Department of Medicine, Pulmonary Division, University of Alberta, Edmonton, Alberta, Canada.
J Appl Physiol (1985). 2012 Aug 15;113(4):541-8. doi: 10.1152/japplphysiol.00404.2012. Epub 2012 Jun 14.
The development of intrapulmonary shunts with increased cardiac output during exercise in healthy humans has been reported in several recent studies, but mechanisms governing their recruitment remain unclear. Dobutamine and dopamine are inotropes commonly used to augment cardiac output; however, both can increase venous admixture/shunt fraction (Qs/Qt). It is possible that, as with exercise, intrapulmonary shunts are recruited with increased cardiac output during dobutamine and/or dopamine infusion that may contribute to the observed increase in Qs/Qt. The purpose of this study was to examine how dobutamine and dopamine affect intrapulmonary shunt and gas exchange. Nine resting healthy subjects received serial infusions of dobutamine and dopamine at incremental doses under normoxic and hyperoxic (inspired O(2) fraction = 1.0) conditions. At each step, alveolar-to-arterial Po(2) difference (A-aDo(2)) and Qs/Qt were calculated from arterial blood gas samples, intrapulmonary shunt was evaluated using contrast echocardiography, and cardiac output was calculated by Doppler echocardiography. Both dobutamine and dopamine increased cardiac output and Qs/Qt. Intrapulmonary shunt developed in most subjects with both drugs and paralleled the increase in Qs/Qt. A-aDo(2) was unchanged due to a concurrent rise in mixed venous oxygen content. Hyperoxia consistently eliminated intrapulmonary shunt. These findings contribute to our present understanding of the mechanisms governing recruitment of these intrapulmonary shunts as well as their impact on gas exchange. In addition, given the deleterious effect on Qs/Qt and the risk of neurological complications with intrapulmonary shunts, these findings could have important implications for use of dobutamine and dopamine in the clinical setting.
在一些最近的研究中已经报道了在健康人体运动期间心输出量增加时肺内分流的发展，但控制其募集的机制仍不清楚。多巴酚丁胺和多巴胺是常用的增强心输出量的正性肌力药；然而，两者都可以增加静脉混合/分流量(Qs/Qt)。在多巴酚丁胺和/或多巴胺输注期间，可能会像运动一样，随着心输出量的增加而募集肺内分流，这可能导致观察到的 Qs/Qt 增加。本研究的目的是研究多巴酚丁胺和多巴胺如何影响肺内分流和气体交换。九名休息健康受试者在常氧和高氧（吸入 O2 分数=1.0）条件下接受递增剂量的多巴酚丁胺和多巴胺的连续输注。在每一步，从动脉血气样本计算肺泡-动脉 Po2 差异（A-aDo2）和 Qs/Qt，使用对比超声心动图评估肺内分流，并通过多普勒超声心动图计算心输出量。多巴酚丁胺和多巴胺均增加心输出量和 Qs/Qt。两种药物均在大多数受试者中产生肺内分流，并与 Qs/Qt 的增加平行。由于混合静脉血氧含量的同时升高，A-aDo2 保持不变。高氧始终消除肺内分流。这些发现有助于我们目前对这些肺内分流募集机制的理解，以及它们对气体交换的影响。此外，鉴于肺内分流对 Qs/Qt 的有害影响以及与肺内分流相关的神经并发症风险，这些发现可能对临床应用多巴酚丁胺和多巴胺具有重要意义。
