Veal C F, Jackson R M, Brannen A L, Fulmer J D
Department of Medicine, University of Alabama, Birmingham.
J Cardiovasc Pharmacol. 1989 Aug;14(2):227-32. doi: 10.1097/00005344-198908000-00007.
Reexpansion pulmonary edema (RPE) is an acute, unilateral lung injury initiated by cytotoxic oxygen metabolites and temporally associated with an influx of polymorphonuclear neutrophils (PMNs); these toxic oxygen products appear to result from reoxygenation of chronically collapsed lung. Lodoxamide tromethamine (U-42585E) reduces infarct size after reperfusion of ischemic myocardium. The possible protective effects of lodoxamide in RPE were examined. Right lungs of rabbits were collapsed for 7 days by injection of air into the pleural space. Reexpansion was accomplished by chest tube with negative pressure in spontaneously ventilating rabbits. Twelve pairs of animals received either lodoxamide (20 mg/kg/h intravenously (i.v.) from 30 min before reexpansion until they were killed) or an equivalent volume of sterile saline. After 2 h, animals were killed by i.v. pentobarbital. Right and left lungs of six pairs of animals were lavaged with 25 ml saline each; the remaining six pairs of animals were studied by measurement of lung wet/dry weight ratio. Albumin concentrations in lavage fluid (BAL) of lodoxamide-treated animals were 243 +/- 165 micrograms/ml in right lung and 29 +/- 15 micrograms/ml in left lung (p less than 0.03); albumin concentration in right lung BAL of untreated animals was 1,180 +/- 319 micrograms/ml (p less than 0.02 vs. lodoxamide-treated animals). PMN percentages in right BAL (3.8 +/- 3.1) and left BAL (2.9 +/- 2.2) did not differ in lodoxamide-treated animals (p greater than 0.65); PMN percentage in right BAL of untreated animals was 18.7 +/- 2.9 (p less than 0.001 vs. lodoxamide-treated animals).(ABSTRACT TRUNCATED AT 250 WORDS)
复张性肺水肿（RPE）是一种急性单侧肺损伤，由细胞毒性氧代谢产物引发，并在时间上与多形核中性粒细胞（PMN）的流入相关；这些有毒氧产物似乎源于长期萎陷肺的再氧合。洛度沙胺 tromethamine（U - 42585E）可减少缺血心肌再灌注后的梗死面积。研究了洛度沙胺在RPE中的可能保护作用。通过向兔胸膜腔内注入空气使右肺萎陷7天。在自主通气的兔中，通过胸管施加负压实现肺复张。12对动物分别接受洛度沙胺（从复张前30分钟开始静脉注射（i.v.），剂量为20 mg/kg/h，直至处死）或等量的无菌生理盐水。2小时后，通过静脉注射戊巴比妥处死动物。6对动物的左右肺分别用25 ml生理盐水灌洗；其余6对动物通过测量肺湿/干重比进行研究。洛度沙胺治疗组动物右肺灌洗液（BAL）中的白蛋白浓度为243±165微克/毫升，左肺为29±15微克/毫升（p<0.03）；未治疗动物右肺BAL中的白蛋白浓度为1180±319微克/毫升（与洛度沙胺治疗组动物相比，p<0.02）。洛度沙胺治疗组动物右BAL（3.8±3.1）和左BAL（2.9±2.2）中的PMN百分比无差异（p>0.65）；未治疗动物右BAL中的PMN百分比为18.7±2.9（与洛度沙胺治疗组动物相比，p<0.001）。（摘要截短于250字）
