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Showing papers by "Mary E. Wlodek published in 1989"


Journal ArticleDOI
TL;DR: Monitoring in unanesthetized fetal sheep in utero during the last third of gestation shows that most spontaneous voids in the fetus begin during LV ECoG, suggesting that voiding is regulated by descending information from the brain.
Abstract: Fetal bladder contractions, indicative of micturition (voiding), and behavioral states were monitored in unanesthetized fetal sheep in utero during the last third of gestation. Fetal voids began during low-voltage electrocortical activity (LV ECoG) at a greater frequency (91.4 +/- 1.0%) than expected (57.2%) and began during high-voltage electrocortical activity (HV ECoG) with a lower frequency (8.7 +/- 1.0%) than expected (42.8%). Fetal voids began significantly sooner after the onset of LV ECoG (5.84 +/- 0.13 min) than after the onset of HV ECoG (10.88 +/- 0.04 min). Electroocular and nuchal muscle activities were associated with 96.2 and 66.0% of the voids, respectively, but there was no significant association between fetal voiding and swallowing episodes. Abolition of spontaneous voiding, by urine drainage (24 h), caused no significant differences, relative to a 24-h control period, in the duration or number of episodes of LV or HV ECoG or percentage of time spent in these states. Also, induction of voiding by infusing saline into the bladder did not significantly alter the time to the next change of ECoG state. However, the mean time to the next void and the mean volume of saline infused into the bladder to induce voiding tended to be less during LV ECoG than HV ECoG, although not significantly less. Our data show that most spontaneous voids in the fetus begin during LV ECoG, suggesting that voiding is regulated by descending information from the brain. Furthermore, these experiments demonstrate that fetal bladder contractions and voiding, either spontaneous or induced, do not influence the normal cycling of fetal ECoG states.

18 citations


Journal Article
TL;DR: The data suggested that the increase in GFR and urine output measured during the third hour of hypoxia and the recovery period may reflect a pressure diuresis.
Abstract: In order to determine the effects of fetal hypoxemia on renal blood flow, glomerular filtration rate (GFR) and urethral and urachal urine output, we examined the effects of 3 h maternally-induced (9% O2, 3% CO2, 88% N2) fetal hypoxaemia on 10 chronically-instrumented fetal sheep between 127-135 days of gestation. Fetal arterial pH fell significantly during the second and third hours of hypoxia and this coincided with a significant increase in fetal arterial blood pressure (P less than 0.05). During the second hour of hypoxia, with mild acidaemia, fetal GFR decreased significantly and then, during the third hour, fetal GFR, urethral and total urine output were significantly elevated. During the 2-h recovery period urachal and total, but not urethral urine output, were significantly elevated (P less than 0.05). The data suggested that the increase in GFR and urine output measured during the third hour of hypoxia and the recovery period may reflect a pressure diuresis.

7 citations