Pituitary and Plasma Concentrations of Adrenocorticotrophin, Growth Hormone, Vasopressin and Oxytocin in Fetal and Maternal Sheep during the Latter Half of Gestation and the Response to Haemorrhage

Dp, Alexander; Hg, Britton; Ml, Forsling; Da, Nixon; Jg, Ratcliffe

doi:10.1159/000240652

Cited by 57 publications

(24 citation statements)

References 23 publications

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“…Hemorrhage of 20 ml/kg fetal weight caused a 15-fold rise in concentration of arginine vasopressin. A 40-50% reduction of blood volume in acutely exteriorized sheep fetuses elicited a maximal response of 80-1000 /iU/ml (Alexander et al, 1974a). Maternal hypoxia caused an increase in sheep fetal arginine vasopressin concentration to 119 and 100 /xU/ml (Alexander et al, 1972).…”

Section: Discussionmentioning

confidence: 93%

“…Changes in heart rate, cardiac output, and distribution of cardiac output to various fetal organs are similar to those seen during fetal hypoxia and suggest that vasopressin release may play an important role in the fetal cardiovascular response to stress. ORE Res 44: 430-436, 1979 ARGININE VASOPRESSIN has been detected in the neurohypophysis (Alexander et al, 1974a;Skowsky and Fisher, 1977; Vizsolyi and Perks, 1976a, b) and plasma (Rurak, 1975;Skowsky et al, 1974) of fetal sheep by midgestation. It is not known, however, whether arginine vasopressin has a role in normal fetal physiology or in the fetal response to stressful stimuli.…”

Section: Discussionmentioning

confidence: 99%

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Hemodynamic responses of the sheep fetus to vasopressin infusion.

Iwamoto¹,

Rudolph²,

Keil³

et al. 1979

Circulation Research

142

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SUMMARYThe effects of intravenous infusion of vasopressin on the circulation of the fetus were studied in lambs in utero with chronically maintained intravascular catheters. Vasopressin infused in doses of 0.91-2.26 mU/min per kg fetal weight resulted in plasma levels of arginine vasopressin of 6.8-36.4 /iU/ml; these levels are similar to those achieved during fetal hypoxia. Petal mean arterial blood pressure increased from control levels of 47 ± 1.7 to 56 ± 1.9 nun Hg, and heart rate fell from 174 ± 4.1 to 144 ± 4.4 beats/min. Fetal cardiac output and its distribution and actual organ blood flows were measured before and during vasopressin infusion by the radionuclide-labeled microsphere technique. Combined ventricular output did not change significantly, but there was a redistribution of flow, with a marked reduction of the proportion of cardiac output to the gastrointestinal and peripheral circulations and an increase in the percent of cardiac output to the umbilical-placental, myocardial, and cerebral circulations. This redistribution was associated with a significant increase in fetal arterial Po» from 22 to 24 torr. Changes in heart rate, cardiac output, and distribution of cardiac output to various fetal organs are similar to those seen during fetal hypoxia and suggest that vasopressin release may play an important role in the fetal cardiovascular response to stress. ORE Res 44: 430-436, 1979 ARGININE VASOPRESSIN has been detected in the neurohypophysis (Alexander et al., 1974a;Skowsky and Fisher, 1977; Vizsolyi and Perks, 1976a, b) and plasma (Rurak, 1975;Skowsky et al., 1974) of fetal sheep by midgestation. It is not known, however, whether arginine vasopressin has a role in normal fetal physiology or in the fetal response to stressful stimuli. Plasma concentrations of arginine vasopressin in the sheep fetus have been shown to be elevated in response to various stimuli such as fetal hemorrhage, hypoxia, increased plasma sodium, and surgical manipulation (Alexander et al., 1974a, b;Rurak, 1975;Skowsky et al., 1973;Alexander et al., 1972).The cardiovascular system of the fetus responds to neurohypophysial hormones; intravenous infusion of arginine vasopressin into the sheep fetus has been shown to cause an increase in blood pressure and a decrease in heart rate (Rurak, 1975;Alexander et al., 1976). At present there is no information regarding the specific actions of arginine vasopressin on the cardiovascular system of the fetus. It is known that, in the adult, arginine vasopressin causes bradycardia and vasoconstriction of certain vascular beds, resulting in an increase in blood pressure (Vizsolyi and Perks, 1976a;Altura and Altura, 1977;Schmid et al., 1974). Our studies were undertaken to determine whether these responses are present in the fetus, and to characterize further the action of vasopressin on the hemodynamics of the sheep fetus. The nuclide-labeled microsphere method (Rudolph and Heymann, 1967;Heymann et al., 1977) was used to determine the distribution of combined ventricular output to v...

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Hemodynamic responses of the sheep fetus to vasopressin infusion.

Iwamoto¹,

Rudolph²,

Keil³

et al. 1979

Circulation Research

142

View full text Add to dashboard Cite

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“…Hypoxia is a known trigger of AVP secretion in the fetal lamb (20), but other stimuli have been identified, e.g. hypovolemia (21). The mode of delivery influences markedly AVP secretion (5).…”

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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“…Data regarding fetal vasopressin physiology, however, are meager. Vasopressin has been identified in the human fetal pituitary at 10-12 weeks of gestation (9, 12) and in the fetal pituitary of other mammalian species, including the guinea pig, sheep, and seal, during the last half of gestation (1,2,10,12,14). In addition, in the sheep and monkey, significant concentrations of circulating vasopressin have been detectable in fetal blood during the last half of gestation (1, 1 l ) , and increases in circulating levels have been evoked either by osmolar or volume (hemorrhage) stimuli (1, 11).…”

Section: Speculationmentioning

confidence: 99%

Arginine Vasopressin Response to an Osmotic Stimulus in the Fetal Sheep

et al. 1978

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Summary MATERIALS AND METHODSBaseline plasma osmolality (pOsm) and plasma arginiie vasopressin (pAVP) were measured in chronically catheterized fetal sheep. Mean baseline pAVP in fetuses from 101-120 days was 1.9 + 0.46 pU/ml (mean * SEM) with a pOsm of 293 rt 1.8 mOsm/kg. In fetuses of 121-141 days of gestation, mean pAVP was significantly lower, 0.77 0.19 pU/ml (P < 0.05), with a similar pOsm (293 2 1.9 mOsm/kg). The logarithmic baseline pAVP values were linearly correlated with pOsm for both groups. Hypertonic saline infusion resulted in a similar increase in the log pAVP corrected for the rise in pOsm in the 101-120-day fetuses and in 121-141-day fetuses. The slope of this response was similar to that of the steady state relationship. The data indicates that the fetal osmoreceptor system for control of arginine vasopressin secretion is fully functional in the last trimester of pregnancy. SpeculationThe fetal hypothalamic posterior pituitary system appears to show a relatively heightened response to increases in plasma osmolality during the last trimester of gestation. This may reflect the heightened hypothalamic activity postulated to explain the high circulating growth hormone levels at this time. The higher baseline plasma vasopressin levels in the younger fetuses would support this view. Alternatively, the augmented responsiveness may represent an adaptive response to the immaturity of the fetal kidney with respect to free water clearance or an adaptive response to some extrarenal function of the hormone on salt and water homeostasis in utero.Vasopressin secretion is regulated by two systems of r e c e p tors: the osmoreceptors located in or near the supraoptic nuclei in the hypothalamus and a series of volume receptors, including left atrial stretch receptors and carotid sinus and aortic arch baroreceptors. Available information suggests that the newborn is capable of secreting vasopressin at birth and that both the osmoreceptor and volume control systems are functional (3-6). Data regarding fetal vasopressin physiology, however, are meager. Vasopressin has been identified in the human fetal pituitary at 10-12 weeks of gestation (9, 12) and in the fetal pituitary of other mammalian species, including the guinea pig, sheep, and seal, during the last half of gestation (1,2,10,12,14). In addition, in the sheep and monkey, significant concentrations of circulating vasopressin have been detectable in fetal blood during the last half of gestation (1, 1 l ) , and increases in circulating levels have been evoked either by osmolar or volume (hemorrhage) stimuli (1, 11). However, little is known about the sensitivity and relative responsiveness of the fetal osmoreceptor control system. The present studies were designed to provide this information. 5Pregnant Columbia or Columbia-Suffolk ewes were obtained from a local source and the gestational age based on the induced ovulation technique (7). The animals were maintained in the vivarium and fasted 4 8 hr before surgery. The pregnant ewes were anesthetized using a m...

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Pituitary and Plasma Concentrations of Adrenocorticotrophin, Growth Hormone, Vasopressin and Oxytocin in Fetal and Maternal Sheep during the Latter Half of Gestation and the Response to Haemorrhage

Cited by 57 publications

References 23 publications

Hemodynamic responses of the sheep fetus to vasopressin infusion.

Hemodynamic responses of the sheep fetus to vasopressin infusion.

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

Arginine Vasopressin Response to an Osmotic Stimulus in the Fetal Sheep

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