Vasopressin and Catecholamine Secretion during Metabolic Acidemia in the Ovine Fetus

Faucher, Daniel; Lowe, T. W.; Magness, Ronald R.; Laptook, Abbot R.; Porter, John C.; Rosenfeld, Charles R.

doi:10.1203/00006450-198701000-00010

Cited by 19 publications

(9 citation statements)

References 29 publications

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“…Baseline data for maternal and fetal (Table I) arterial blood gases, pH, and hematocrit are similar to data previously reported from our laboratory (1 1, 13,19). Maternal Pao2 increased significantly at 10 min of Oz exposure ( Fig.…”

Section: Resultssupporting

confidence: 86%

“…Each sample of fetal blood collected for AVP and catecholamine measurements was centrifuged immediately, the plasma was removed, and the erythrocytes were resuspended in a volume of sterile isotonic saline equal to the plasma volume and reinfused into the fetus in the manner previously reported (1 5). This procedure has been shown to have no effect on AVP secretion (13). Maternal blood was handled similarly, but red cells were not reinfused.…”

Section: Methodsmentioning

confidence: 99%

“…respiratory acidosis) results in relatively small increases in plasma AVP (1 1). Because this suggested that hypoxemia alone may not be the major determinant of AVP release during asphyxia, we examined the role of acute metabolic acidemia in the release of this peptide hormone in fetal sheep of similar gestational ages (13). In those studies, NH4C1 infusion resulted in a fall in fetal arterial pH to 7.04 ?…”

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

et al. 1991

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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...

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Section: Resultssupporting

confidence: 86%

Section: Methodsmentioning

confidence: 99%

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

et al. 1991

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“…However, it does enter the blood, and reaches average plasma levels of (1·2 ± 0·3) ² 10¦Í Ò (means ± s.d.) in late fetal sheep, and rises to (1·2 ± 0·4) ² 10¦Ì Ò just before delivery (calculated from Jones, 1980;Faucher et al 1987;Reid et al 1990). The highest levels reported in fetal plasma are seen in rats, where, despite some decline in late gestation, they remain at 1·3 ² 10¦Ì Ò at birth, 2-3 times those of the mother, and constitute about 20-30% of the total plasma catecholamines (Ben-Johnathan & Maxson, 1978).…”

Section: Discussionmentioning

confidence: 99%

The effect of dopamine on lung liquid production by in vitro lungs from fetal guinea‐pigs

Chua

Perks

1998

The Journal of Physiology

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During gestation, fetal lungs produce large quantities of fluid which contribute substantially to the amniotic fluid, particularly in the guinea-pig, where production rates appear to be higher than those for urine (Strang, 1991;Perks et al. 1992). This production is based on a Na¤-K¤-2Cl¦ cotransport system, probably located in type II cells (Strang, 1991). However, at birth it is vital for this process to be replaced by fluid reabsorption, and it is generally agreed that this is brought about by an amiloride-sensitive, Na¤-based transport system, probably augmented by colloid osmotic effects (Strang, 1991). The first agent shown to activate fluid reabsorption was adrenaline (sheep: Walters & Olver, 1978; goat: Perks & Cassin, 1989). However, in the guinea-pig, reabsorption can be produced by both adrenaline and noradrenaline, which, unlike the â_receptor activation in sheep, act through Journal of Physiology (1998), 513.1, pp. 283-294 283The effect of dopamine on lung liquid production by in vitro lungs from fetal guinea-pigs 1. The neuroendocrine system of the lungs has no clear function. However, previous studies of one of its products, somatostatin, have implicated it in lung liquid removal at birth. The present study extends this concept by investigating the effects of dopamine, a major product of this system, on lung liquid reabsorption. 2. The effects of dopamine on fetal lung liquid production and reabsorption were tested on in vitro lungs from fetal guinea-pigs of 60 ± 2 days of gestation (term = 67 days). Dopamine was placed in the outer bathing saline during the middle hour of 3 h incubations. Fluid movements across the pulmonary epithelium were monitored by a dye dilution method, and changes in rates over 1 h intervals were tested for significance by analysis of variance and regression analysis. 3. Dopamine was able to reduce fluid production or cause reabsorption (based on 42 preparations). Control preparations and those given 10¦Ì Ò dopamine showed no significant changes; those given higher concentrations showed significant reductions in production or reabsorption (P < 0·025 to P < 0·0005), according to dose (42·6 ± 10·8 % reduction at 10¦Ê Ò; 75·4 ± 5·9 % reduction at 10¦É Ò; 92·1 ± 7·0 % reduction at 10¦Ç Ò and 121·4 ± 12·8 % (reabsorption) at 10¦AE Ò dopamine). The linear log dose-response curve (r = 0·99) showed a theoretical threshold at 1·7 ² 10¦Í Ò dopamine. 4. Effects were mediated through specific dopamine receptors (based on 78 preparations).Dopamine at 10¦É Ò was tested together with each of three dopamine receptor antagonists at 10¦Ç Ò. The general dopamine receptor antagonist haloperidol and the more specific Dµ receptor blocker domperidone both abolished responses, but the D1 receptor antagonist SCH23390 was without effect. This suggested that Dµ dopamine receptors mediated the responses, and that responses were not due to conversion of dopamine to adrenaline or noradrenaline. 5. There was no evidence that responses involved amiloride-sensitive Na¤ transport (based on 54 preparat...

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“…Asphyxia is the most likely mechanism responsible for the AVP secretion during parturition (5). In fetal sheep (35), metabolic acidosis produces only a 2-fold and hypoxemia a 4-fold rise of AVP release, compared to about 200-fold increase in response to a combination of hypoxemia, metabolic acidosis, and hypercapnia (i.e. asphyxia).…”

Section: Discussionmentioning

confidence: 99%

Cord Plasma Vasopressin, Erythropoietin, and Hypoxanthine as Indices of Asphyxia at Birth

et al. 1988

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ABSTRACT. To assess the value of cord plasma arginine vasopressin (AVP), erythropoietin (EP), and hypoxanthine (HX) as indices of asphyxia, we studied 62 infants of mothers with preeclampsia, 34 acutely asphyxiated infants, with 5-min Apgar score 5 6 and/or umbilical arterial pH 57.05, and 38 control infants. Umbilical arterial AVP in the asphyxia group (geometric mean; 95% confidence interval: 180; 92-350 pg/ml) was higher than in the control group (23; 8-66, p = 0.002) and correlated with umbilical arterial pH ( r = -0.447, p = 0.028). AVP levels in the preeclampsia group did not differ from controls. Cord venous E P was higher in infants delivered by elective cesarean section from women with severe preeclampsia (115; 75-177 mU/ml, p < 0.001) than in control infants (23; 18-27); in the whole group EP correlated with pH (r = -0.493, p < 0.001). E P in the asphyxia group was similar (46; 35-65) to controls (40; 33-47) and did not correlate with pH. Cord arterial HX in the preeclampsia group was similar to controls (12.3; 9.5-16.0 pmol/liter), but elevated in the asphyxia group (23.7; 17.6-31.8, p = 0.001), in which HX correlated with pH ( r = 0.558, p = 0.008) and AVP ( r = 0.588, p = 0.005). E P did not correlate with AVP or HX in any group, nor did any of the variables correlate with the Apgar score. We conclude that cord plasma AVP and HX reflect acute asphyxia, whereas E P is elevated after more prolonged hypoxia. (Pediatr Res 24: 490-494,1988) Abbreviations AVP, arginine vasopressin EP, erythropoietin HX, hypoxanthine Fetal asphyxia and delivery trigger a rapid increase in the secretion of several "stress" hormones, e.g. catecholamines, glucocorticoids, ACTH, p-endorphin, and AVP, which in turn mediate the cardiovascular and metabolic adaptation to asphyxia (4-6). A more specific response to hypoxia is an increase in the synthesis of EP, followed by elevation of plasma levels (7,8). If tissue hypoxia becomes more severe, cellular ATP concentrations cannot be maintained, and increased concentrations of the purine nucleotide catabolic products, HX, xanthine, and uric acid, appear in body fluids (9).The aim of our study was to assess if three components of this physiological response, AVP, EP, and HX, could be useful as biochemic indices of the severity of asphyxia. Two different clinical conditions were studied: acute severe birth asphyxia and maternal preeclampsia, the latter as an example of a chronic but less severe compromise in fetal oxygen and nutrient supply.

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Vasopressin and Catecholamine Secretion during Metabolic Acidemia in the Ovine Fetus

Cited by 19 publications

References 29 publications

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

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

The effect of dopamine on lung liquid production by in vitro lungs from fetal guinea‐pigs

Cord Plasma Vasopressin, Erythropoietin, and Hypoxanthine as Indices of Asphyxia at Birth

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