Ketamine modulates fetal hemodynamic and endocrine responses to umbilical cord occlusion

Umbilical cord occlusion (UCO) is a hypoxic insult that has been used to model birth asphyxia and umbilical cord compression in utero. UCO triggers vigorous neural and endocrine responses that include increased plasma ACTH and cortisol concentrations, increased blood pressure (BP), and decreased hea...

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Main Authors:	Zarate, Miguel A., Chang, Eileen I., Antolic, Andrew, Wood, Charles E.
Format:	Online
Language:	English
Published:	John Wiley and Sons Inc. 2016
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5027363/

id	pubmed-5027363
recordtype	oai_dc
spelling	pubmed-50273632017-03-07 Ketamine modulates fetal hemodynamic and endocrine responses to umbilical cord occlusion Zarate, Miguel A. Chang, Eileen I. Antolic, Andrew Wood, Charles E. Original Research Umbilical cord occlusion (UCO) is a hypoxic insult that has been used to model birth asphyxia and umbilical cord compression in utero. UCO triggers vigorous neural and endocrine responses that include increased plasma ACTH and cortisol concentrations, increased blood pressure (BP), and decreased heart rate (HR). We have previously reported that ketamine, a noncompetitive N‐methyl‐D‐aspartate receptor antagonist, can modify the fetal hemodynamic and ACTH responses to ventilatory hypoxia and cerebral ischemia‐reperfusion. We performed the present experiments to test the hypothesis that ketamine has similar effects on the neuroendocrine and cardiovascular responses to UCO. Fetal sheep were chronically catheterized at gestational day 125. Ketamine (3 mg/kg) was administered intravenously to the fetus 10 min prior to the insult. UCO was induced for 30 min by reducing the umbilical vein blood flow until fetal PaO2 levels were reduced from 17 ± 1 to 11 ± 1 mm Hg. UCO produced an initial increase on fetal BP in both control and ketamine groups (P = 0.018 time), followed by a decrease in the control group, but values remained higher with ketamine. HR decreased after UCO (P = 0.041 stimulustime) in both groups, but the reduction was greater initially in control compared to ketamine groups. Fetal Pa CO 2 levels increased after UCO (P < 0.01 stimulustime), but values were higher in the control versus ketamine groups. UCO significantly decreased fetal pH values (P < 0.01 stimulustime) with a greater effect on the control versus ketamine group. Ketamine delayed the cortisol responses to UCO (P < 0.001 stimulustime), and UCO produced a robust increase in ACTH levels from 19 ± 2 to 280 ± 27 pg/mL (P < 0.001 stimulus*time), but there were no differences in ACTH levels between UCO groups. We conclude that ketamine augmented the cardiovascular response to UCO, but did not alter the ACTH response to UCO. John Wiley and Sons Inc. 2016-09-05 /pmc/articles/PMC5027363/ /pubmed/27597770 http://dx.doi.org/10.14814/phy2.12962 Text en © 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Zarate, Miguel A. Chang, Eileen I. Antolic, Andrew Wood, Charles E.
spellingShingle	Zarate, Miguel A. Chang, Eileen I. Antolic, Andrew Wood, Charles E. Ketamine modulates fetal hemodynamic and endocrine responses to umbilical cord occlusion
author_facet	Zarate, Miguel A. Chang, Eileen I. Antolic, Andrew Wood, Charles E.
author_sort	Zarate, Miguel A.
title	Ketamine modulates fetal hemodynamic and endocrine responses to umbilical cord occlusion
title_short	Ketamine modulates fetal hemodynamic and endocrine responses to umbilical cord occlusion
title_full	Ketamine modulates fetal hemodynamic and endocrine responses to umbilical cord occlusion
title_fullStr	Ketamine modulates fetal hemodynamic and endocrine responses to umbilical cord occlusion
title_full_unstemmed	Ketamine modulates fetal hemodynamic and endocrine responses to umbilical cord occlusion
title_sort	ketamine modulates fetal hemodynamic and endocrine responses to umbilical cord occlusion
description	Umbilical cord occlusion (UCO) is a hypoxic insult that has been used to model birth asphyxia and umbilical cord compression in utero. UCO triggers vigorous neural and endocrine responses that include increased plasma ACTH and cortisol concentrations, increased blood pressure (BP), and decreased heart rate (HR). We have previously reported that ketamine, a noncompetitive N‐methyl‐D‐aspartate receptor antagonist, can modify the fetal hemodynamic and ACTH responses to ventilatory hypoxia and cerebral ischemia‐reperfusion. We performed the present experiments to test the hypothesis that ketamine has similar effects on the neuroendocrine and cardiovascular responses to UCO. Fetal sheep were chronically catheterized at gestational day 125. Ketamine (3 mg/kg) was administered intravenously to the fetus 10 min prior to the insult. UCO was induced for 30 min by reducing the umbilical vein blood flow until fetal PaO2 levels were reduced from 17 ± 1 to 11 ± 1 mm Hg. UCO produced an initial increase on fetal BP in both control and ketamine groups (P = 0.018 time), followed by a decrease in the control group, but values remained higher with ketamine. HR decreased after UCO (P = 0.041 stimulustime) in both groups, but the reduction was greater initially in control compared to ketamine groups. Fetal Pa CO 2 levels increased after UCO (P < 0.01 stimulustime), but values were higher in the control versus ketamine groups. UCO significantly decreased fetal pH values (P < 0.01 stimulustime) with a greater effect on the control versus ketamine group. Ketamine delayed the cortisol responses to UCO (P < 0.001 stimulustime), and UCO produced a robust increase in ACTH levels from 19 ± 2 to 280 ± 27 pg/mL (P < 0.001 stimulus*time), but there were no differences in ACTH levels between UCO groups. We conclude that ketamine augmented the cardiovascular response to UCO, but did not alter the ACTH response to UCO.
publisher	John Wiley and Sons Inc.
publishDate	2016
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5027363/
_version_	1613654492313550848

Ketamine modulates fetal hemodynamic and endocrine responses to umbilical cord occlusion

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