Effects of Acute Hypercapnia on Maternal and Fetal Vasopressin and Catecholamine Release

Abstract

ABSTRACT. Although fetal asphyxia, i.e. hypoxemia, acidosis, and hypercapnia, increases plasma arginine vasopressin (AVP) >40-fold, hypoxemia and metabolic acidosis occurring independently cause only 5-fold and 2-fold increases, respectively. To determine the effects of hypercapnia on AVP release, we examined the effects of acute hypercapnia on AVP secretion in six pregnant sheep and their fetuses a t 135 f 4 d (x f SD), exposing the ewe successively to room air, 30% 02, 30% O 2 plus 10% C 0 2 , 30% 02, and room air, and monitoring uterine blood flow, a s well as maternal and fetal mean arterial pressure, heart rate, arterial blood gases, and plasma AVP and catecholamines. Oxygen exposure had no effect on the ewe or fetus. During O 2 plus COz exposure, the ewes and fetuses developed hypercapnia in the absence of hypoxia, arterial C 0 2 tension increasing to 8.38 f 0.87 kPa (62.9 f 6. respectively. Hypercapnia alone is not a major determinant of AVP secretion in the mother or fetus; thus, the marked rise in fetal AVP secretion observed during asphyxia1 insults may reflect interaction between the effects of hypercapnia and hypoxemia. (Pediatr Res 30: 368-374,1991) Abbreviations MAP, mean arterial pressure E, epinephrine NE, norepinephrine PaOz, arterial O 2 tension PaCOZ, arterial COz tension ANOVA, analysis of variance pH,, arterial p H Alterations in the homeostatic milieu trigger a complex series of events that serve to protect the individual organism against environmental insults. Asphyxia, i.e. the simultaneous occurrence of hypoxemia, acidosis, and hypercapnia, is a striking illustration of an intense "stress," and subsequent adaptive responses reflect a complex interaction of factors related to the metabolic, neuroendocrine, and cardiovascular systems. Although these responses have been examined in adult animals of several species (1-6), the ontogeny of these responses during fetal development is not fully understood.In fetal sheep the response to stress has been characterized by increased secretion of AVP and adrenal catecholamines (7). By using the fetal sheep as a model, we and others (5, 8-12) have observed that fetal asphyxia, regardless of method of induction, results in substantial increases in plasma AVP concentrations, i.e. >40-fold rises over baseline levels. In contrast, we have shown ( I I) that during moderate fetal hypoxemia, i.e. a 45% decrease in Pa02 without alterations in either arterial pH or PcoZr plasma levels of AVP rose only modestly (5-fold over baseline values). Furthermore, induction of marked metabolic acidemia had little effect on fetal AVP secretion, i.e. only a 2-fold rise over baseline levels (I 3). Because neither hypoxemia alone nor pure metabolic acidosis resulted in the substantial increase in plasma AVP seen during fetal asphyxia, the role of hypercapnia in fetal secretion of AVP, as well as the interaction of these variables, remained to be elucidated.Catecholamines are also released during asphyxia. Rose ef a/.(14) demonstrated that acute hypercapnic acidosis resulte...

Cardiovascular Responses of Goat Fetuses to Hypercapnia during Extrauterine Incubation Using Extracorporeal Membrane Oxygenation

“…In these studies, fetal hypercapnia was induced through the ewe. It was reported that amniotic fluid pressure in creased during hypercapnia [5] and maternal cortisol crossed the placental barrier [8,9], With our extrauterine fetal incubation system, it was possible to observe fetal physiological change without maternal influence.…”

“…But very few studies have reported on changes of fetal physiological parameters such as heart rate and blood pressure during hypercapnia [4][5][6]8]. Therefore, responses of the fetal peripheral chemoreccptor to changes in PaCCE have not yet been quantified.…”

“…Therefore, responses of the fetal peripheral chemoreccptor to changes in PaCCE have not yet been quantified. Faucher et al [5] reported that fetal heart rate and mean blood pressure were unchanged during hypercapnia (75.2 ± 4.6 mm Hg) at 30 min of exposure using fetal sheep at 135 ± 5 days' gestation. Chen and Wood [7] reported that fetal heart rate increased significantly, but mean blood pressure was unchanged due to hypercapnia (55.2 ± 1.8 mm Hg) induced by maternal hypercapnia.…”

“…Fetal cerebral blood flow is increased during hypercap nia because of its direct effect on vascular dilatation [1][2][3], but fetal peripheral chemoreceptor response to changes in arterial C 0 2 tension was not yet been quantified minutely [4], The changes in fetal heart rate, mean arterial blood pressure, and other parameters in fetal circulation due to the hypercapnia are contradictory [4][5][6][7]. In most of these previous studies, fetal hypercapnia was induced through the ewe.…”

“…In most of these previous studies, fetal hypercapnia was induced through the ewe. Accordingly, fetal cardiovascular responses might be influenced by maternal physiological status, for example uterine contraction and maternal cortisol secre tion [5,8,9].…”