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To define the dose response of apnea and breathing to morphine we studied 12 fetuses at 116-141 days of gestation using our window technique. We instrumented the fetus to record electrocortical activity (ECoG), eye movements (EOG), diaphragmatic activity (integral of EMGdi), heart rate, carotid blood pressure, and amniotic pressure. Saline and morphine in doses of 0.03, 0.1, 0.5, 1, and 3 mg/kg were injected in random order in the jugular vein of the fetus during low-voltage ECoG. Fetuses were videotaped for evaluation of fetal behavior. We found 1) that saline did not elicit a response; 2) apnea, associated with a change from low- to high-voltage ECoG, increased from 2.2 +/- 1.5 (SE) min in two fetuses at a dose of 0.03 mg to 20 +/- 6.3 min in seven fetuses at 3 mg/kg (P less than 0.005); 3) the length of the breathing responses, associated with a change from high- to low-voltage ECoG, were 15 +/- 1.8 and 135.9 +/- 18.1 min (P less than 0.0005); 4) integral of EMGdi X frequency, an index equivalent to minute ventilation, increased from 1,763 +/- 317 arbitrary units to 10,658 +/- 1,843 at 1.0 mg/kg and then decreased to 7,997 +/- 1,335 at 3.0 mg/kg. These changes were related to a steady increase in integral of EMGdi, whereas frequency decreased at 3 mg/kg. There was an increase in breathing response to morphine plasma concentrations or morphine doses.(ABSTRACT TRUNCATED AT 250 WORDS)

The disposition and cardiovascular effects of ethanol were studied in near-term pregnant sheep and their fetuses after intravenous infusions either to the mother or the fetus. Placental transfer of ethanol from mother to fetus was rapid, but transfer from the fetal to maternal circulation was impaired when ethanol was administered directly to the fetus. Plasma clearance of ethanol was similar from the mother and fetus in utero. In the maternal infusion experiments, both maternal and fetal heart rate increased with plasma ethanol concentration. However, in the fetal infusion experiments, both maternal and fetal heart rate increased with plasma ethanol concentration. However, in the fetal infusion experiments, fetal heart rate was inversely related to plasma ethanol concentrations while maternal mean arterial blood pressure increased with maternal plasma ethanol concentration. Further studies in neonatal lambs are needed to determine if ethanol has adverse effects on hemodynamics when the neonate is separated from its protective intrauterine environment.

Arterial and portal norepinephrine and epinephrine levels, and hepatic blood volumes were measured in cats anesthetized with pentobarbital sodium to determine the basal levels after surgery and adrenalectomy in comparison with levels during intravenous infusions of norepinephrine and epinephrine that produced hepatic venoconstriction. In addition, the hypothesis that norepinephrine released into portal blood during mesenteric nerve stimulation might produce hepatic venous responses was tested. No epinephrine was detected in any plasma samples except during intravenous epinephrine infusions. Surgery did not increase, and adrenalectomy did not decrease, the basal norepinephrine levels measured after anesthesia (0.8 +/- 0.1 ng/ml). These basal levels were below the minimal levels required to produce hepatic venous responses. Equal plasma levels of norepinephrine and epinephrine produced similar hepatic venous responses and maximal responses required increases in plasma levels of 100 times the basal levels. Stimulation of mesenteric nerves at 2 Hz produced no change in portal norepinephrine levels, whereas at 8 Hz it produced a doubling of these levels. No significant changes in hepatic volume occurred. It is concluded that although basal levels of circulating catecholamines may reflect overall sympathetic nervous activity, they are not high enough to produce hepatic venous responses. Sympathetic control of the hepatic venous bed is mediated through the hepatic innervation, and circulating catecholamines play at most a minor role.

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