骨骼肌缺血再灌注损伤及发病机制初探

Mechanisms of postischemic injury in cremaster muscle

目的 探讨骨骼肌缺血再灌注损伤过程的微循环变化、组织学改变以及多肽含量变化和意义。方法 42只雄性大鼠随机分为留伴行神经组和去伴行神经组 ,建立标准骨骼肌缺血再灌注模型。采用激光多谱勒及显微放大分析系统、组织学方法以及凝胶电泳方法等观察缺血再灌注损伤变化。结果 缺血再灌注损伤后的骨骼肌微血管管径在 2 0分钟时恢复率基本达到高峰约 6 0 % ,此后为平台期 :90分钟最高峰 ,为 75 %。主干血管流速率亦在 2 0分钟基本达到上限。病理检查显示 :缺血的骨骼肌纤维呈空泡状 ,核形态增大 ,染色加深 ,红细胞严重聚集。凝胶蛋白电泳提示 :缺血骨骼肌中分子量2 0KD左右的多肽显著增加。结论 骨骼肌缺血再灌注损伤发生后 ,骨骼肌的微循环发生不同程度的破坏 ,及因之导致骨骼结构损伤和异常的 2 0KD多肽含量明显增加 ,以及红细胞凝聚 ,白细胞的改变 。

Objective*'To study the changes of microcirculation,histology and polypeptide content in cremaster muscle after reperfusion following ischemia Methods*'42 Sprague Daley rats were divided into two groups:innervation group and denervation group,and standard ischemia/reperfusion injury models were established.Laser Doppler,microscopic analysis system,histological study and gel electrophoresis were applied to analyse the course of ischemia and reperfusion.Results*'At 20 minutes after ischemia/reperfusion injury,the recovery ratio of capillary vessel diameter in cremaster muscle was 60% which was close to peak.Following period was balcony stage,and till 90 minutes it reached to top value-75%.The pathologic examination showed that ischemia cremaster muscle fiber of vacuoles appearance,increased and deeply dying cell nuclear and accumulation of RBC.The gel electrophoresis test showed that the content of polypeptide of molecular weight about 20KD in ischemic cremaster muscle obviously increased.Conclusion*'All of the above outcomes indicated that the microvascular changes in the postischemic cremaster muscle were severe,while leads to failure of functional recovery after surgery.The mechanism of postischemic injury is not completely understood,but it may be incited by categories of ischemia,intimal damage,and systemic or local responses.The first tissue thought to be irreversibly injured is the endothelium and white blood cell.