Devitt H H, Burka J F, Jones R, Amy R W, King E G
Department of Pathology and Biochemistry, University of Alberta Hospital, Edmonton, Canada.
Surgery. 1988 Feb;103(2):213-20.
Oleic acid (OA) injection into the lungs of dogs produces pulmonary edema and decreased cardiac output, and the result is combined hypoxic and stagnant hypoxia. Prostacyclin (PGI2) has some effects that may be beneficial in the alleviation of hypoxia. We studied 18 anesthetized dogs that were divided into three groups: (1) Six dogs acted as controls and did not receive OA or PGI2, (2) six dogs received OA but no PGI2, and (3) six dogs were first given OA and 1 hour later an infusion of PGI2 (100 ng/kg/min) was started and continued for 4 hours. All dogs were killed at the end of the study and their lungs were removed for weighing and preparation for microscopic examination. Compared with controls, OA caused a low cardiac output, high systemic and pulmonary vascular resistance, and increased right-to-left intrapulmonary shunt. The group that received OA and PGI2 demonstrated a well-maintained cardiac output and a low systemic vascular resistance. Right-to-left intrapulmonary shunt, however, increased in these dogs compared with the dogs not given PGI2. All animals given OA had similar wet/dry lung weights and histologic appearances. Our results suggest that the only beneficial effect of PGI2 in OA-induced lung injury is to improve the stagnant hypoxia, but this is associated with an aggravation of the hypoxic hypoxia. The result of these competing effects appears to be a mild overall improvement in oxygen delivery as suggested by the slightly higher mixed venous PO2 in the group that received PGI2.
向犬肺内注射油酸（OA）会导致肺水肿和心输出量降低，结果是合并了低氧性和淤血性缺氧。前列环素（PGI2）具有一些可能有助于缓解缺氧的作用。我们研究了18只麻醉犬，将其分为三组：（1）6只犬作为对照组，未接受OA或PGI2；（2）6只犬接受OA但未接受PGI2；（3）6只犬先给予OA，1小时后开始输注PGI2（100 ng/kg/分钟），并持续4小时。在研究结束时处死所有犬，取出它们的肺进行称重并制备用于显微镜检查。与对照组相比，OA导致心输出量降低、全身和肺血管阻力升高以及肺内右向左分流增加。接受OA和PGI2的组显示心输出量维持良好且全身血管阻力较低。然而，与未给予PGI2的犬相比，这些犬的肺内右向左分流增加。所有给予OA的动物肺湿/干重和组织学表现相似。我们的结果表明，PGI2在OA诱导的肺损伤中的唯一有益作用是改善淤血性缺氧，但这与低氧性缺氧的加重有关。这些相互竞争作用的结果似乎是氧输送有轻微的总体改善，如接受PGI2组的混合静脉血氧分压略高所提示的那样。
