Malik A B, van der Zee H, Lee B C
Lymphology. 1979 Sep;12(3):149-57.
The effects of hemorrhage on pulmonary hemodynamics and lung transvascular fluid dynamics were studied in sheep. We found that 2 hr of hemorrhage caused a fall in lung lymph flow (p less than 0.05) and no significant change in lymph protein concentration. The fall in lymph flow was not due to decreased vascular surface area since the regional distribution of pulmonary perfusion was not altered during hemorrhage; however, the decrease in lymph flow was associated with decrease (p less than 0.05) in the calculated pulmonary microvascular pressure. The extravascular lung water lung content per g bloodless dry lung was increased (p less than 0.05) in the hemorrhaged sheep from the control values. Pulmonary edema was not due to increased lung vascular endothelial permeability since the net transvascular protein flux was not increased. The finding that pulmonary edema occurred despite the consistent decreases in lymph flow suggests that edema may be due to hemorrhage-induced lymphatic "failure" or that edema fluid is sequestered in spaces (e.g., endothelial cells) where if cannot be drained by the lymphatics.
在绵羊身上研究了出血对肺血流动力学和肺跨血管液体动力学的影响。我们发现，出血2小时导致肺淋巴流量下降（p<0.05），而淋巴蛋白浓度无显著变化。淋巴流量下降并非由于血管表面积减少，因为出血期间肺灌注的区域分布未改变；然而，淋巴流量的减少与计算出的肺微血管压力降低（p<0.05）有关。与对照值相比，出血绵羊每克无血干肺的血管外肺水含量增加（p<0.05）。肺水肿并非由于肺血管内皮通透性增加，因为跨血管蛋白净通量未增加。尽管淋巴流量持续下降但仍发生肺水肿这一发现表明，水肿可能是由于出血诱导的淋巴“功能衰竭”，或者水肿液被隔离在淋巴管无法引流的空间（如内皮细胞）中。
