Abstract
Acute asphyxia results in AVP hypersecretion in fetal sheep. Since acidosis, hypoxia, and hypercapnea occur simultaneously with asphyxia, it is unclear which is primarily responsible for AVP release. We have shown that hypoxia has no effect until aortic PO2 (PaO2) is <12mmHg, and AVP levels were only 10±3μU/ml (X̄±SE). To further examine the asphyxial components in fetal AVP release, we studied the effects of metabolic acidosis in 8 fetal sheep at 137±1.4 days. Each was infused with .03-.07mEq NH4Cl/min·kg for 120min while monitoring mean arterial pressure (MAP), heart rate (HR), PaO2, pHa, and PaCO2, and plasma AVP before, during (20min intervals) and repeatedly after NH4Cl. MAP, PaO2, and PaCO2 were unchanged; pHa fell progressively from 7.376±.012 to 6.986±.066* during NH4Cl, rising to 7.356±.021 by 24h. Plasma AVP rose gradually from 2.85±.23 to 5.26±1.1μU/ml* during NH4Cl, falling to 2.77±.41 by 4h. After NH4Cl, HR rose 24±1.1%*. The rise in AVP during NH4Cl was linearly correlated with pHa, r=-.67 (p<.0001, n=37), and PaO2 tended to rise. In only one animal (not included), with pH=7.12 and PaO2=12mmHg, AVP rose >8μU/ml, 30.2μU/ml. We conclude that: 1) acidosis, like hypoxemia alone, does not result in marked fetal AVP release; 2) whereas AVP release is related linearly to pHa, there appears to be a threshold value for PaO2; and 3) acidosis and hypoxia appear synergistic for AVP release, but the role of PaCO2 is unknown. *p<.05.
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Faucher, D., Lowe, T., Laptook, A. et al. ACUTE METABOLIC ACIDOSIS: EFFECTS ON ARGININE IN VASOPRESSIN(AVP) RELEASE IN FETAL SHEEP. Pediatr Res 18 (Suppl 4), 137 (1984). https://doi.org/10.1203/00006450-198404001-00264
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DOI: https://doi.org/10.1203/00006450-198404001-00264