Amrinone administration in endotoxin shock
Vincent, J.L.; Domb, M.; Van der Linden, P.; Motte, S.; de Boelpaepe, C.; Contempré, B.; Cantraine, F.
Circulatory Shock 25(2): 75-83
1988
ISSN/ISBN: 0092-6213 PMID: 3292077 Document Number: 321121
This study explored the hemodynamic effects of amrinone, a phsophodiesterase inhibitor, in association with intravenous fluids, in the treatment of endotoxin shock. Mongrel dogs were anesthetized with pentobarbital and mechanically ventilated with room air. Treatment was started 30 min after slow intravenous administration of 3 mg/kg of Escherichia coli endotoxin. In the first part of the study, ten dogs were resuscitated for 30 min with intravenous saline alone (10 ml/kg) and for the next 3 h by saline (10 mg/kg/h) and amrinone 40 .mu.g/kg/min. During this latter period, arterial pressure remained stable while cardiac output significantly increased from 3.1 .+-. 0.5 to 5.1 .+-. 0.7 1/min (P < 0.01), and oxygen delivery increased from 616 .+-. 92 to 983 .+-. 156 ml/min (P < 0.01). Comparison with control animals revealed that amrinone infusion prevented the decrease in left ventricular stroke work and markedly increased oxygen delivery. In the second part of the study, 18 dogs were treated by saline infusion titrated to maintain pulmonary artery balloon-occluded pressure at baseline level. In ten dogs, amrinone was added 60 min after endotoxin administration at a dose of 40 .mu.g/kg/min. Total amount of fluids infused averaged 87 .+-. 14 ml in the amrinone-treated dogs and 64 .+-. 15 ml in the control dogs (differences nonsignificant). Oxygen delivery and oxygen consumption increased significantly in the amrinone-treated dogs (from 541 .+-. 36 to 1063 .+-. 176 ml/min, P < 0.01, and from 145 .+-. 23 to 202 .+-. 38 ml/min. P < 0.01, respectively) but not in the control dogs. The amrinone-treated dogs had lower PaO2 and higher venous adminsture than the control dogs. These results therefore indicate that, in endotoxin shock, amrinone can increase oxygen supply without significant alteration in aterial pressure or dramatic effects on the cardiovascular tolerance in fluids.