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目的 探讨肢体缺血再灌注后微血管痉挛的发生机制。方法 应用兔后肢止血带常温缺血模型及足背肌腱表面微循环观察法 ,观察肢体缺血 2小时及 5小时再灌注后微动脉对局部滴注血管收缩剂 [去甲肾上腺素 (10 - 6 mol/ L ) ]、内皮依赖性血管舒张剂 [乙酰胆碱 (10 - 6 mol/ L ) ]及内皮非依赖性血管舒张剂 [硝酸甘油(10 - 4 mol/ L) ]的反应性变化。结果 与缺血前比较 ,肢体缺血 2小时再灌注后 ,微动脉对上述三种血管活性物质的反应性均无显著性变化 ;缺血 5小时再灌注后 ,微动脉对去甲肾上腺素的收缩反应仍无显著性变化 ,但对乙酰胆碱及硝酸甘油的舒张反应均见减弱 ,对乙酰胆碱的反应减弱非常显著 (P<0 .0 1) ,对硝酸甘油的反应减弱显著 (P<0 .0 5 )。结论 肢体缺血 2小时再灌注后 ,微动脉内皮依赖性和非依赖性舒张机制均无显著损害 ,但缺血 5小时再灌注后则上述两种血管舒张机制均受妨碍 ,尤以内皮依赖性舒张为著 ,这可能是长时间缺血肢体再灌注后发生微血管痉挛的主要原因。
Objective To investigate the mechanism of microvascular spasm after limb ischemia reperfusion. Methods Arterial ischemia model of rabbit hind limb tourniquet and microcirculation of tendon surface of dorsal flexor tendon were used to observe the effects of arteriole microinvasion (norepinephrine (10 - 6 mol / L)], the reactivity of endothelium - dependent vasodilator [acetylcholine (10 - 6 mol / L)] and endothelium - independent vasodilator [10-4 mol / L] Results Compared with those before ischemia, the reactivity of the arterioles to the above three vasoactive substances did not change significantly after reperfusion for 2 hours. After 5 hours of reperfusion, the reactivity of arterioles to norepinephrine The contractile response still showed no significant change, but the relaxation responses to acetylcholine and nitroglycerin were weakened, the response to acetylcholine was weakened significantly (P <0.01), and the response to nitroglycerin was weakened significantly (P <0. 0 5). Conclusions There was no significant impairment in endothelium-dependent and independent relaxation of arterioles after 2-hour reperfusion of limb ischemia, but both of the above-mentioned vasodilation mechanisms were impaired after 5-hour reperfusion, especially in endothelium-dependent Diastolic, this may be the main reason for the occurrence of micro-vascular spasm after long-term ischemic limb reperfusion.