Ducas J, Stitz M, Gu S, Schick U, Prewitt R M
Department of Medicine, University of Manitoba Health Sciences Centre, Winnipeg, Canada.
Am Rev Respir Dis. 1992 Aug;146(2):307-12. doi: 10.1164/ajrccm/146.2.307.
We compared the general hemodynamic effects of dopamine and dobutamine in dogs with acute pulmonary hypertension complicated by a decrease in cardiac output (CO). The pulmonary hypertension was induced by injection of autologous blood clot. Emboli markedly increased mean pulmonary artery pressure (Ppa) and decreased CO (both p < 0.001). Both dopamine and dobutamine increased CO 50% (p < 0.05) and decreased pulmonary vascular resistance (PVR) (p < 0.05), calculated as (PAP - left ventricular end diastolic pressure)/CO. Mean PVR (mm Hg/L/min) decreased from 16.1 to 12.4 with dopamine and from 16. to 11.9 with dobutamine, both p < 0.05. Ventricular filling pressures were not affected. In another 12 dogs we investigated the effects of both drugs on pulmonary pressure-flow (P-Q) characteristics. P-Q characteristics were determined in dogs with normal Ppa values and in those with embolic pulmonary hypertension. The slope of the P-Q relationship defines the incremental vascular resistance and the extrapolated pressure intercept, the effective vascular outflow pressure. All P-Q relationships were described well by a linear equation. Despite significant systemic effects in both groups and despite a decrease in PVR with both drugs in embolized dogs, neither drug significantly affected pulmonary P-Q characteristics. The discrepancy between PVR and incremental resistance is explained by an incorrect assumption in PVR that the left ventricular filling pressure is the effective vascular outflow pressure. We conclude that both before and after the induction of pulmonary hypertension, both dopamine and dobutamine improve CO without affecting pulmonary vascular tone.
我们比较了多巴胺和多巴酚丁胺对伴有心输出量（CO）降低的急性肺动脉高压犬的一般血流动力学效应。肺动脉高压通过注射自体血凝块诱导产生。栓子显著增加平均肺动脉压（Ppa）并降低CO（两者p<0.001）。多巴胺和多巴酚丁胺均使CO增加50%（p<0.05），并降低肺血管阻力（PVR）（p<0.05），肺血管阻力计算为（肺动脉压 - 左心室舒张末期压力）/CO。多巴胺使平均PVR（mmHg/L/min）从16.1降至12.4，多巴酚丁胺使其从16.降至11.9，两者p<0.05。心室充盈压未受影响。在另外12只犬中，我们研究了两种药物对肺压力 - 流量（P - Q）特性的影响。在Ppa值正常的犬和患有栓塞性肺动脉高压的犬中测定P - Q特性。P - Q关系的斜率定义了增量血管阻力，外推压力截距定义了有效血管流出压力。所有P - Q关系均可用线性方程很好地描述。尽管两组均有显著的全身效应，且栓塞犬使用两种药物后PVR均降低，但两种药物均未显著影响肺P - Q特性。PVR与增量阻力之间的差异可通过PVR中一个错误假设来解释，即左心室充盈压是有效血管流出压力。我们得出结论，在肺动脉高压诱导前后，多巴胺和多巴酚丁胺均可改善CO而不影响肺血管张力。
