O2 tensions of blood from uterine wall venules, maternal placental venules, and uterine vein.
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Biomedical subjects
Publications and source records attributed to R E Forster.
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The dynamics of CO(2) exchange in the lungs of man was studied by observing the rate of disappearance of a stable isotope of CO(2) ((13)CO(2)) from the alveolar gas during breath holding. Over 50% of the inspired isotope disappeared within the first 3 sec followed by a moderately rapid logarithmic decline in which one-half of the remaining (13)CO(2) disappeared every 10 sec. The large initial disappearance of (13)CO(2) indicated that alveolar (13)CO(2) equilibrated in less than 3 sec with the CO(2) stored in the pulmonary tissues and capillary blood. The volume of CO(2) in the pulmonary tissues calculated from this initial disappearance was 200 ml or 0.33 ml of CO(2) per milliliter of pulmonary tissue volume. The alveolar to end-capillary gradient for (13)CO(2) was calculated by comparing the simultaneous disappearance rates of (13)CO(2) and acetylene. At rest and during exercise this gradient for (13)CO(2) was either very small or not discernible, and diffusing capacity for CO(2) (D(LCO2)) exceeded 200 ml/(min x mm Hg). After the administration of a carbonic anhydrase inhibitor the rate of disappearance of (13)CO(2) decreased markedly. D(LCO2) fell to 42 ml/(min x mm Hg) and at least 70% of the exchange of (13)CO(2) with the CO(2) stores in the pulmonary tissues and blood was blocked by the inhibitor. These changes were attributed to impairment of exchange of (13)CO(2) with the bicarbonate in the pulmonary tissues and blood. The pH of the pulmonary tissues (V(tis)) was determined by a method based on the premise that the CO(2) space in the pulmonary tissues blocked by the inhibitor represented total bicarbonate content. At an alveolar P(CO2) of 40 mm Hg pH of V(tis) equalled 6.97 +/- 0.09.
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A technique is described for studying the respiratory function of the placenta using carbon monoxide, a gas whose exchange across the placenta between the maternal and fetal circulations is limited by diffusion rather than blood flow. During the steady state before the introduction of CO, the normal concentration of carboxyhemoglobin in the ewe, [COHb](M), is approximately 0.90%, and that in the fetus is 2.9%, the ratio [COHb](F)/[COHb](M) being 3.2. In dogs the corresponding values are 1.9%, 4.8%, and 2.4%. After the introduction of CO into the mother animal, CO diffused across the placenta slowly with an equilibration half-time of approximately 2 hours. The average carbon monoxide diffusing capacity (D(Pco)) of the placenta during maternal to fetal exchange was 0.54 ml per (minute x mm Hg x kg fetal weight) (SD +/- 0.13) in sheep and 0.57 ml per (minute x mm Hg x kg) (SD +/- 0.18) in dogs. The fetal to maternal placental diffusing capacity in two sheep was 0.54 ml per (minute x mm Hg x kg). Calculations considering the relative rates of reaction of O(2) and CO with red cell hemoglobin and the relative rates of diffusion of the two gases suggest that the true D(Po2) should be about 1.2 to 2 times greater than the D(Pco) or 0.65 to 1.1 per (minute x mm Hg x kg). This is about 5 times greater than the reported value of D(Po2) calculated from measurements of P(O2) in the mixed uterine and umbilical venous blood. With a diffusing capacity of this magnitude the maternal and fetal placental end capillary P(O2) would approach equilibrium, becoming too small to measure, and the calculation of D(Po2) would be unreliable. We suggest that the apparent end capillary P(o2) gradients of 15 to 20 mm Hg, obtained from sampling uterine and umbilical venous blood, result from a combination of uneven distribution of maternal and fetal placental blood flow and from placental oxygen consumption.
A technique is described for studying the distribution of blood flow to the maternal and fetal placental vessels in sheep and dogs with radioactive labeled macroaggregates of albumin. When the maternal animal breathed room air the distribution of maternal placental blood flow was uneven among the cotyledons as well as within a given cotyledon. Fetal blood flow was also distributed nonuniformly among and within the cotyledons. The relation of maternal to fetal placental blood flow was also markedly uneven (coefficient of correlation, tau = 0.066). After the animal was made hypoxic by breathing 10-12% O(2) the distribution of maternal, fetal, and maternal/fetal placental flows became more uniform. The coefficient of correlation of maternal to fetal flow was high (tau = 0.53, P < 0.01). While the maternal animal breathed room air, after ligation of a major branch of the umbilical artery the distribution of maternal, fetal, and maternal/fetal flows in the remaining two-thirds to three-fourths of the placenta became more uniform. The correlation coefficient for maternal to fetal flow was high (tau = 0.35, P < 0.01).It appears that under normal circumstances with uneven distribution of blood flows there is a considerable portion of the placenta that does not receive blood flow in optimum quantities to promote efficient O(2) exchange. Failure to consider the influence of nonuniform maternal flow/fetal flow will result in overestimation of mean maternal-fetal oxygen tension gradients, and thus underestimation of the placental diffusing capacity for oxygen. In response to maternal hypoxia or compromise of the fetal placental circulation the distribution of maternal, fetal, and maternal/fetal flows becomes more uniform, thereby increasing the efficiency of placental O(2) exchange.
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Using a double-beam stopped-flow apparatus estimations were made of the velocity constant for the initial uptake of oxygen by fully reduced erythrocytes (k'(c)). Mammalian cells were studied with volumes varying from 20 micro(3) (goat) to 90 micro(3) (man), as were bullfrog cells (680 micro(3)). Measurements were made under physiological conditions of pH, P(CO2), and temperature. In man k'(c) was 80 mM(-1) sec(-1) and in other species smaller cells generally had a greater value for k'(c) than did the larger cells. In the goat it was 1.8 times as great as the human value; in the bullfrog it was only one-fifth as great. These differences could not be accounted for by interspecific differences in hemoglobin kinetics. The differences probably represent a true effect of size conferring some biological advantage on the species with the smaller cells. The cell membrane offered resistance to oxygen passage. Using the usual red cell model of an infinite sheet of reduced hemoglobin, membrane permeability appeared to differ among mammals. If, as is likely, the effective cell halfthickness differs among mammals, actual membrane permeability differences may be less. A method for measurement of oxygen saturation of dilute cell suspensions is also described.
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