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The effect of acute maternal hypoglycaemia on fetal cardiovascular control

The effect of acute maternal hypoglycaemia on fetal cardiovascular control
The effect of acute maternal hypoglycaemia on fetal cardiovascular control
Aims: To investigate the effect of acute maternal hypoglycaemia on fetal cardiovascular (CV) function, as a sub-optimal environment in utero has been implicated in the development of CV disease in adult life.
Subjects: Fetal sheep (n = 7) were studied in utero at 125 and 126 days gestational age (dGA, term = 147 days) following implantation of vascular catheters and an umbilical cord occluder at 119 dGA.
Study design: Fetal CV parameters were measured during a maternal saline (day 125) and insulin (day 125) infusion. Fetal CV function was assessed by: (a) generating a dose response curve to angiotensin II; (b) a 90 sec total umbilical cord occlusion; (c) administration of phenylephrine to assess baroreflex function.
Outcome measures: (a) Area under the mean arterial blood pressure (MAP) response (AUC) to increasing doses of angiotensin II; (b) MAP and heart rate (HR) response to cord occlusion; (c) sensitivity and operating point of the baroreflex response. Results: Maternal insulin infusion resulted in maternal and fetal hypoglycaemia. (a) The angiotensin II MAP AUC was not affected by hypoglycaemia. (b) The increase in MAP and decrease in HR following a 90 sec cord occlusion was not affected by hypoglycaemia. (c) Hypoglycaemia resulted in reduced fetal baroreflex sensitivity (P <0.05, paired t test).
Conclusions: Our finding of reduced fetal baroreflex sensitivity during fetal hypoglycaemia indicates altered CV homeostatic mechanisms. Such fetal adaptations to a poor intrauterine environment could contribute towards the development of altered cardiovascular phenotype in adult life.
cardiovascular, fetal, maternal
0378-3782
p.S88
Cleal, J.K.
18cfd2c1-bd86-4a13-b38f-c321af56da66
Hanson, M.A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Gardiner, H.M.
e4167ce0-dc23-4479-9bdf-6a51a2ee6f23
Green, L.R.
8a601974-efe5-4916-9268-9e7bc72d89c5
Cleal, J.K.
18cfd2c1-bd86-4a13-b38f-c321af56da66
Hanson, M.A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Gardiner, H.M.
e4167ce0-dc23-4479-9bdf-6a51a2ee6f23
Green, L.R.
8a601974-efe5-4916-9268-9e7bc72d89c5

Cleal, J.K., Hanson, M.A., Gardiner, H.M. and Green, L.R. (2007) The effect of acute maternal hypoglycaemia on fetal cardiovascular control. Early Human Development, 83 (supplement 1), p.S88. (doi:10.1016/S0378-3782(07)70191-3).

Record type: Meeting abstract

Abstract

Aims: To investigate the effect of acute maternal hypoglycaemia on fetal cardiovascular (CV) function, as a sub-optimal environment in utero has been implicated in the development of CV disease in adult life.
Subjects: Fetal sheep (n = 7) were studied in utero at 125 and 126 days gestational age (dGA, term = 147 days) following implantation of vascular catheters and an umbilical cord occluder at 119 dGA.
Study design: Fetal CV parameters were measured during a maternal saline (day 125) and insulin (day 125) infusion. Fetal CV function was assessed by: (a) generating a dose response curve to angiotensin II; (b) a 90 sec total umbilical cord occlusion; (c) administration of phenylephrine to assess baroreflex function.
Outcome measures: (a) Area under the mean arterial blood pressure (MAP) response (AUC) to increasing doses of angiotensin II; (b) MAP and heart rate (HR) response to cord occlusion; (c) sensitivity and operating point of the baroreflex response. Results: Maternal insulin infusion resulted in maternal and fetal hypoglycaemia. (a) The angiotensin II MAP AUC was not affected by hypoglycaemia. (b) The increase in MAP and decrease in HR following a 90 sec cord occlusion was not affected by hypoglycaemia. (c) Hypoglycaemia resulted in reduced fetal baroreflex sensitivity (P <0.05, paired t test).
Conclusions: Our finding of reduced fetal baroreflex sensitivity during fetal hypoglycaemia indicates altered CV homeostatic mechanisms. Such fetal adaptations to a poor intrauterine environment could contribute towards the development of altered cardiovascular phenotype in adult life.

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More information

Published date: September 2007
Additional Information: 5th International Congress on Developmental Origins of Health & Disease (Poster P1-21)
Keywords: cardiovascular, fetal, maternal

Identifiers

Local EPrints ID: 60998
URI: http://eprints.soton.ac.uk/id/eprint/60998
ISSN: 0378-3782
PURE UUID: e3d6f33c-662c-4423-bde0-b0df7238f34b
ORCID for J.K. Cleal: ORCID iD orcid.org/0000-0001-7978-4327
ORCID for M.A. Hanson: ORCID iD orcid.org/0000-0002-6907-613X
ORCID for L.R. Green: ORCID iD orcid.org/0000-0001-7423-9696

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Date deposited: 29 Sep 2008
Last modified: 16 Mar 2024 03:23

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Contributors

Author: J.K. Cleal ORCID iD
Author: M.A. Hanson ORCID iD
Author: H.M. Gardiner
Author: L.R. Green ORCID iD

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