Figueras J, Weil M H
Circulation. 1977 Jan;55(1):195-9. doi: 10.1161/01.cir.55.1.195.
Colloid osmotic pressure (COP) was measured in 95 patients with clinical and radiological evidence of acute cardiogenic pulmonary edema. Fifty patients who were admitted for coronary observation but in whom acute myocardial infarctin was excluded, and 21 patients who had sustained acute myocardial infarction without evidence of left ventricular failure served as controls. Significantly higher values of COP, total plasma protein, and hematocrit were observed in patients with pulmonary edema. Increases in COP during pulmonary edema were best explained by transudation of hypooncotic fluid into extravascular spaces. Following treatment of pulmonary edema in 76 patients with furosemide, morphine, and oxygen, pulmonary edema was reversed in 65 patients. Reabsorption of hypooncotic fluid from extravascular sites with a significant decline in COP, total protein and hematocrit followed reversal of pulmonary edema. No significant changes in these parameters were observed in patients who failed to respond to therapy. These observations implicate filtration of hypooncotic fluid from the intravascular compartment during onset of cardiogenic pulmonary edema and reabsorption of hypooncotic fluid into the intravascular compartment during reversal of pulmonary edema.
对95例有急性心源性肺水肿临床和影像学证据的患者测量了胶体渗透压(COP)。50例因冠状动脉观察入院但排除急性心肌梗死的患者,以及21例发生急性心肌梗死但无左心室衰竭证据的患者作为对照。肺水肿患者的COP、总血浆蛋白和血细胞比容值明显更高。肺水肿期间COP的升高最好用低渗液渗入血管外间隙来解释。76例患者用呋塞米、吗啡和氧气治疗肺水肿后,65例患者的肺水肿得到逆转。肺水肿逆转后,血管外部位的低渗液重吸收,COP、总蛋白和血细胞比容显著下降。对治疗无反应的患者这些参数无明显变化。这些观察结果表明,在心源肺水肿发作期间,低渗液从血管内滤出,在肺水肿逆转期间,低渗液重吸收进入血管内。