高位脊髓损伤对大鼠心肌功能的影响

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。

Effect of high level spinal cord injury on rat heart function

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: Forty-eight 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 ventricle 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 cardiac 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.