Acute carbon monoxide intoxication and hyperbaric oxygen in pregnancy.

Modalities of oxygen therapy for pregnant women intoxicated with carbon monoxide (CO) are ill defined. Hyperbaric oxygen (HBO) is presumed to be hazardous to the pregnancy. On the other hand CO entails anoxic injuries in the mother and fetus. We have entered 44 pregnant women who sustained an acute carbon monoxide poisoning at home, into a prospective study in order to assess HBO tolerance. They were treated within 5.3 +/- 3.7 h (range: 1-12) of the intoxication with a combination of 2 h of HBO at a pressure of 2 atmospheres absolute (ATA) and 4 h of normobaric oxygen, irrespective of the clinical severity of the intoxication and of the age of pregnancy. Six patients were lost to obstetric follow-up. Only 2 patients sustained a spontaneous abortion: 1 within 12 h and 1 within 15 days of the intoxication. Thirty-four women gave birth to normal newborns. Finally 1 elected to undergo abortion for reasons unrelated to the intoxication and 1 gave birth to a baby with Down's syndrome. There is no evidence that HBO was involved with either abortion of our study. We conclude that HBO may be carried out in pregnant women acutely intoxicated with carbon monoxide.

Effects of an intravenous infusion of noradrenaline on the plasma concentration of free and sulfoconjugated catecholamines in anesthetized dogs.

Exogenous noradrenaline (NA) was infused intravenously at increasing rate from zero (control) to 10, 25, 50, 100, 200 and 600 ng/kg/min during 20 min in anesthetized and ventilated dogs; the mean (+/- SEM) plasma concentration of free NA was increased from 130 +/- 23 pg/ml (basal) to 7,826 +/- 787 pg/ml. This had no measurable effect on the plasma concentration of dopamine and adrenaline in either free or sulfoconjugated form; a lack of change was also observed in dogs given a 600-ng/kg/min infusion during more than 2 h. The increase of free NA concentration was highly correlated both with the infusion rate, and with the blood pressure. Contrary to expectations, the plasma concentration of NA sulfate decreased in all 5 dogs when plasma NA concentration was progressively increased from basal to about 1,600 pg/ml; beyond this apparently crucial level (i.e. from about 1,600 to 7,826 pg/ml), the response of NA sulfate concentration was erratic, as it was in dogs given a 600-ng/kg/min infusion during more than 2 h. If the response of canine blood pressure is examined in the light of the level of free NA concentration, two mechanisms can be suspected: (1) when the NA level increased from basal to about 1,600 pg/ml, a direct action upon peripheral resistances was likely to be the predominant hypertensive mechanism; (2) beyond about 1,600 pg/ml, a combined effect of NA on both peripheral resistances and cardiac hemodynamics could have a role in the hypertensive process. Thus, a concentration of NA of about 1,600 pg/ml appears to be a landmark for both CA metabolism and circulatory homeostasis. Further studies will have to be carried out to investigate whether this represents the upper physiological concentration in the anesthetized dog.