Department of Rehabilitation Medicine, The First Affiliated Hospital of Nanjing Medical University, China.
Am J Phys Med Rehabil. 2011 Feb;90(2):97-105. doi: 10.1097/PHM.0b013e3182017483.
The aim of this study was to investigate the protective effect of physiologic ischemic training of normal skeletal muscle against myocardial infarction.
Thirty-five rabbits were implanted with water balloon constrictors in the left ventricular branch to cause myocardial ischemia and an electrode near the left sciatic nerve for electric muscle stimulation for physiologic ischemic training. Three groups were randomly selected: the pure ischemia (PI) group received myocardial ischemia for 2 mins, two times a day, five times a week; the exercise training (ET) group received myocardial ischemia as did the PI group, plus 4 mins of physiologic ischemic training, two times a day, five times a week; and the sham-operated (SO) group was the sedentary controls. After 4 wks of training, the left ventricular branch was occluded to cause infarction. Infarct size was measured by magnetic resonance imaging; left ventricular ejection fraction, by echocardiogram; capillary density, by immunohistochemistry; and collateral circulation blood flow, by a microsphere technique.
The ET group's infarct size was significantly smaller than that of the PI group (P < 0.01) and the SO group (P < 0.01). Change in left ventricular ejection fraction in the ET group was significantly lower than in the SO group (P < 0.01), and capillary density in the ET group was significantly higher than in the PI group (P< 0.01) and the SO group (P < 0.01). Collateral circulation blood flow in the ET group was significantly higher than in the PI group (P < 0.01) and the SO group (P< 0.01). Capillary density was significantly correlated with endpoint collateral circulation blood flow (r = 0.91, P = 0.000), infarct size (r = -0.91, P = 0.000), and change in left ventricular ejection fraction (r = -0.94, P = 0.000).
Physiologic ischemic training of skeletal muscle may induce collateral circulation development in the myocardium, thus decreasing infarct size when infarction occurs.
本研究旨在探讨正常骨骼肌的生理性缺血训练对心肌梗死的保护作用。
35 只兔子被植入左心室分支的水囊缩窄器以引起心肌缺血，并在左坐骨神经附近植入电极进行生理性缺血训练的电肌肉刺激。随机选择三组：单纯缺血（PI）组接受 2 分钟、每天两次、每周五次的心肌缺血；运动训练（ET）组接受与 PI 组相同的心肌缺血，外加每天两次、每周五次的 4 分钟生理性缺血训练；假手术（SO）组为久坐对照组。经过 4 周的训练后，左心室分支被阻断以引起梗死。通过磁共振成像测量梗死面积；通过超声心动图测量左心室射血分数；通过免疫组织化学测量毛细血管密度；通过微球技术测量侧支循环血流。
ET 组的梗死面积明显小于 PI 组（P<0.01）和 SO 组（P<0.01）。ET 组左心室射血分数的变化明显低于 SO 组（P<0.01），毛细血管密度明显高于 PI 组（P<0.01）和 SO 组（P<0.01）。ET 组的侧支循环血流明显高于 PI 组（P<0.01）和 SO 组（P<0.01）。毛细血管密度与终点侧支循环血流（r=0.91，P=0.000）、梗死面积（r=-0.91，P=0.000）和左心室射血分数变化（r=-0.94，P=0.000）显著相关。
骨骼肌的生理性缺血训练可能诱导心肌侧支循环的发展，从而减少梗死发生时的梗死面积。
