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Biomedical subjects

L D Longo

Publications and source records attributed to L D Longo.

At least 181 records · Page 10Linked to original sources

Carbon monoxide uptake and elimination in fetal and maternal sheep.

We studied the relation of carboxyhemoglobin concentration in the fetus, [HbCOf], to that of the pregnant mother, [HbCOm], and inspired CO concentrations in unanesthetized sheep. We exposed ewes with catheters chronically implanted in maternal and fetal blood vessels to varying inspired CO concentrations. At 30 parts per million (ppm) CO, [HbCOm] increased from base-line levels of about 1.1% to about 4.6% over a course of 8-10 h. [HbCOf] increased more slowly from base-line values of 1.8% to steady-state values of 7.4% by 36-48 h. At 50 ppm, steady-state [HbCOm] = 7.2% and [HbCOf] = 11.3%. At 100 ppm, steady-state [HbCOm] = 12.2%, [HbCOf] = 19.8%. The increase in [HbCOm] resembled a simple exponential process with a half-time of 1.5 h. The time for [HbCOf] to reach half its final value was 5 h. The decay curve for CO elimination showed similar reactions, with fetal washout occurring slower than in the mother. Elevated [HbCOf] significantly decreased the PO2 values in the fetal descending aorta and inferior vena cava. These decreases in PO2 values can cause hypoxia and fetal death.

Animals↗

Fetal O2 changes in response to hypoxic stress: a mathematical model.

We developed a mathematical model to compute the time course of PO2 changes in fetal blood vessels during hypoxia. The model represents the circulation and major organs as a system of paths and nodes. We calculated outflow O2 for a path from its inflow O2 content and its distribution of transit times. The O2 content at a given node equals the flow-weighted sum of O2 delivered by different paths. Placental O2 transfer and organ O2 consumption are related to their arterial PO2 levels. We simulated the effects of uterine contractions with Gaussian-shaped decreases in placental O2 transfer. Increasing the intensity and increasing the duration of hypoxic episodes have comparable effects. Liver O2 consumption decreases more than that of other organs during hypoxic episodes. At the peak of a contraction, fetal systemic PO2 values decrease only about one-fourth as much as those in end-capillary placental blood. This indicates that despite rapid circulation times, fetal O2 reserves protect it against severe, short term hypoxia.

Brain↗

Placental diffusing capacity for carbon monoxide and oxygen in unanesthetized sheep.

We measured placental diffusing capacity for carbon monoxide (DpCO) in 10 unanesthetized sheep with catheters chronically implanted in maternal and fetal vessels. Serially measured DpCO during the last third of gestation averaged 0.55 +/- 0.02 (SEM) ml.(min.Torr.kg fetal wt)-1, essentially the same value as that previously reported in anesthetized, acutely operated animals. While placental CO diffusing capacity increased as a function of gestational age when expressed as ml.(min.Torr)(-1), it remained constant when calculated per kg fetal wt. In eight experiments, DpCO showed no change following the administration of several drugs which combine with cytochrome P450. We interpret this as evidence against the carrier hypothesis for placental CO exchange. We calculated the placental diffusing capacity for oxygen to be 0.68 ml.(min.Torr.kg)-1 and the mean maternal-to-fetal capillary Po2 difference to be 10 Torr. Caculations predict that maternal and fetal oxygen partial pressures equilibrate in end-capillary blood during the course of a single transit in placental exchange vessels; thus placental oxygen exchange is not limited by diffusion.

Animals↗

Carbon monoxide: effects on oxygenation of the fetus in utero.

The partial pressure of oxygen in fetal blood decreases in proportion to the carboxyhemoglobin concentrations in fetal and maternal blood. Because fetal oxygen tensions normally equal 20 to 30 percent of the values for adults, this reduction can result in severe hypoxia of vital tissues. Decreases in oxygen tension may be a factor in the lower birth weights of infants born to women who smoke or are exposed to severe air pollution.

Air Pollutants↗

Mercury toxicity in the pregnant woman, fetus, and newborn infant. A review.

This paper reviews the reported cases of mercury poisoning in pregnancy and the data based on sources of contamination, maternal uptake, and distribution. It analyzes current knowledge of placental transfer of various mercury compounds, fetal uptake, and distribution. It identifies the embryopathic and fetal toxic effects of mercury in general while emphasizing the greater toxicity of methylmercury compounds. Since maternal exposure to methylmercury is primarily through fish consumption, it recommends that women of childbearing age should not consume more than 350 Gm. of fish per week. In addition, they should not be occupationally exposed to air concentrations of mercury vapor greater than 0.01 mg. per cubic meter, of inorganic and phenylmercuric compounds greater than 0.02 mg. per cubic meter, or any detectable concentration of methylmercury.

Abnormalities, Drug-Induced↗