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低蛋白血症对肺和软组织水肿形成的影响。

Effect of hypoproteinemia on pulmonary and soft tissue edema formation.

作者信息

Harms B A, Kramer G C, Bodai B I, Demling R H

出版信息

Crit Care Med. 1981 Jul;9(7):503-8. doi: 10.1097/00003246-198107000-00001.

Abstract

The effect of acute hypoproteinemia on the rate of fluid flux across the pulmonary and soft tissue microcirculation was studied in the unanesthetized sheep. Lymph flow was used to monitor fluid flux, a protein depletion of 30-50% of baseline value was produced by plasmapheresis. Vascular hydrostatic pressures and cardiac output were maintained constant with crystalloid infusion. The measured oncotic pressure in plasma, pi rho rapidly decreased as did the oncotic gradient between plasma and lymph. Lung and soft tissue lymph flow increased 2- to 3-fold immediately after protein depletion. Lung interstitial oncotic pressure, pi L, as measured in lymph, decreased to return the oncotic gradient and lymph flow to baseline by 24 h. Soft tissue oncotic gradient also returned to baseline by 24 h, but lymph flow remained significantly elevated for the next 48 h, indicating an increase in fluid flux unrelated to changes in oncotic pressure. Lymph flow rapidly returned to baseline when protein was returned. Protein depletion may alter the soft tissue interstitial matrix, allowing for edema formation. More effective mechanisms prevent this from occurring in the lung.

摘要

在未麻醉的绵羊身上研究了急性低蛋白血症对肺和软组织微循环中液体通量率的影响。采用淋巴流量来监测液体通量,通过血浆置换使蛋白质含量降至基线值的30%-50%。通过输注晶体液维持血管静水压和心输出量恒定。血浆中测得的胶体渗透压πρ迅速下降,血浆与淋巴之间的胶体渗透压梯度也迅速下降。蛋白质耗竭后,肺和软组织的淋巴流量立即增加2至3倍。通过测量淋巴液得出的肺间质胶体渗透压πL下降,使胶体渗透压梯度和淋巴流量在24小时内恢复到基线水平。软组织胶体渗透压梯度在24小时时也恢复到基线水平,但在接下来的48小时内淋巴流量仍显著升高,这表明液体通量增加与胶体渗透压变化无关。补充蛋白质后,淋巴流量迅速恢复到基线水平。蛋白质耗竭可能会改变软组织间质基质,从而导致水肿形成。肺中有更有效的机制可防止这种情况发生。

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