EFFECT OF PRECONDITIONING ISCHEMIA ON REPERFUSION ARRHYTHMIAS AFTER CORONARY-ARTERY OCCLUSION AND REPERFUSION IN THE RAT

EFFECT OF PRECONDITIONING ISCHEMIA ON REPERFUSION ARRHYTHMIAS AFTER CORONARY-ARTERY OCCLUSION AND REPERFUSION IN THE RAT
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DOI:
10.1161/01.res.68.1.61
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发表时间:
1991-01-01
影响因子:
20.1
通讯作者:
KLONER, RA
KLONER, RA
中科院分区:
医学1区
文献类型:
--
作者:
HAGAR, JM;HALE, SL;KLONER, RA

文献摘要

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在大鼠冠状动脉闭塞5分钟后再灌注时可预期地发生严重心律失常。关于心脏缺血预处理(PC)是否能降低此类心律失常的发生率,现有的数据很少。研究了PC(3个周期,每个周期为冠状动脉闭塞2分钟和再灌注5分钟)对随后冠状动脉闭塞5分钟再灌注后心律失常发生的影响。大鼠(每组n = 16)单独进行5分钟闭塞和再灌注,或在PC预处理后进行;在缺血期间和再灌注10分钟内监测心律失常,并取左心室缺血区和非缺血区的组织进行磷酸肌酸和三磷酸腺苷检测。PC降低了闭塞期间室性心动过速(VT)的发生率(对照组为81%,PC组为13%,p < 0.001)。在随后的再灌注中,PC组无动物发生室颤(VF),而对照组有13只(81%)发生(p < 0.001),PC组无动物发生不可逆性VF,而对照组有7只(44%)发生(p = 0.007)。PC组有4只(25%)发生VT,而对照组全部(100%)发生(p < 0.001)。PC将VT加VF的平均持续时间从320 ± 54秒减少到5 ± 1秒(p < 0.001),并将再灌注后心律失常发作延迟从8 ± 2秒推迟到85 ± 35秒。与无不可逆性VF的对照组相比,PC组动物再灌注结束时缺血区的磷酸肌酸水平无差异(16.2 ± 4.1与15.5 ± 3.9 nmol/mg蛋白,p =无显著差异)。磷酸肌酸水平与VT或VF的发生无关(发生VF为14.0 ± 5.6 nmol/mg蛋白,未发生VF为16.7 ± 3.3;发生VT为16.4 ± 3.5,未发生VT为15.4 ± 4.5;p =无显著差异)。缺血区的三磷酸腺苷水平不受PC影响(PC组为15.5 ± 2.1,对照组为14.5 ± 1.9 nmol/mg蛋白)。当在冠状动脉闭塞5分钟之前进行PC预处理时,通常严重的再灌注心律失常明显减轻。PC的这种保护作用不太可能与高能磷酸化合物的改变有关。
Severe arrhythmias occur predictably on reperfusion after 5 minutes of coronary occlusion in the rat. There is little data available on whether ischemic preconditioning (PC) of hearts can reduce the incidence of such arrhythmias. The effect of PC (three cycles of 2 minutes of coronary occlusion and 5 minutes of reperfusion) on development of arrhythmias after a subsequent 5-minute coronary artery occlusion and reperfusion was studied. Rats (n = 16 each group) underwent 5-minute occlusion and reperfusion alone or preceded by PC; arrhythmias were monitored during ischemia and for 10 minutes of reperfusion, and biopsies were taken for creatine phosphate and adenosine triphosphate in ischemic and nonischemic zones of the left ventricle. PC reduced the incidence of ventricular tachycardia (VT) during occlusion (81% control versus 13% PC, p < 0.001). On subsequent reperfusion, ventricular fibrillation (VF) developed in zero PC animals versus 13 (81%) of controls (p < 0.001), and irreversible VF in zero of PC versus seven (44%) of controls (p = 0.007). VT occurred in four (25%) of PC versus all (100%) of controls (p < 0.001). PC reduced mean duration of VT plus VF from 320 +/- 54 to 5 +/- 1 seconds (p < 0.001) and delayed arrhythmia onset from 8 +/- 2 to 85 +/- 35 seconds after reperfusion. There was no difference in creatine phosphate levels in the ischemic zone at the end of reperfusion in PC animals compared with controls without irreversible VF (16.2 +/- 4.1 versus 15.5 +/- 3.9 nmol/mg protein, p = NS). There was no relation between creatine phosphate levels and occurrence of VT or VF (14.0 +/- 5.6 nmol/mg protein VF versus 16.7 +/- 3.3 no VF; 16.4 +/- 3.5 VT versus 15.4 +/- 4.5 no VT; p = NS). Adenosine triphosphate levels in the ischemic zone were unaffected by PC (15.5 +/- 2.1 versus 14.5 +/- 1.9 nmol/mg protein, PC versus control). When a coronary occulusion of 5 minutes duration is preceded by PC, the usually severe reperfusion arrhythmias are markedly attenuated. This protective effect of PC is not likely to be related to alterations in high-energy phosphate compounds.