Effects of dopamine and nifedipine infusions on the pulmonary circulation of the lamb.

T F Feltes, C D Fike, T N Hansen
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Abstract

The purpose of this study was to test the hypothesis that nifedipine when given with dopamine will lower pulmonary vascular resistance in hypoxic lambs without altering systemic vascular resistance. We studied six unanesthetized lambs (ranging in age from 13 to 35 days) as they breathed air or on a separate day as they breathed 10% O2 and 3% CO2 in nitrogen. First, we infused dopamine at progressively higher rates (10, 20, 40, 80, and 160 micrograms/kg/min) while measuring mean aortic, pulmonary arterial, and left atrial pressures and heart rate continuously and cardiac output and arterial blood gas tensions at frequent intervals. Then, while maintaining the dopamine infusion at 160 micrograms/kg/min, we infused boluses of nifedipine intravenously (10 micrograms/kg) every 5 min until a cumulative dose of 50 micrograms/kg had been administered. In both groups of lambs, cardiac output increased with increasing rates of dopamine infusion (baseline to maximum dopamine: 260 +/- 20 ml/kg/min to 420 +/- 60 ml/kg/min for normoxic lambs and 400 +/- 50 ml/kg/min to 560 +/- 80 ml/kg/min for hypoxic lambs). While systemic vascular resistance and pulmonary vascular resistance did not change significantly in either group during dopamine infusion, the ratio of pulmonary vascular resistance to systemic vascular resistance increased at low rates of infusion and decreased at high rates. The peak in this ratio occurred at a rate of infusion of 20-40 micrograms/kg/min in normoxic lambs and 40-80 micrograms/kg/min in hypoxic lambs. Infusion of nifedipine did not affect cardiac output in normoxic lambs but decreased it significantly in hypoxic lambs. Nifedipine infusion did not affect pulmonary vascular resistance in the normoxic lambs and increased pulmonary vascular resistance in the hypoxic lambs. We conclude that nifedipine, even when given with high doses of dopamine, is not a specific pulmonary vasodilator.

注射多巴胺和硝苯地平对羔羊肺循环的影响。
本研究的目的是验证一种假设,即硝苯地平与多巴胺联合使用会降低缺氧羔羊的肺血管阻力,而不会改变全身血管阻力。我们研究了6只未麻醉的羔羊(年龄从13天到35天不等)呼吸空气或在单独的一天呼吸10%的O2和3%的CO2氮。首先,我们逐渐以较高的速率(10、20、40、80和160微克/千克/分钟)注入多巴胺,同时连续测量平均主动脉、肺动脉和左房压和心率,并频繁测量心输出量和动脉血气张力。然后,在维持160微克/千克/分钟的多巴胺输注量的同时,我们每5分钟静脉输注硝苯地平(10微克/千克),直到累计剂量达到50微克/千克。在两组羔羊中,心输出量随着多巴胺输注率的增加而增加(正常缺氧羔羊的基线至最大多巴胺:260 +/- 20 ml/kg/min至420 +/- 60 ml/kg/min,缺氧羔羊的400 +/- 50 ml/kg/min至560 +/- 80 ml/kg/min)。在多巴胺输注期间,两组大鼠全身血管阻力和肺血管阻力均无明显变化,但肺血管阻力与全身血管阻力之比在低输注速率下升高,在高输注速率下降低。正常缺氧羔羊在20-40微克/公斤/分钟、缺氧羔羊在40-80微克/公斤/分钟时,该比值达到峰值。输注硝苯地平对正常氧合羔羊的心输出量无影响,但对缺氧羔羊的心输出量有显著降低。硝苯地平对正常氧合羔羊肺血管阻力无影响,对缺氧羔羊肺血管阻力有增加作用。我们得出结论,硝苯地平,即使给予高剂量多巴胺,也不是一种特定的肺血管扩张剂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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