Angle M R, Molloy D W, Penner B, Jones D, Prewitt R M
Department of Medicine, Health Sciences Centre, Winnipeg, Manitoba.
Chest. 1989 Jun;95(6):1333-7. doi: 10.1378/chest.95.6.1333.
Autologous blood clot was injected into six dogs to produce a graduated decrease in cardiac output (CO). The effects of an infusion of norepinephrine, titrated to specific end points, were recorded before embolization and at two levels of pulmonary hypertension. Simultaneous measurements of systemic and renal hemodynamics were made. Sequential blood clot injection increased (p less than .01) pulmonary vascular resistance (PVR) from 1.3 to 13 to 33 mm Hg.L-1.min and reduced CO 45 percent and 75 percent (p less than .01). Norepinephrine increased both stroke volume and CO (p less than .01) in each condition and did not increase PVR. Since the biventricular filling pressures remained constant or fell slightly with norepinephrine, the increase in CO is best explained by an improvement in pump performance. There was no deterioration in renal blood flow or creatinine clearance with norepinephrine. The data suggested that in this model of right ventricular dysfunction, norepinephrine consistently improved myocardial performance without provoking further vasoconstriction in either the pulmonary or renal circulations.
将自体血凝块注入六只狗体内,使心输出量(CO)逐渐降低。在栓塞前以及两种肺动脉高压水平下,记录滴定至特定终点的去甲肾上腺素输注效果。同时进行全身和肾脏血流动力学测量。连续注入血凝块使肺血管阻力(PVR)从1.3升高至13再至33 mmHg·L⁻¹·min(p < 0.01),心输出量降低45%和75%(p < 0.01)。在每种情况下,去甲肾上腺素均增加了每搏输出量和心输出量(p < 0.01),且未增加肺血管阻力。由于去甲肾上腺素使双心室充盈压保持恒定或略有下降,心输出量的增加最好用泵功能的改善来解释。去甲肾上腺素未导致肾血流量或肌酐清除率恶化。数据表明,在这种右心室功能障碍模型中,去甲肾上腺素持续改善心肌功能,而不会在肺循环或肾循环中引发进一步的血管收缩。