高位脊髓损伤对大鼠心肌功能的影响

Effect of high level spinal cord injury on rat heart function

目的 探讨高位脊髓损伤(SCI)对大鼠心肌的影响以及内皮素-1(ET-1)在其中的作用。方法 采用Allens打击法制备中度高位SCI动物模型。大鼠随机分为假手术对照组以及C7损伤后4、12、24、48和 72 h 6组(n=8).记录各组平均动脉压(MAP)、心率(HR)、左室收缩峰压(LVSP)和左室内压变化最大速率 (±dp／dt max);测定各组血清乳酸脱氢酶(LDH)、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)和ET-1的含 量变化;取心肌组织匀浆,测定心肌组织ET-1含量变化。另取心肌内壁组织作透射电镜扫描,观察心肌超微 结构的变化。结果 各损伤组的HR、MAP、LVSP及±dp／dt max均显著下降(P<0.05或P<0.01).尤以伤 后12 h下降最显著(P均<0.01);而3种心肌酶均显著升高(P<0.05或P<0.01)。血浆和心肌ET-1在损 伤后4 h即明显升高(P均<0.05),12 h达高峰。高位SCI 12 h后,大鼠心肌肌丝轻度溶解,线粒体空泡变性。 结论 高位SCI后大鼠心肌受到一定程度损害,全身和心肌局部ET-1产生过多可能是参与因素之一。

Objective To study the effects of high level spinal cord injury (SCI) on rat heart, and investigate the role of endothelin - 1(ET - 1) in the harmful effects on heart after SCI. Methods Fortyeight male SD rats were randomly divided into six groups of 8 animals each: control group;4 - hour group: 4 th hour after injury to spinal cord at cervical 7 level;12 -hour group: 12 th hour after injury to 7 spinal cord at C7 level; 24 - hour group with same injury; 48 - hour group and 72 - hour group, all with same injury. Mean arterial pressure (MAP), heart rate(HR), left ventrical systolic pressure (LVSP), and left ventricular maximum velocities of contraction (±dp/dt max) were recorded in each group. Lactate dehydrogenase (LDH), creatine kinase(CK), MB isoenzyme of creatine kinase (CK - MB) and ET - 1 contents in the myocardium, were also measured. Specimens of the myocardium were harvested for ultrastructure examination with transmission electron microscopy. Results Hemodynamics variables including HR, MAP, LVSP and ±dp/dtmax were significantly decreased in all the injury groups compared with that of control group (P<0. 05 or P<0. 01). These variables in 12 -hour group showed lowest values among all the groups (all P<0. 01). But the values of cardiac enzymes were much higher in five injury groups compared with that of control group (P<0. 05 or P<0. 01). ET - 1 contents in serum and cardie tissue raised markedly after the injury was inflicted to the animals (P<0. 05), reaching peak at 12 hours (P<0.01). Ultrastructural examination of the myocardial tissue demonstrated that there were mild dissolution of myocardial fibriles and vacuolation of mitochondria at 12 hours after injury. Conclusion High level SCI could induce myocardial injuries and an excessive production of ET -1 in circulation and myocardial tissue might play a role in myocardial damage after injury of the spinal cord at a high level.