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应用光镜及电镜 ,对急性缺氧状态下大鼠的肺小动脉内皮细胞 (pulmonarysmallarteryendothelialcell,PSAEC)及肺毛细血管内皮细胞 ( pulmonarycapillaryendothelialcell,PCEC)进行形态学观察 ,并用显微分光光度仪对急性缺氧状态下PSAEC的乳酸脱氢酶 (lacticdehydrogenase,LDH)活性进行定量分析。发现 :急性缺氧可引起PSAEC和PCEC发生各种损伤性形态变化 ,损伤程度随缺氧时间延长而加重 ;与缺氧前相比 ,急性缺氧后各组PSAEC的LDH活性均下降 ,且随缺氧时间的延长 ,LDH活性下降得更明显。提示 :急性缺氧可引起血管内皮细胞 (VEC)损伤 ,损伤程度随缺氧时间的延长而加重 ,血管内皮细胞损伤的程度与其LDH活性密切相关。
The morphological changes of pulmonary arteriolar endothelial cells (PSAECs) and pulmonary capillaries endothelial cells (PCECs) of rats under acute hypoxic conditions were observed by light microscope and electron microscope. Acute hypoxia The PSAEC lactic dehydrogenase (LDH) activity in oxygen state was quantified. It was found that acute hypoxia could cause various morphological changes of PSAEC and PCEC, and the degree of injury aggravated with the prolongation of hypoxia. Compared with pre-hypoxia, LDH activity of PSAEC in each group decreased after acute hypoxia Hypoxia time, LDH activity decreased more significantly. Hint: Acute hypoxia can cause vascular endothelial cell (VEC) injury, the degree of injury aggravates with the prolongation of hypoxia, and the degree of vascular endothelial cell injury is closely related to its LDH activity.