摘要
目的明确降钙素基因相关肽（ＣＧＲＰ）是否在整体大鼠心肌缺血预适应（ＩＰＣ）中起作用。方法将 ９６只 ＳＤ大鼠随 机分为 ８组。所有动物均接受 ３０ ｍｉｎ缺血／ ２ ｈ再灌注，缺血预适应方案由 ３次 ５ ｍｉｎ缺血／ ５ ｍｉｎ再灌注组成。 ３０ ｍｉｎ缺血前 ２０ ｍｉｎ静脉注射 ＣＧＲＰ １０μｇ／ｋｇ·ｂ．ｗ．。预适应前 ３０ ｍｉｎ静脉注射优降糖（ＧＬＩ） ０．３ ｍｇ／ｋｇ·ｂ．ｗ．。首次预适应 缺血前静脉注射ＣＧＲＰ多抗（ＰｃＡｂ）２．５ｍｇ／ｋｇ·ｂ．ｗ．。梗死大小由硝基四唑氮篮染色判定，并以坏死区（ＩＳ）占危险区的百 分比表示。血浆ＣＧＲＰ浓度用放射免疫法测定。结果首次和第３次预适应缺血的血浆ＣＧＲＰ浓度均较对照组显著增 加（Ｐ＜０．０１），且后者增加更为明显（Ｐ＜０．０１）。ＩＰＣ能明显缩小心肌梗死范围和几乎完全抑制缺血和再灌注时室性心律 失常的发生，预先用ＣＧＲＰ－ＰｃＡｂ能明显减弱上述作用。ＣＧＲＰ预适应具有ＩＰＣ样心肌保护作用，但程度不及ＩＰＣ明显。 预先用ＧＬＩ均能取消ＩＰＣ和ＣＧＲＰ预适应缩小心肌梗死范围的作用，但对室性心律失常无影响。结论ＣＧＲＰ在整 体大鼠缺血预适应中可能起重要作用；
Objective The aim of this study was to investigate whether calcitonin gene-related peptide (CGRP) plays a role in ischemic preconditioning (IPC) in an intact rat model. Methods Ninety-six SD rats were randomly divided into 8 groups, all of whom were subjected to 30-min regional ischemic followed by 2-h reperfusion, after preconditioning disposal. The IPC protocol consisted of 3 cycles of 5-min regional ischemia and 3 cycles of 5-min reperfusion. The preconditioning disposal for different groups were as the following: CGRP (10 μg/kg·b.w.) was given 20 min before 30-min ischemia (CGRP group); glibenclamide (GLI) was given 30 min before CGRP (GLI＋CGRI, group) or IPC (GLI+ICP group); CGRP polyclonal antibody (PcAb, 2.5mg/kg) was given 20 min before first ischemic insult (PcAb group). Plasma CGRI, level was determined by radioimmunoassay (RIA), and the infarct size by nitro blue tetrazolium, expressed as percentage of the area at risk. Results Compared with control group, the mean plasma CGRP level at the end of first and especially the third ischemic insult was markedly increased in IPC group (p<0.01), and obvious reduction of the infarct size and declined incidence of ventricular arrhythmia during 30-min ischemia and the subsequent 2-h reperfusion were noted. These effects, however, were attenuated by pretreatment with CGRP PcAb. Pretreatment with CGRP also resulted in the reduction of the infarct size and inhibition of ventricular arrhythmia, only not so obvious as ICP did. GLI pretreatmed completely abolished the infarct-limiting effect of CGRP or IPC, but did not affect there antiarrhythmic effects. Conclusion As an endogenous myocardial protective substance, CGRP may play an important role in IPC, and its infarct-limiting effect was probably mediated by ATP-sensitive K+ channel.
出处
《第一军医大学学报》
CSCD
北大核心
2001年第1期25-28,共4页
Journal of First Military Medical University
关键词
降钙素基因相关肽
缺血预适应
心肌缺血
钾离子通道
ATP
大鼠
calcitonin gene-related peptide
ischemic preconditioning
cardioprotection
potassium channel
reperfusion injury
myocardial infarct
arrhythmia
