摘要
ＯｂｊｅｃｔｉｖｅＴｏｉｎｖｅｓｔｉｇａｔｅｔｈｅｅｆｅｃｔｓｏｆｉｓｃｈｅｍｉｃｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇ（ＰＣ）ａｎｄＡＴＰｓｅｎｓｉｔｉｖｅＫ＋ｃｈａｎｎｅｌｓ（Ｋ＋ＡＴＰ）ｏｐｅｎｅｒｎｉｃｏｒａｎｄｉｌｏｎｒｅｐｅｒｆｕｓｉｏｎａｒｈｙ...
Objective To investigate the effects of ischemic preconditioning (PC) a nd ATP sensitive K + channels (K + ATP ) opener nicorandil on reperfusion arrhythmias and electrophysiology.Langendorff perfused rat hearts were subjected to ischemic PC with three cycles of 2 minutes of global ischemia or infusion of K + ATP o pene r nicorandil with subsequent 5 minutes global ischemia and reperfusion. The inci dence of reperfusion arrhythmias, ventricular fibrillation threshold (VFT), effe ctive refractory period (ERP) and monophasic action potential duration (MAPD) o f the left and right ventricles were compared to those from control rat hearts.Results The results indicated that PC reduced the incidence of total ar rhythmias and ventricular fibrillation during reperfusion (P<0.0 5, vs controls). PC markedly delayed the onset of arrhythmia after reper f usion (P<0.01, vs controls). PC significantly enhanced the VFT v alues during reperfusion and shorte ned the ERP and the MAPD during ischemia. VFT was restored more rapidly than tha t in controls. K + ATP opener nicorandil neither reduced the incidence of total arrhythmias and VF nor delayed arrhythmia onset. Nicorandil shortened ERP and MAPD 90 without enhancing the VFT values, and VFT returned to normal as slowly as that in controls.Conclusions We conclude that PC protects the globally ischemic rat hear ts from reperfusion arrhythmias. The antiarrhythmic effect of PC is likely to be related to a significant increase of VFT. K + ATP opener nicorandil has n o potential antiarrhythmic action and K + ATP channels may not play a majo r role in the antiarrhythmic effects of ischemic PC in isolated rat hearts. Chin Med J 1999; 112(5):424 429 Experiments suggest that repeated brief coronary artery occlusions protect t he heart from irreversible injury during subsequent longer episodes of ischemia. Murry et al. 1 used the term “ischemic preconditioning” to describe this pa radox ical increase in ischemic tolerance of the myocardium. Ischemic preconditioning (PC) reduces myocadial infarct size and improves postischemic recovery of ventri cular function. 2,3 Interestingly, several papers related that ischemic PC can reduce the burst of ventricular arrhythmias induced by coronary occlusion a nd reperfusion in anesthetized rats, 3,4 but little is known about the mec hanism. 5 Another question is whether the results in vivo and in vitro are ide ntical or not. Furthermore, whether ATP sensitive K + channels (K + ATP ) play a major role in the antiarrhythmic effect of PC remains contraversial 5, 6 Thus the present investigation was designed to study the effects of ischemic PC and K + ATP opener nicorandil on the r eperfusion arrhythmias and electrophysiologic characters, including ventricular fibrillation threshold (VFT), effective refractory period (ERP) and monophasic a ction potential duration (MAPD) in the globally ischemic rat hearts.
