Gorin A B, Kohler J, DeNardo G
J Clin Invest. 1980 Nov;66(5):869-77. doi: 10.1172/JCI109953.
Onset of lung edema is usually associated with increase in the pulmonary transvascular flux of water and proteins. Clinical measurement of these parameters may aid in early diagnosis of pulmonary edema, and allow differentiation between "cardiogenic" and "noncardiogenic" types base on the magnitude of the detected changes. We have previously described a noninvasive method for estimating transvascular protein flux in lung (Gorin, A. B., W. J. Weidner, R. H. Demling, and N. C. Staub, 1978. Noninvasive measurement of pulmonary transvascular protein flux in sheep. J. Appl. Physiol. 45: 225-233). Using this method we measured the net transvascular flux of [113mIn]transferrin (mol wt, 76,000 in lungs of nine normal human volunteers. Plasma clearance of [113In]transferrin occurred with a T1/2 = 7.0 +/- 2.6 h (mean +/- SD). The pulmonary transvascular flux coefficient, alpha, was 2.9 +/- 1.4 X 10(-3) ml/s (mean +/- SD) in man, slightly greater than that previously measured in sheep (2.7 +/- 0.7 X 10(-3) ml/s; mean +/- SD). The pulmonary transcapillary escape rate is twofold greater than the transcapillary escape rate for the vascular bed as a whole, indicating a greater "porosity" of exchanging vessels in the lung than exists for the "average" microvessel in the body. Time taken to reach half-equilibrium concentration of tracer protein in the lung interstitium was quite short, 52 +/- 13 min (mean +/- SD). We have shown that measurement of pulmonary transvascular protein flux in man is practical. The coefficient of variation of measurements of alpha (between subjects) was 0.48, and of measurements of pulmonary transcapillary escape rates was 0.39. In animals, endothelial injury commonly results in a two- to threefold increase in transvascular protein flux. Thus, external radioflux detection should be a suitable means of quantitating lung vascular injury in human disease states.
肺水肿的发生通常与肺血管内水和蛋白质的跨血管通量增加有关。对这些参数进行临床测量可能有助于早期诊断肺水肿，并根据检测到的变化幅度区分“心源性”和“非心源性”类型。我们之前描述了一种估算肺血管内蛋白质通量的非侵入性方法（戈林，A.B.，W.J.魏德纳，R.H.德姆林，和N.C.斯塔布，1978年。绵羊肺血管内蛋白质通量的非侵入性测量。《应用生理学杂志》45: 225 - 233）。使用这种方法，我们测量了9名正常人类志愿者肺部[113mIn]转铁蛋白（分子量76,000）的净跨血管通量。[113In]转铁蛋白的血浆清除半衰期T1/2 = 7.0 +/- 2.6小时（平均值 +/- 标准差）。人类的肺跨血管通量系数α为2.9 +/- 1.4×10(-3)毫升/秒（平均值 +/- 标准差），略高于之前在绵羊中测量的值（2.7 +/- 0.7×10(-3)毫升/秒；平均值 +/- 标准差）。肺毛细血管逃逸率比整个血管床的毛细血管逃逸率高两倍，这表明肺中交换血管的“孔隙率”比身体中“平均”微血管的孔隙率更大。示踪蛋白在肺间质中达到半平衡浓度所需的时间相当短，为52 +/- 13分钟（平均值 +/- 标准差）。我们已经表明，测量人类肺血管内蛋白质通量是可行的。α测量值（受试者之间）的变异系数为0.48，肺毛细血管逃逸率测量值的变异系数为0.39。在动物中，内皮损伤通常会导致跨血管蛋白质通量增加两到三倍。因此，外部放射性通量检测应该是定量人类疾病状态下肺血管损伤的合适方法。
