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大鼠68只,分为对照组、单纯缺氧组、单纯栓塞组和缺氧复合肺微栓塞组。在减压舱内模拟6000m高原48h造成低压缺氧;自尾静脉注入20％甲醛固定的蟾蛛红细胞造成肺微栓塞。各组动物在麻醉下,测右心室内压,然后经股静脉注入~(51)Cr标记的大鼠红细胞,10min后自颈动脉取血1ml,立即开胸取肺。称量血和肺湿重后,分别测定其放射活性,然后将标本置70℃恒温箱内烤干、称量肺和血干重。根据公式计算无血肺组织干重、肺体指数、肺血管外含水量。结果表明,缺氧和栓塞均使右心室收缩压升高,缺氧复合肺微栓塞组右心室收缩压最高。单纯缺氧时无血肺组织干重增加,缺氧复合肺微栓时,干重增加更明显。缺氧复合肺微栓塞组的肺血管外含水量显著高于对照组和单纯栓塞组。
Sixty-eight rats were divided into control group, simple hypoxia group, simple embolization group and hypoxic composite pulmonary micro-embolization group. Hypobaric hypoxia was induced in the decompression cabin simulating a 6000-m plateau for 48 hours, and 20% formalin-fixed toadstool cells were injected into the caudal vein to cause pulmonary micro-embolism. Each group of animals under anesthesia, measured right ventricular pressure, and then injected into the femoral vein ~ (51) Cr-labeled rat erythrocytes, 10min after taking blood from the carotid artery 1ml, chest immediately take the lung. Weigh blood and lung wet weight, respectively, measured radioactivity, and then the specimen was set at 70 ℃ oven dry, weighed lung and blood dry weight. Calculated according to the formula without dry weight of lung tissue, lung index, pulmonary extravascular water content. The results showed that both hypoxia and embolization increased right ventricular systolic pressure, and the highest right ventricular systolic pressure in hypoxic composite pulmonary microembolism group. When hypoxia alone did not increase the dry weight of hematopoietic tissue, hypoxia combined pulmonary micro-embolism, dry weight increased more significantly. The extra-pulmonary extravascular water content in hypoxic combined pulmonary microembolism group was significantly higher than that in control group and simple embolization group.