Marber M S, Walker D M, Eveson D J, Walker J M, Yellon D M
Hatter Institute for Cardiovascular Studies, Division of Cardiology, University College Hospital, London, United Kingdom.
Cardiovasc Res. 1993 Apr;27(4):597-601. doi: 10.1093/cvr/27.4.597.
Rapid pacing has been shown to precondition the dog heart against ischaemic dysrhythmia. The aim of this study was to determine whether rapid pacing could also limit infarct size.
Rabbits (n = 5) were rapidly paced via the left atrium at 420-480 beats.min-1. Five min of rapid pacing and 10 min of recovery in sinus rhythm were followed by 45 min of regional ischaemia and 120 min of reperfusion. Control rabbits (n = 9) were treated identically without prior rapid pacing. Infarct size was determined in both groups using tetrazolium and expressed as a percentage of the area at risk demarcated by fluorescent microspheres. In a separate series of experiments, rapidly paced Langendorff perfused rabbit hearts (n = 9) were used to determine coronary flow under perfusion conditions designed to simulate the in vivo situation during rapid pacing.
Rapid pacing caused a fall in systolic pressure from 91.4(SEM 4.5) to 47.0(5.9) mm Hg (p < 0.01) and diastolic pressure from 67.2(2.9) to 23.6(3.2) mm Hg (p < 0.01). Both recovered within 30 s of cessation of pacing. During rapid pacing the action potential duration shortened from 192(13) to 128(5) ms (p = 0.01) and developed electrical alternans (n = 4). Following rapid pacing the ECG showed either ST depression or T wave inversion (n = 4). Despite these profound changes, rapid pacing did not reduce infarct size v control [52.7(4.6)% v 60.8(9.1)% of the area at risk, respectively]. The in vitro experiments estimated that rapid pacing would result in a reduction in coronary flow to 44% of that in sinus rhythm without a significant rise in lactate efflux.
In our model, pretreatment with rapid pacing fails to reduce infarct size. The most likely reason for this is that rapid pacing at a rate of 480 beats.min-1 does not cause myocardial ischaemia of sufficient severity to trigger the preconditioning response.
快速起搏已被证明可使犬心脏对缺血性心律失常产生预处理作用。本研究的目的是确定快速起搏是否也能限制梗死面积。
对5只兔子经左心房以420 - 480次/分钟的频率进行快速起搏。快速起搏5分钟并在窦性心律下恢复10分钟后，进行45分钟的局部缺血和120分钟的再灌注。对照组9只兔子进行相同处理，但无预先快速起搏。两组均使用四氮唑测定梗死面积，并表示为荧光微球划定的危险区域面积的百分比。在另一系列实验中，使用经快速起搏的Langendorff灌注兔心脏（9只），在旨在模拟快速起搏期间体内情况的灌注条件下测定冠状动脉血流量。
快速起搏使收缩压从91.4（标准误4.5）降至47.0（5.9）mmHg（p < 0.01），舒张压从67.2（2.9）降至23.6（3.2）mmHg（p < 0.01）。两者在起搏停止后30秒内均恢复。快速起搏期间动作电位时程从192（13）缩短至128（5）ms（p = 0.01）并出现电交替（4只）。快速起搏后心电图显示ST段压低或T波倒置（4只）。尽管有这些显著变化，但与对照组相比，快速起搏并未减少梗死面积[分别为危险区域面积的52.7（4.6）%和60.8（9.1）%]。体外实验估计，快速起搏会使冠状动脉血流量降至窦性心律时的44%，而乳酸流出量无显著增加。
在我们的模型中，快速起搏预处理未能减少梗死面积。最可能的原因是480次/分钟的快速起搏不会引起严重程度足以触发预处理反应的心肌缺血。
