1984
DOI: 10.1159/000123933
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Effects of Hypoxia on Vasopressin Concentrations in Cerebrospinal Fluid and Plasma of Sheep

Abstract: The relationship between concentrations of vasopressin in plasma and cerebrospinal fluid (CSF) was examined under basal and hypoxic conditions in unanesthetized and unrestrained adult female sheep. Under basal conditions mean (± SE) concentration of vasopressin (4.1 ± 0.3 pg/ml) in CSF was significantly (p< 0.001) higher than the concentration in arterial plasma (2.4 + 0.2 pg/ml). There was a significant positive correlation between CSF and plasma vasopressin concentrations (r = 0.66, p < 0.01). The introducti… Show more

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Cited by 19 publications
(5 citation statements)
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“…These sites include noncardiac vagal afferents as well as central nervous system receptors. [36][37][38][39][40][41][42][43] The rise of AVP in the presence of combined sinoaortic and cardiac denervation occurred in the presence of marked hypotension, which could have induced cerebral ischemia with concomitant AVP release.36'4042-44 In addition, a recent study by Wood et a145 demonstrated that in fetal sheep AVP responses to hemorrhage were related to changes in arterial pH, also suggesting that AVP release could be mediated by chemoreceptors. In that study, there were also no differences in the AVP responses to hemorrhage in the intact and vagotomized sheep.45 Furthermore, it has been proposed that nicotinic synapses in the central nervous system have an important role in mediating AVP release in response to hypotension.46,47 Because these pathways can be inhibited by ganglionic blockade,46,47 we examined a subset of intact dogs with ganglionic blockade in response to hemorrhage.…”
Section: Discussionmentioning
confidence: 99%
“…These sites include noncardiac vagal afferents as well as central nervous system receptors. [36][37][38][39][40][41][42][43] The rise of AVP in the presence of combined sinoaortic and cardiac denervation occurred in the presence of marked hypotension, which could have induced cerebral ischemia with concomitant AVP release.36'4042-44 In addition, a recent study by Wood et a145 demonstrated that in fetal sheep AVP responses to hemorrhage were related to changes in arterial pH, also suggesting that AVP release could be mediated by chemoreceptors. In that study, there were also no differences in the AVP responses to hemorrhage in the intact and vagotomized sheep.45 Furthermore, it has been proposed that nicotinic synapses in the central nervous system have an important role in mediating AVP release in response to hypotension.46,47 Because these pathways can be inhibited by ganglionic blockade,46,47 we examined a subset of intact dogs with ganglionic blockade in response to hemorrhage.…”
Section: Discussionmentioning
confidence: 99%
“…occurs in measurable amounts in the cerebrospinal fluid (CSF) of several species. A rise in the osmolality of the extracellular fluid [7,24], severe hemorrhage [25], and hy poxia [23] cause AVP levels to increase in both the systemic circulation and in the CSF. A prominent diurnal rhythm has been demonstrated for AVP in the CSF of cats and monkeys 118, 19], rats [17,21], and recently in that of rabbits [12].…”
mentioning
confidence: 99%
“…These stimuli include hypoxia, hemorrhage, shock, emesis, and intracranial hypertension. 7 -11 -34 - 37 Our results imply that these plasma levels of vasopressin have marked effects on blood flow to the choroid plexus.…”
Section: Functional Implicationsmentioning
confidence: 68%