山羊烟雾吸入性损伤血栓素和前列环素的变化

本实验制作慢性肺淋巴瘘模型13只,行烟雾吸入致伤。观测了伤后6小时内TXA_2和PGI_2含量,EVLW、Q_L和L/P、血流动力指标、血气、血小板及白细胞计数。EVLW、Q_L和L/P 1小时均明显增加,2小时达高峰,6小时仍在较高水平,提示为通透性肺水肿。TXA_2和PGI_2伤后均增加,TXA_2和TXA_2/PGI_2比值与EVLW和L/P在时间和程度上变化一致,提示它们可能与肺水肿形成有关。其机理可能通过直接作用和/或使血小板、白细胞聚集,释放化学介质,导致肺微血管通透性增加。此外,TXA_2在早期PAP增加中也可能起一定作用。

Changes of Thromboxane and Prostacyclin after Smoke Inhalation Injury in Goats

Smoke inhalation injury was inflicted to 13 goats with chrnoic lung lymph fistula. The contents of thromboxane A2(TXA2) and prostacyclin(PGI2) in plasma, lung lymph fluid, and lung tissues were measured in the 6-hour-periodafter injury with radioimmunoassay. Extravascular lung water(EVLW), thequantity of lymph fluid (QL), the ratio of protein contents in lung lymph and plasma(L/P), hemodynamic parameters, blood gases, platelet count and WBCcount were also determined.It was found that EVLW. QL and L/P increased markedly in the 1st hour, reached the peak of elevation in the 2nd hour, and remained higher than the pre-injury level in the 6th hour after injury, which implies the existence of permea-bility pulmonary edema . Both TXA2 and PGI2 also increased markedly after, injury. The changes of TXA2 and TXA2/PGI2 ratio were in parallelto those of EVLW, QL and L/P in time course and in degree, which implies that the changes of TXA2 and PGI2 might play an important role in the genesis of permeability pulmonary edema. The mechanism might be the direct injury of the two substances and/or the precipitation of platelet and WBC aggregation which can release certain chemical mediators to increase the permeability of the capillaries. In addition, TXA2 might also result in the early elevation of pulmonary arterial pressure.