Drummond W H, Gause G E, Polak M J, Lyles D, Cassin S
Department of Pediatrics, University of Florida College of Medicine, Gainesville 32610.
Exp Lung Res. 1989 May;15(3):447-58. doi: 10.3109/01902148909087870.
Ethanol is a pulmonary vasoconstrictor in rat lungs perfused in situ with Krebs-Henseleit salt solution. Pentobarbital-anesthetized rats were tracheotomized, and an in situ recirculating isolated lung perfusion was instituted using a Krebs-Henseleit buffer with 3% bovine albumin at 37 degrees C. Changes in pulmonary arterial pressure and tracheal inspiratory pressure during intravenous ethanol infusion at four different cumulative doses were measured in normoxic (n = 6) and hyperoxic (n = 6) lungs, compared to normoxic perfusate (no ethanol infusion) controls (n = 6). Perfusate alcohol levels progressively increased in experimental groups. Perfusate gas and pH values were normal and not altered by ethanol. PAP increased by the end of ethanol infusion from 9.7 +/- 2 to 26 +/- 13 mm Hg in the normoxic group and from 10.6 to 22 +/- 9 mm Hg in the hyperoxic lungs (p less than .02); no change occurred in control lungs. Severe pulmonary edema occurred in 83% of the ethanol exposed lungs (vs. 0% of perfusate controls). Postethanol wet/dry weight ratios were twice normal (p less than .02). Pulmonary arterial pressure rose in two stages. First there was a 25-100% increase before airway pressure increased, representing pulmonary vasoconstriction. This was followed by a precipitous 100-500% transmitted pressure rise as severe pulmonary edema developed. Thus, we conclude that the vasoconstrictor effect of ethanol on the pulmonary circulation occurs in rats as well as in lambs, dogs, and humans. In isolated perfused rat lungs, the response is locally mediated.
在使用克氏-亨氏盐溶液原位灌注的大鼠肺中，乙醇是一种肺血管收缩剂。对戊巴比妥麻醉的大鼠进行气管切开，并在37℃下使用含3%牛白蛋白的克氏-亨氏缓冲液建立原位循环离体肺灌注。在常氧（n = 6）和高氧（n = 6）肺中，测量在静脉输注四种不同累积剂量乙醇期间肺动脉压和气管吸气压力的变化，并与常氧灌注液（未输注乙醇）对照组（n = 6）进行比较。实验组灌注液中的酒精水平逐渐升高。灌注液气体和pH值正常，不受乙醇影响。在常氧组中，乙醇输注结束时肺动脉压从9.7±2升高至26±13 mmHg，在高氧肺中从10.6升高至22±9 mmHg（p < 0.02）；对照组肺中无变化。83%暴露于乙醇的肺出现严重肺水肿（而灌注液对照组为0%）。乙醇处理后的湿/干重比是正常的两倍（p < 0.02）。肺动脉压分两个阶段升高。首先，在气道压力升高之前有25%-100%的升高，代表肺血管收缩。随后，随着严重肺水肿的发展，传导压力急剧升高100%-500%。因此，我们得出结论，乙醇对肺循环的血管收缩作用在大鼠以及羔羊、狗和人类中均会发生。在离体灌注的大鼠肺中，这种反应是由局部介导的。
