ethanol in adult rats and humans leads to reduced AVP-producing neurons, and prenatal ethanol (PE) exposure has been reported to cause changes in the morphology of AVP-producing cells in the suprachiasmatic nucleus of young rats. The present studies further characterize the effects of PE exposure on AVP in the young adult rat, its hypothalamic synthesis, pituitary storage, and osmotically stimulated release. Pregnant rats were fed a liquid diet with 35% of the calories from ethanol or a control liquid diet for days 7-22 of pregnancy. Water consumption and urine excretion rate were measured in the offspring at 60 -68 days of age. Subsequently, the offspring were infused with 5% NaCl at 0.05 ml ⅐ kg Ϫ1 ⅐ min Ϫ1 with plasma samples taken before and at three 40-min intervals during infusion for measurement of AVP and osmolality. Urine output and water intake were ϳ20% greater in PEexposed rats than in rats with no PE exposure, and female rats had a greater water intake than males. The relationship between plasma osmolality and AVP in PE-exposed rats was parallel to, but shifted to the right of, the control rats, indicating an increase in osmotic threshold for AVP release. Pituitary AVP was reduced by 13% and hypothalamic AVP mRNA content was reduced by 35% in PEexposed rats. Our data suggest that PE exposure can cause a permanent condition of a mild partial central diabetes insipidus. fetal alcohol syndrome; vasopressin; plasma osmolality; thirst; vasopressin messenger ribonucleic acid; neurohypophysis CHRONIC CONSUMPTION of alcohol has been shown to significantly reduce the number of AVP-producing neurons in the rat supraoptic nucleus (19). More recently, chronic alcoholism in humans has also been shown to reduce AVP-producing neurons in a dose-related and time-dependent manner (13). Furthermore, AVP synthesis is reduced, as evidenced by reduced AVP mRNA in the hypothalamus of rats chronically administered alcohol, and there is a reduced AVP mRNA response to an osmotic stimulus in similarly treated rats (28). Correspondingly, chronic exposure to alcohol in humans has been reported to reduce plasma levels of AVP (7, 14) and cerebrospinal fluid levels of AVP (23). Thus the AVP system would appear to be impaired by chronic alcohol exposure in adult rats and humans.Previous work has also demonstrated that brain weight is reduced in adult rats that were prenatally exposed to ethanol during the second half of pregnancy (29), and other studies have demonstrated a dose dependence of alcohol-induced brain damage and that some brain structures are more sensitive to the damage than others (21). More specifically, Rojas-Castaneda et al. (26) have reported evidence of morphological changes in the AVP-producing cells of the suprachiasmatic nucleus of 15-dayold rats that were prenatally exposed to ethanol. However, the number of AVP-producing cells was not observed to be significantly reduced in similar studies by the same group (27).Last, there is evidence that AVP systems are nearly fully developed during gestation. AVP has bee...

AVP synthesis, storage, and osmotically stimulated release are reduced in young adult rats exposed prenatally to ethanol (PE). Whether the reduced release of AVP to the osmotic stimulus is due to impairment of the vasopressin system or specifically to an osmoreceptor-mediated release is not known. The present experiments were done, therefore, to determine whether a hemorrhage-induced AVP response would also be diminished in PE-exposed rats. Pregnant rats were fed either a control liquid diet [no prenatal ethanol (NPE)] or a liquid diet with 35% of the calories from ethanol from days 7-21 of pregnancy. Offspring were weaned at 3 wk of life. At 11 wk of age, femoral arterial catheters were surgically placed, and blood volumes were determined at 12 wk. Three days later, two hemorrhages of 10% of the blood volume were performed with samples taken before and 10 min after the hemorrhages. After a 20% blood loss, plasma AVP was 19% higher in NPE rats than in the PE rats despite no differences in mean arterial blood pressure (MABP). Also, hypothalamic AVP mRNA and pituitary AVP content were reduced in PE rats. Furthermore, confirming an earlier report of sex differences in AVP release, the hemorrhage-induced hormone response was twofold greater in female rats than male rats, regardless of previous ethanol exposure. These studies demonstrate that the AVP response to hemorrhage is reduced in PE rats independently of differences in MABP. The data are compatible with a theory of a reduced number of hemorrhage-responsive vasopressinergic neurons capable of stimulated AVP release in PE rats.

A 26-year-old female with a history of preterm labor and cerclage placement presented at 29 weeks gestation. Twin girls were delivered at 29 1 7 weeks. Twin A presented with clinical sepsis at birth. Twin A's blood cultures became positive for Actinomyces species on day of life 15. Despite aggressive medical management twin A died at 35 days of life.