Aggregation fo blood platelets and increased hydraulic conductivity of pulmonary exchange vessels.

Acta physiologica Scandinavica Pub Date : 1976-10-01
J Vaage, G Nicolaysen, B A Waaler
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Abstract

Pulmonary microembolization secondary to platelet aggregation has been suggested to be a pathogenetic component of the shock lung syndrome. In vitro experiments have also shown that platelets can release factors with a permeability-enhancing activity. We studied the effect of collagen-induced platelet aggregation on the hydraulic conductivity of thexchange vessels in isolated, blood-perfused rabbit lungs. The net rate of fluid filtration in each pair of lungs was determined during standardized elevations of left atrial pressure before and after platelet aggregation induced by intraarterial collagen infusions. Such infusions were followed by a significant, but transient increase in the net rate of fluid filtration. These lungs were papaverinized so that collagen infusions caused only minor increases in inflow pressure. Separate experiments indicated that the observed increase in pulmonary arterial pressure could not explain the increase in net filtration rate after collagen infusion. When platelet-poor plasma was used as a perfusate no change in the net rate of fluid filtration was observed after collagen infusion. The conclusion from these experiments is then that intravascular platelet aggregation induced by collagen infusion caused a transient increase in the permeability of the pulmonary exchange vessels.

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血小板聚集和肺交换血管的水力传导能力增加。
继发于血小板聚集的肺微栓塞已被认为是肺休克综合征的一个致病因素。体外实验也表明,血小板可以释放具有增强通透性活性的因子。我们研究了胶原诱导的血小板聚集对离体血灌注兔肺交换血管水力传导的影响。在动脉内注射胶原蛋白诱导血小板聚集前后左房压标准化升高时,测定每对肺的液体滤过净率。这样的注入之后,液体过滤的净速率显著但短暂地增加。这些肺被罂粟碱化,因此胶原蛋白输注只引起流入压力的轻微增加。单独实验表明,观察到的肺动脉压升高并不能解释胶原蛋白输注后净滤过率的增加。当使用血小板不足的血浆作为灌注液时,胶原输注后未观察到液体滤过净率的变化。这些实验的结论是,胶原输注诱导的血管内血小板聚集引起肺交换血管通透性的短暂增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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