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未麻醉绵羊肺微血管对前列环素(PGI2)输注的反应。

Pulmonary microvascular response to prostacyclin (PGI2) infusion in unanesthetized sheep.

作者信息

Gunther R, Zaiss C, Demling R H

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1982 May;52(5):1338-42. doi: 10.1152/jappl.1982.52.5.1338.

Abstract

We studied the effect of prostacyclin (PGI2) infusion and cessation of infusion on the pulmonary microcirculation. We used lung lymph flow (QL) and the lymph to plasma protein ratio as sensitive indices of net fluid (QF) and protein flux (CP). After a 4-h base line period, we infused PGI2 (0.2 micrograms . kg(-1).min(-1) into eight unanesthetized sheep for 2 h. We monitored vascular pressures and lymph during infusion and for another 18 h after PGI2. During infusion, QL and cardiac output increased by 75 and 50%, respectively, over base line, whereas the lymph-to-plasma ratio (L/P) remained constant for both albumin and globulin. This resulted in a significant increase in both fluid and protein flux. Pulmonary vascular pressures remained unchanged, whereas mean aortic pressure decreased. The increase in QF and CP was felt to be due to an increase in the surface area of fluid exchange vessels rather than increased permeability. After infusion, cardiac output rapidly returned to base line, whereas mean QL remained increased by 70% over base line for 2-8 h. Mean L/P decreased from 0.65 to 0.53. Pulmonary arterial pressure and pulmonary vascular resistance increased. The increase in QL and decrease in L/P indicate a rebound increase in pulmonary microvascular pressure in the postperfusion period.

摘要

我们研究了输注前列环素(PGI2)及停止输注对肺微循环的影响。我们将肺淋巴流量(QL)以及淋巴与血浆蛋白比值作为净液体(QF)和蛋白通量(CP)的敏感指标。在4小时的基线期后,我们对8只未麻醉的绵羊输注PGI2(0.2微克·千克-1·分钟-1),持续2小时。在输注期间以及PGI2输注后另外18小时内,我们监测血管压力和淋巴情况。输注期间,QL和心输出量分别比基线增加了75%和50%,而白蛋白和球蛋白的淋巴与血浆比值(L/P)保持恒定。这导致液体和蛋白通量均显著增加。肺血管压力保持不变,而平均主动脉压力下降。QF和CP的增加被认为是由于液体交换血管表面积增加而非通透性增加所致。输注后,心输出量迅速恢复至基线水平,而平均QL在2至8小时内仍比基线增加70%。平均L/P从0.65降至0.53。肺动脉压和肺血管阻力增加。QL的增加和L/P的降低表明在灌注后时期肺微血管压力出现反弹性增加。

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