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 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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