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肺对低蛋白血症和贺斯输注的跨血管液体滤过反应。

Pulmonary transvascular fluid filtration response to hypoproteinemia and Hespan infusion.

作者信息

Harms B A, Rosenfeld D J, Pahl A C, Conhaim R L, Starling J R

机构信息

Department of Surgery, University of Wisconsin, Madison 53792.

出版信息

J Surg Res. 1990 May;48(5):408-14. doi: 10.1016/0022-4804(90)90004-l.

Abstract

Management of major blood loss utilizing protein-free fluids for volume replacement frequently results in plasma protein depletion and plasma volume expansion. These factors can increase pulmonary transvascular fluid filtration which may lead to life-threatening pulmonary edema. We studied the combined effects of plasma protein depletion and plasma volume expansion on lung lymph flow (QL) in awake sheep prepared with chronic lung lymph fistulae. Animals were first chronically protein-depleted by batch plasmapheresis and then infused for 2 hr with either lactated Ringer's (Hypo/LR; n = 7) or 6% hydroxyethyl starch (Hespan) (Hypo/HES; n = 6). Control normoproteinemic animals (Norm/LR; n = 13) only received lactated Ringer's. Hypoproteinemia alone resulted in an average 2-fold increase in QL over normoproteinemic baseline levels (P less than or equal to 0.05). Infusion of LR into hypoproteinemic animals caused a 7.9-fold increase in QL (P less than or equal to 0.05). By comparison, HES infusion under similar hypoproteinemic conditions limited the increase in QL to 3.2-fold over baseline. We attributed this reduced rise in QL to Hespan's high oncotic pressure, which dramatically widened (by 4-5 mm Hg) the pulmonary-to-lymph oncotic pressure gradient. We did not observe this with LR infusion, or in previous studies employing intravenous infusion of plasma protein. Thus, the oncotic pressure of Hespan appears to significantly limit pulmonary fluid filtration during hypoproteinemia compared to LR. We do not believe that these effects are the results of any changes in microvascular porosity.

摘要

利用无蛋白液体进行容量替代来处理大量失血,常常会导致血浆蛋白耗竭和血浆容量扩张。这些因素会增加肺血管跨膜液体滤过,进而可能导致危及生命的肺水肿。我们研究了血浆蛋白耗竭和血浆容量扩张对清醒绵羊肺淋巴流量(QL)的联合影响,这些绵羊已制备慢性肺淋巴瘘。首先通过分批血浆置换使动物长期处于蛋白缺乏状态,然后分别用乳酸林格液(Hypo/LR;n = 7)或6%羟乙基淀粉(贺斯)(Hypo/HES;n = 6)输注2小时。对照的正常蛋白血症动物(Norm/LR;n = 13)仅接受乳酸林格液。单独的低蛋白血症导致QL较正常蛋白血症基线水平平均增加2倍(P≤0.05)。向低蛋白血症动物输注乳酸林格液使QL增加7.9倍(P≤0.05)。相比之下,在类似的低蛋白血症条件下输注羟乙基淀粉,使QL的增加限制在较基线水平增加3.2倍。我们将QL这种增加幅度的降低归因于贺斯的高胶体渗透压,它使肺与淋巴之间的胶体渗透压梯度显著增大(增大4 - 5 mmHg)。在输注乳酸林格液时以及之前采用静脉输注血浆蛋白的研究中,我们未观察到这种情况。因此,与乳酸林格液相比,羟乙基淀粉的胶体渗透压在低蛋白血症期间似乎能显著限制肺液体滤过。我们认为这些作用并非微血管孔隙率任何变化的结果。

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