Vaage J, Nicolaysen G, Waaler B A
Acta Physiol Scand. 1976 Oct;98(2):175-84.
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.
血小板聚集继发的肺微栓塞被认为是休克肺综合征发病机制的一个组成部分。体外实验也表明，血小板能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、血液灌注兔肺交换血管水力传导率的影响。在通过动脉内注入胶原诱导血小板聚集之前和之后，在左心房压力标准化升高期间，测定每对肺的液体滤过净速率。注入胶原后，液体滤过净速率显著但短暂增加。这些肺用罂粟碱处理，使得注入胶原仅引起流入压力的轻微增加。单独的实验表明，观察到的肺动脉压力升高不能解释注入胶原后滤过净速率的增加。当使用血小板贫乏血浆作为灌注液时，注入胶原后未观察到液体滤过净速率的变化。这些实验的结论是，注入胶原诱导的血管内血小板聚集导致肺交换血管通透性短暂增加。
