Abstract
Techniques of fetal monitoring, including fetal blood sampling in utero, were employed to study the physiological effects of acute maternal carbon monoxide intoxication upon the fetal rhesus monkey. Nine term-pregnant female monkeys were exposed to 0.1-0.3 % inspired CO over 1-3 hours. The mothers tolerated car-boxyhemoglobin (COHb) levels exceeding 60 % without clinical sequelae. The fetuses promptly developed profound hypoxia upon exposure of the mothers to CO. However, the fetal COHb levels rose only gradually over the 1-3 hours and thus contributed only slightly to the development of the early fetal hypoxia. Fetal hypoxia was associated with bradycardia, hypotension, and metabolic and, later, respiratory acidosis. A close correlation was noted between the severity of intrauterine hypoxia and the appearance of brain damage. Severe brain damage (brain swelling associated with hemorrhagic necrosis of the cerebral hemispheres) appeared only in those fetuses whose arterial O2 content had fallen below 2.0 ml/100 ml for at least 45 min during the maternal CO intoxication.