Longitudinal distribution of pulmonary vascular resistance after endotoxin administration in sheep
Longitudinal distribution of pulmonary vascular resistance after endotoxin administration in sheep
复制标题
绵羊内毒素注射后肺血管阻力的纵向分布
DOI：
10.1097/00003246-199201000-00024
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发表时间：
1992
影响因子：
8.8
通讯作者：
S. Rice
中科院分区：
文献类型：
--
作者：
R. Pearl;Edward R. Baer;L. Siegel;G. Benson;S. Rice
背景和方法肺动脉高压可能增加肺毛细血管压力并加剧急性呼吸衰竭时的肺水肿。肺动脉高压对肺毛细血管压力的影响取决于肺血管阻力的纵向分布。由于肺动脉高压发生在急性呼吸衰竭期间，我们假设急性呼吸衰竭可能会导致肺血管阻力纵向分布发生时间依赖性变化。因此，我们测量了急性呼吸衰竭动物模型中的肺毛细血管压力和肺血管阻力的纵向分布。在 1 小时内对 8 只麻醉羊施用大肠杆菌内毒素（2.5 至 5.0 μg/kg）。在接下来的 5 小时内测量肺和全身血流动力学，包括肺动脉闭塞压 (PAOP)、肺毛细血管压力和肺血管阻力的纵向分布。通过分析肺动脉球囊膨胀后的压力衰减来估计肺毛细血管压力。结果在接下来的 5 小时研究中，内毒素给药导致持续性肺动脉高压。内毒素输注期间，肺毛细血管压力在 0.5 小时和 0.75 小时时比基线增加 7 mm Hg，但在 1.5 小时时恢复到基线值。尽管肺动脉高压持续存在，但肺毛细血管压力在研究期间仍保持在基线值。与肺毛细血管压力类似，开始内毒素给药后0.5和0.75小时，肺静脉（或毛细血管后）阻力比基线增加约四倍，但在内毒素给药结束时恢复到基线值，并在研究的其余部分保持在基线值。相反，在输注期间和整个研究期间，肺动脉（或毛细血管前）阻力保持在大约基线三倍的值。结论在急性呼吸衰竭实验模型中，内毒素对肺血管阻力纵向分布的影响具有时间依赖性。如果这些来自动物的数据可以外推到人类，我们推测肺静脉收缩在急性呼吸衰竭患者肺水肿恶化中的重要性可能会随着时间的推移而变化。 （重症监护医学 1992 年；20:119）
Background and MethodsPulmonary hypertension may increase pulmonary capillary pressure and exacerbate pulmonary edema in acute respiratory failure. The effects of pulmonary hypertension on pulmonary capillary pressure depend on the longitudinal distribution of pulmonary vascular resistance. Since pulmonary hypertension occurs during acute respiratory failure, we hypothesized that acute respiratory failure may produce time-dependent changes in the longitudinal distribution of pulmonary vascular resistance. Therefore, we measured pulmonary capillary pressure and the longitudinal distribution of pulmonary vascular resistance in an animal model of acute respiratory failure. Escherichia coli endotoxin (2.5 to 5.0 μg/kg) was administered over a 1-hr period in eight anesthetized sheep. Pulmonary and systemic hemodynamics, including pulmonary artery occlusion pressure (PAOP), pulmonary capillary pressure, and the longitudinal distribution of pulmonary vascular resistance, were measured over the next 5 hrs. Pulmonary capillary pressure was estimated by analysis of the pressure decay following pulmonary artery balloon inflation. ResultsEndotoxin administration resulted in sustained pulmonary hypertension for the subsequent 5 hrs of the study. Pulmonary capillary pressure was increased 7 mm Hg above baseline at 0.5 and 0.75 hrs during the infusion of endotoxin but returned to baseline values at 1.5 hrs. Despite sustained pulmonary hypertension, pulmonary capillary pressure remained at baseline values for the duration of the study. Similar to pulmonary capillary pressure, pulmonary venous (or postcapillary) resistance was increased approximately four-fold over baseline at 0.5 and 0.75 hrs after initiating endotoxin administration, but returned to baseline values by the end of endotoxin administration and remained at baseline values throughout the remainder of the study. In contrast, pulmonary arterial (or precapillary) resistance remained at values approximately three times baseline during the infusion and throughout the duration of the study. ConclusionsIn this experimental model of acute respiratory failure, the effects of endotoxin on the longitudinal distribution of pulmonary vascular resistance are time-dependent. If these data from animals can be extrapolated to humans, we speculate that the importance of pulmonary venoconstriction in exacerbating pulmonary edema may vary over time in patients with acute respiratory failure. (Crit Care Med 1992; 20:119)