COCAINE DOES NOT COMPROMISE CEREBRAL OR MYOCARDIAL OXYGEN DELIVERY INFETAL SHEEP

Eight time-dated pregnant ewes at 125 days' gestation (145 days = term ) underwent surgery for placement of fetal vascular catheters, electro des for recording fetal behavioural state, and maternal venous cathete rs. Three days later, fetal cerebral and myocardial blood flow were de termined by the coloured microsphere technique under four conditions: (1) during rapid-eye movement (REM) sleep, before fetal cocaine infusi on, (2) 30 min after initiation of a cocaine infusion to the fetus at 0.2 mg/kg per min, (3) during REM sleep, before maternal cocaine infus ion, and (4) 30 min after initiation of a cocaine infusion to the ewe at 0.3 mg/kg per min. Cocaine infusion directly to the fetal lamb did not cause hypoxaemia or significantly change cerebral or myocardial bl ood flow or oxygen delivery. Cocaine administered to the ewe led to a drop in fetal oxygen tension from 3.0 +/- 0.5 to 2.5 +/- 0.3 kPa (P < 0.0001) and in fetal oxygen content from 3.8 +/- 0.7 to 2.8 +/- 0.4 mm ol O-2/L (P < 0.0001). Prior to maternal cocaine administration, fetal cerebral blood flow was 146 +/- 103 mL/100 g per min and during mater nal cocaine infusion it went to 184 +/- 147 mL/100 g per min (P = NS) while myocardial blood flow increased from 156 +/- 92 to 333 +/- 178 m L/100 g per min (P < 0.002). This increase in blood flow negated the e ffects of hypoxaemia so that cerebral oxygen delivery was unaffected w hile myocardial oxygen delivery increased an average of 67%. It is con cluded that cocaine administration to pregnant sheep does not impede f etal cerebral or myocardial oxygen delivery.