An Evaluation of Fetal Renal Function in a Chronic Sheep Preparation

Gresham, Edwin L.; Rankin, John; Makowski, Edgar L.; Meschia, Giacomo; Battaglia, Frederick C.

doi:10.1172/jci106785

Cited by 119 publications

(27 citation statements)

References 22 publications

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“…Gresham and co-workers [19] have shown that, after fetal surgery, up to 4 days are required for fetal renal function to return to normal. It is probable, therefore, that, in the present experiments, fetal recovery from an acute acid load was achieved mainly by slow placental clearance of chloride or lactate.…”

Section: Discussionmentioning

confidence: 99%

Elimination of Hydrogen Ion by the Lamb Fetus and Newborn

et al. 1972

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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

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Section: Discussionmentioning

confidence: 99%

Elimination of Hydrogen Ion by the Lamb Fetus and Newborn

et al. 1972

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“…D. 9 mented with 2.5% sodium pentobarbital (Diabutal®) solution given intravenously when necessary. Details of surgery have been described by GRESHAM et al [14]. In addition to implanting catheters in fetal artery and vein, catheters were implanted in the amniotic cavity and fetal bladder via the urachus äs well äs maternal femoral artery.…”

Section: Curriculum Vitaementioning

confidence: 99%

Renal response to acid loading in the developing lamb fetus, intact in utero

Daniel¹,

Bowe²,

Lallemand³

et al. 1975

Journal of Perinatal Medicine

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“…The length of infusion was 120 min or a time necessary to reach an arterial pH of -7.10; two preparations were infused 80 min, one 100 min, and six 120 min. All animals were infused at a rate of 0.382 ml/min, or 0.03 to 0.07 mEq/min.kg; fetal weight at the time of study was estimated at birth or sacrifice by the method of Gresham et al (20). Control experiments were performed in five additional animals by infusing either saline (n = 4) or glucose (n = 5) in the same concentration, volume, and rate as with NH4CI.…”

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confidence: 99%

Vasopressin and Catecholamine Secretion during Metabolic Acidemia in the Ovine Fetus

et al. 1987

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ABSTRACT. It has been suggested that the substantial rise in fetal plasma arginine vasopressin (AVP) during intrauterine hypoxia/asphyxia reflects decreases in P a 0 2 and/or pHa; however, the components of these "stresses," i.e. PO2, PC02, and pH, have not been controlled. Recently, only modest increases in fetal AVP secretion were seen during hypoxia independent of changes in pH and PC02. Since the independent effects of metabolic acidosis on fetal AVP secretion are unknown, we induced acute metabolic acidemia in fetal sheep at 137 f 4 (mean f SD) days gestation with 1 M NH4CI, while monitoring mean arterial pressure, heart rate, Pa02, PaC02, pHa, plasma osmolality, and blood concentrations of electrolytes, AVP, dopamine, norepinephrine, and epinephrine. Mean arterial pressure, Pa02, PaC02, and plasma osmolality and sodium were unchanged; pHa decreased from 7.37 f 0.01 to 7.04 f 0.05 (p < 0.05) during NH4CI and did not return to control levels until 24 h later. AVP increased from 2.85 f 0.23 to 5.26 f 1.11 ~U / m l (p < 0.05) at the time of maximum acidosis, correlating with the fall in pHa (r = -0.67, p = 0.001); however, after stopping NH4CI, AVP returned to baseline levels although pHa remained <7.15. In control studies using the same osmolar load, volume, and rate of infusion, AVP levels were unchanged. Only epinephrine was significantly (p < 0.05) elevated during acidosis, but did not correlate with pHa or plasma AVP.Marked metabolic acidemia appears to have little or no effect on fetal AVP secretion, and fetal catecholamine secretion is variable. (Pediatr Res 21: 38-43, 1987) Abbreviations AVP, arginine vasopressin DA, dopamine NE, norepinephrine E, epinephrine MAP, mean arterial pressure HR, heart rate ANOVA, analysis of variance plasma of human infants (2-5) and shown to reflect not only the route and "stresses" of delivery, but also the occurrence of additional intrauterine "stresses" (2, 5,6). Furthermore, elevated plasma levels of AVP are seen in fetal sheep during hemorrhage (7-9) and hypoxia/asphyxia (10)(11)(12)(13)(14). Thus it appears that, as in the adult, AVP may be considered a "stress" hormone in the fetus.Whereas the stimulus for fetal hypersecretion of AVP during hemorrhage is clear, i.e. hypovolemia and baroreceptor mechanisms (9), the mechanisms(s) responsible for fetal AVP release during hypoxia/asphyxia is less clear. For example, although it has been suggested that during hypoxic insults (1 1, 13, 15) and parturition (14) the fall in PO2 is responsible for the elevated plasma levels of AVP, neither pH nor PC02 were controlled. Recently, we (12) reported that during mild to moderate fetal hypoxemia (a fall in Pa02 from 20 to 1 1 mm Hg) in the absence of alterations in either pHa or PaC02, plasma AVP levels rose from 2 to 10 pU/ml (2.5 pg/ml = 1.0 pU/ml) in contrast to the substantially greater increases reported by others and the nearly 200-fold rise observed during asphyxia, i.e. in the presence of hypoxemia, hypercapnia and acidosis (12). Moreover, we observed that maximum AVP le...

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An Evaluation of Fetal Renal Function in a Chronic Sheep Preparation

Cited by 119 publications

References 22 publications

Elimination of Hydrogen Ion by the Lamb Fetus and Newborn

Elimination of Hydrogen Ion by the Lamb Fetus and Newborn

Renal response to acid loading in the developing lamb fetus, intact in utero

Vasopressin and Catecholamine Secretion during Metabolic Acidemia in the Ovine Fetus

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