Nakatsuka M, Gehr L C, Glauser F L
Department of Anesthesiology, Medical College of Virginia, Virginia Commonwealth University, Richmond.
Acta Anaesthesiol Scand. 1993 Feb;37(2):219-22. doi: 10.1111/j.1399-6576.1993.tb03704.x.
The effects of amrinone and CaCl2 on pulmonary vasculature and biventricular function in sheep with acute lung injury (ALI) were studied. Seven sheep were ventilated with a tidal volume of 10-12 ml.kg-1 with end-tidal CO2 of 40 +/- 5 mmHg (5.3 +/- 0.7 kPa) after acute lung injury was induced with up to 30 mg kg-1 of ethchlorvynol (ECV). Biventricular function and hemodynamic profiles were estimated with a rapid computerized thermodilution method and modified pulmonary artery catheters after acute lung injury, following a loading dose (1 mg kg-1) and maintenance dose (5 micrograms kg-1 min-1) of amrinone and after a bolus dose of CaCl2 (20 mg kg-1). ECV successfully induced acute lung damage in sheep, causing significant increases in pulmonary artery pressure (PAP) and pulmonary vascular resistance index (PVRI). Amrinone reversed the unfavorable changes induced by ECV, significantly reducing PAP, PVRI and left ventricular end-diastolic volume (LVEDV). CaCl2, however, reversed the effect of amrinone and increased PAP, PVRI, and LVEDV but decreased left ventricular ejection fraction.
研究了氨力农和氯化钙对急性肺损伤(ALI)绵羊肺血管和双心室功能的影响。在用高达30mg/kg的ethchlorvynol(ECV)诱导急性肺损伤后,7只绵羊以10-12ml·kg-1的潮气量通气,呼气末二氧化碳分压为40±5mmHg(5.3±0.7kPa)。在急性肺损伤后,采用快速计算机热稀释法和改良肺动脉导管评估双心室功能和血流动力学参数,给予氨力农负荷剂量(1mg/kg)和维持剂量(5μg/kg·min-1)以及氯化钙推注剂量(20mg/kg)后进行评估。ECV成功诱导了绵羊的急性肺损伤,导致肺动脉压(PAP)和肺血管阻力指数(PVRI)显著升高。氨力农逆转了ECV诱导的不利变化,显著降低了PAP、PVRI和左心室舒张末期容积(LVEDV)。然而,氯化钙逆转了氨力农的作用,增加了PAP、PVRI和LVEDV,但降低了左心室射血分数。