Hemodynamic and vasoactive mediator response to experimental respiratory failure.
Hemodynamic and vasoactive mediator response to experimental respiratory failure.
复制标题
血流动力学和血管活性介质对实验性呼吸衰竭的反应。
DOI：
10.1152/jappl.1982.52.5.1230
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Mellins,RB
中科院分区：
文献类型：
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作者：
O'Brodovich,HM;Stalcup,SA;Pang,LM;Mellins,RB
我们测定了慢性插管非麻醉绵羊急性呼吸衰竭时血流动力学和循环内源性血管活性物质浓度的变化。吸入高碳酸-低氧混合气体(PHA=7.16，PaCO2=84Torr，PaO2=48Torr，n=5)2小时，心输出量(热稀释)增加一倍，体循环和肺动脉高压。在2小时的实验气期内，体循环阻力逐渐降低，而肺血管阻力逐渐增加。恢复室内空气呼吸后，肺动脉高压持续45min。血浆肾素活性增加两倍，循环中缓激肽浓度增加25倍(放射免疫法)。血浆去甲肾上腺素和肾上腺素浓度显著升高，其初始值(15min)分别为23.9+/-9.5(SE)和26.7+/-13.3 ng/ml(基线小于0.2)。吸入低氧(n=4)或高碳酸盐富氧(n=7)混合气体没有产生类似的结果。我们得出结论，实验性呼吸衰竭的血流动力学反应是高碳酸中毒和低氧共同作用的结果。这些变化部分是通过交感肾上腺活性增加和H+、O2和内源性血管活性介质浓度的改变来调节的。
We determined the changes in hemodynamics and circulating concentrations of endogenous vasoactive mediators during acute respiratory failure in chronically catheterized unanesthetized sheep. Inhalation of a hypercarbic-hypoxic gas mixture for 2 h (pHa = 7.16, PaCO2 = 84 Torr, PaO2 = 48 Torr, n = 5) resulted in a doubling of cardiac output (thermodilution) and systemic and pulmonary hypertension. Systemic vascular resistance decreased, whereas pulmonary vascular resistance gradually increased throughout the 2-h experimental gas period. Pulmonary hypertension persisted for 45 min after return to room air breathing. Plasma renin activity tripled, and circulating bradykinin concentration increased 25-fold (radioimmunoassay). Plasma norepinephrine and epinephrine concentrations (radioenzymatic assay) dramatically increased with respective initial values (15 min) of 23.9 +/- 9.5 (SE) and 26.7 +/- 13.3 ng/ml (base line less than 0.2). Inhalation of hypoxic (n = 4) or hypercarbic-enriched O2 (n = 7) gas mixtures did not produce similar findings. We concluded that the hemodynamic response to experimental respiratory failure results from the combination of hypercarbic acidosis and hypoxia. These changes were mediated in part by increased sympathoadrenal activity and altered concentrations of H+, O2, and endogenous vasoactive mediators.