０．０５，２．３０±０．２２，０．２５±０．０３，０．３０±０．０８，２．６０±０．１５，０．２４±０．０５，２．７０±０．２０和０．２５±０．０７μｍｏｌ·ｍｉｎ－１·ｇ－１湿组织．这些结果提示：１）ＰＣ对ＬＰＣ所致心肌损伤具有保护作用；２）ＰＣ的保护作用是由ＣＧＲＰ所介导；３）ＣＧＲＰ或辣椒素可模拟ＰＣ的保护作?
To study the effect of ischemic preconditioning (PC) on the myocardial injury induced by hemolytic phosphatidylcholine (LPC), and to explore the role of calcitonin gene related peptide (CGRP) in PC. Heart rate, coronary flow, left ventricular pressure and maximal rate of increase of left ventricular pressure (+ dp / dtmax) were recorded by Langendorf perfusion in vitro. The content of creatine phosphokinase (CPK) in perfusate was measured. The results showed that LPC can reduce each cardiac function index and increase the release of CPK; PC (ischemic 5min, reperfusion 5min, repeated 3 times) can reduce the injury of LPC; PC myocardial protection can be selectively CGRP The blockade of CGRP8-37 was abolished; pretreatment with CGRP or capsaicin produced the same cardioprotection as PC. The release of CPK in control group, LPC, PC + LPC, CGRP8-37, CGRP8-37 + PC + LPC, CGRP + LPC, CGRP8-37 + CGRP + LPC and capsaicin + LPC groups were 0.26 ± 0.05, 2.30 ± 0.22 and 0.25 ± 0.30 ± 0.08, 2.60 ± 0.15, 0.24 ± 0.05, 2.70 ± 0.20 and 0.25 ± 0.07 μmol · min-1 · g- 1 wet tissue. These results suggest that: 1) PC protects against LPC-induced myocardial injury; 2) the protective effect of PC is mediated by CGRP; 3) CGRP or capsaicin can mimic the protection of PC;