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灌注羊肺中压力升高或渗漏性水肿增加后的恢复情况。

Recovery from increased pressure or increased leakiness edema in perfused sheep lungs.

作者信息

Fukue M, Serikov V B, Jerome E H

机构信息

Cardiovascular Research Institute, University of California, San Francisco 94143.

出版信息

J Appl Physiol (1985). 1994 Jul;77(1):184-9. doi: 10.1152/jappl.1994.77.1.184.

Abstract

Two routes by which interstitial pulmonary edema liquid may leave the lung during recovery are reabsorption into the pulmonary circulation and clearance by lung lymphatics. We hypothesized that reabsorption of edema liquid of low protein concentration into the pulmonary circulation would be greater than reabsorption of edema liquid of high protein concentration because of the greater protein osmotic gradient in the former. On the basis of previous studies, lymph flow should contribute minimally to the recovery. In 22 in situ perfused sheep lungs with lymph fistulas, we produced approximately 100 g of osmotic or hydrostatic edema (low protein) or increased leakiness edema by calcium depletion (high protein). To induce reabsorption, we changed the perfusate from low- (1% albumin, osmotic pressure = 4 cmH2O) to high-protein (7% albumin, osmotic pressure = 22 cmH2O) solution in the osmotic group, decreased capillary pressure from 29 +/- 9 to 11 +/- 6 cmH2O in the hydrostatic group, or reversed leakiness by adding CaCl2 to the perfusate in the increased leakiness group. Reabsorption occurred only during recovery from osmotic (40 +/- 22% of filtered liquid) and hydrostatic (15 +/- 11%) edema. Total lung lymph flow during recovery from osmotic, hydrostatic, or increased leakiness edema was 4.9 +/- 3.4, 4.3 +/- 3.4, or 3.5 +/- 1.9 g, respectively. We conclude that during recovery from pulmonary edema interstitial liquid is reabsorbed into the circulation in inverse proportion to its protein concentration. We confirm that only a small fraction of the interstitial edema liquid is cleared by the lymphatics during recovery from any type of edema.

摘要

间质性肺水肿液在恢复过程中离开肺的两条途径是重新吸收进入肺循环和通过肺淋巴管清除。我们假设,低蛋白浓度的水肿液重新吸收进入肺循环的量会大于高蛋白浓度的水肿液,因为前者的蛋白渗透梯度更大。根据先前的研究,淋巴液流动对恢复的贡献应最小。在22只带有淋巴瘘的原位灌注绵羊肺中,我们通过钙缺乏(高蛋白)产生了约100克渗透性或静水压性水肿(低蛋白)或通透性增加性水肿。为诱导重新吸收,在渗透性水肿组中,我们将灌注液从低蛋白(1%白蛋白,渗透压 = 4 cmH₂O)改为高蛋白(7%白蛋白,渗透压 = 22 cmH₂O)溶液;在静水压性水肿组中,将毛细血管压力从29 ± 9 cmH₂O降至11 ± 6 cmH₂O;在通透性增加性水肿组中,通过向灌注液中添加氯化钙来逆转通透性。重新吸收仅发生在渗透性水肿(滤过液的40 ± 22%)和静水压性水肿(15 ± 11%)的恢复过程中。从渗透性、静水压性或通透性增加性水肿恢复过程中,全肺淋巴液流量分别为4.9 ± 3.4克、4.3 ± 3.4克或3.5 ± 1.9克。我们得出结论,在肺水肿恢复过程中,间质液以与其蛋白浓度成反比的比例被重新吸收进入循环。我们证实,在从任何类型的水肿恢复过程中,只有一小部分间质水肿液通过淋巴管清除。

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