J Kermode1, W Butt, F Shann. 1. Intensive Care Unit, Royal Children's Hospital, Parkville, Victoria, Australia.
Abstract
OBJECTIVE: To study the dose response characteristics of prostaglandin E1 and epoprostenol (prostacyclin) and directly to compare their effectiveness as pulmonary vasodilators in infants with pulmonary hypertension. DESIGN: A crossover design with each patient receiving both drugs in random order. SETTING: Infants were studied in the intensive care unit while they were sedated, paralysed, and ventilated. PATIENTS: Twenty infants who had undergone corrective cardiac surgery and who were in sinus rhythm, had stable haemodynamic function, and had a pulmonary artery catheter in place. All infants were receiving dopamine and phenoxybenzamine. INTERVENTIONS:Baseline haemodynamic measurements were taken and an infusion of the first drug was started at the lowest dose: after 20 minutes the measurements were repeated and the dose increased. This protocol was repeated for all doses of both drugs: 10, 30, and 100 ng/kg/min of prostaglandin E1 and 5, 10, and 25 ng/kg/min of epoprostenol. Cardiac output was measured by the pulsed Doppler ultrasound method. MAIN OUTCOME MEASURES: Pulmonary and systemic vascular resistances were calculated from the cardiac output and compared by the Wilcoxon signed ranks test. RESULTS: Both prostaglandin E1 and epoprostenol were effective vasodilators: 5 ng/kg/min of epoprostenol was equivalent to 30 ng/kg/min of prostaglandin E1. CONCLUSIONS: Neither drug showed pulmonary specificity.
RCT Entities:
OBJECTIVE: To study the dose response characteristics of prostaglandin E1 and epoprostenol (prostacyclin) and directly to compare their effectiveness as pulmonary vasodilators in infants with pulmonary hypertension. DESIGN: A crossover design with each patient receiving both drugs in random order. SETTING:Infants were studied in the intensive care unit while they were sedated, paralysed, and ventilated. PATIENTS: Twenty infants who had undergone corrective cardiac surgery and who were in sinus rhythm, had stable haemodynamic function, and had a pulmonary artery catheter in place. All infants were receiving dopamine and phenoxybenzamine. INTERVENTIONS: Baseline haemodynamic measurements were taken and an infusion of the first drug was started at the lowest dose: after 20 minutes the measurements were repeated and the dose increased. This protocol was repeated for all doses of both drugs: 10, 30, and 100 ng/kg/min of prostaglandin E1 and 5, 10, and 25 ng/kg/min of epoprostenol. Cardiac output was measured by the pulsed Doppler ultrasound method. MAIN OUTCOME MEASURES: Pulmonary and systemic vascular resistances were calculated from the cardiac output and compared by the Wilcoxon signed ranks test. RESULTS: Both prostaglandin E1 and epoprostenol were effective vasodilators: 5 ng/kg/min of epoprostenol was equivalent to 30 ng/kg/min of prostaglandin E1. CONCLUSIONS: Neither drug showed pulmonary specificity.
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