The hemodynamic and cardiometabolic effects of
dopamine were evaluated in
propoxyphene-induced circulatory
shock in eight
pentobarbital anesthetized pigs. Circulatory
shock was induced by an infusion of
propoxyphene chloride 15 mg . min-1 i.v. At
shock, i.e. CI less than or equal to 2.0 l . min-1 . m-2 and/or MAP less than or equal to 60 mmHg,
dopamine was infused
at 10, 20, 40, 80 and 160 micrograms . kg-1 . min-1 with an interval between increments of 8 min. After 30 min at 160 micrograms . kg-1 . min-1, the infusion rate was reversibly decreased. The
propoxyphene infusion of 15 mg . min-1 was continued throughout the study.
Dopamine improved the circulation in seven animals; one animal died in refractory
shock during
dopamine infusion.
Dopamine infusion at
shock level resulted in an increase of the following variables (% of baseline value): MAP (69%),
HR (109%), CI (138%) and SVI (129%). Normalisation was seen in MRAP (120%) and in MPAOP (100%). A profound decrease in systemic vascular resistance was unchanged. Increases were seen in left and right ventricular
stroke work index, to 88% and 176% of baseline, respectively. Left ventricular dP/dt increased (170%). In the coronary circulation myocardial blood flow increased (133%) as did myocardial oxygen consumption (65%) concomitant with a decrease in myocardial
oxygen uptake (41%), but coronary vascular resistance progressively decreased (38%). The myocardial
propoxyphene extraction changed from +54% to -86% during peak
dopamine infusion. In conclusion,
dopamine reversed
cardiac failure in
propoxyphene overdose by a marked positive inotropic stimulation restoring contractility. A marked positive chronotropic stimulation maintained a sufficient cardiac index and a normal blood pressure in spite of a profound vasodilatation which was unresponsive to
dopamine.