Elimination of Hydrogen Ion by the Lamb Fetus and Newborn

Abstract

Response of the fetal lamb to metabolic acidosis in the absence of hypoxia or maternal acidosis was studied and compared with that of the newborn Iamb. Experiments were conducted on nonanesthetized fetuses intact in utero, catheters having been implanted previously at hysterotomy. Metabolic acidosis was produced by infusion of 28 mmoles of lactic or hydrochloric acid (0.25 M) into the femoral vein of fetus or newborn.Similar changes in acid-base state were produced with hydrochloric and lactic acids. In fetuses, pH fell 0.28 pH units; this decrease was greater than that observed in newborns (0.20 pH units). Newborns hyperventilated during and following infusion, lowering P C o, by an average of 8 mm Hg and partially compensating for the metabolic acidosis. In fetuses, arterial P co , rose during infusion by an average of 6 mm Hg, but values for P C o 2 in umbilical vein and maternal artery did not change. Thus fetal A-V difference for P CO2 across the placenta increased, whereas the P c02 gradient between fetus and mother remained constant. These observations suggest that fetal ability to compensate for metabolic acidosis is limited by the maternal Pa co ,.Upon completion of the acid infusion, pH rose and base deficit fell at approximately the same rate in both fetus and newborn, but the rate of recovery was slow. After 1 hr, pH was still significantly lower than the control value (by 0.1 pH unit) and base deficit was lower by 9 mEq/liter. By 12 hr, all acid-base values had returned to normal. SpeculationThese experiments indicate that the transfer of hydrogen ion across the placenta is relatively slow, even when the circulatory status of both mother and fetus is normal, and there is no fetal hypoxia or uterine contraction. In this respect the placental membrane has properties similar to the blood brain "barrier." With strong uterine contractions, maternal perfusion of the intervillous space is reduced or ceases, which leads to successive episodes of fetal hypoxia and acidosis. Slow placental transfer of hydrogen ion may explain the development of metabolic acidosis in the fetus during the course of labor. 584Elimination of hydrogen ion by lamb fetus and newborn 585

Renal Acid–Base And Sodium Handling In Hypoxia And Subsequent Mild Metabolic Acidosis In Foetal Sheep

“…In the normoxic foetus, induction of acidaemia by infusion of either hydrochloric or lactic acid is followed by a rapid fall in urinary pH and rises in urinary titratable acid, ammonium and net acid excretion 2,4,5 . In contrast, in the present study, in which foetuses developed a mild metabolic acidosis as a result of hypoxia, there were no rapid changes in renal acid excretion.…”

“…Thus, in the present study, the fall in plasma pH was more gradual and the minimum plasma pH (which actually occurred during the recovery period) was not as low as in acid infusion studies. Second, in acid infusion studies, 2,4,5 foetal arterial P CO 2 rose, but in the present study the foetuses were hypocapnic. This was because the ewes hyperventilated when they were made hypoxic by nitrogen infusion into the trachea and, because CO 2 rapidly crosses the placenta, foetal P CO 2 also fell 21 .…”

“…Foetal acid–base balance is controlled by both the placenta and the foetal kidneys. The placenta is responsible for rapid transfer of carbon dioxide, but the transfer of hydrogen ions and bicarbonate ions, at least in the sheep, is quite slow 1,2 . The foetal kidneys, like adult kidneys, reabsorb filtered bicarbonate and generate new bicarbonate by excreting acid in the form of titratable acid and ammonium 3 .…”

“…The foetal kidneys, like adult kidneys, reabsorb filtered bicarbonate and generate new bicarbonate by excreting acid in the form of titratable acid and ammonium 3 . When foetuses are made acidaemic by infusion of either hydrochloric or lactic acid, net acid excretion by the foetal kidney increases quite rapidly and the kidneys contribute to the subsequent recovery of acid–base balance 2,4,5 …”

The effects of metabolic acidosis on renal function of fetal sheep.

“…infusion of hydrochloric acid (Univar, AR) at a dose of 6-7-19-3 mmol/kg fetal body weight (molarity: 0-15-0-25 M). Initially it was decided to infuse 15 mmol/kg body weight of acid, a dose similar to that used by Smith & Schwartz (1970) and Daniel, Baratz, Bowe, Hyman, Morishima, Sarcia & James (1972). However four animals died during or shortly after these doses were infused and in other animals, arterial pressure rose sharply and heart rate fell during the first 30 min of infusion, so the infusion was terminated when only half the dose had been given.…”