Document Detail


The late gestation fetal cardiovascular response to hypoglycaemia is modified by prior peri-implantation undernutrition in sheep.
MedLine Citation:
PMID:  19103677     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Undernourished late gestation fetuses display asymmetric growth restriction, suggestive of a redistribution of nutritional resources. The modification of fetal organ blood supply in response to acute hypoxia is well characterized, but it is not known whether similar responses occur in response to acute reductions in nutrition, or if such late gestation responses can be influenced by early gestation nutrition. In pregnant sheep, total nutrient requirements were restricted during the peri-implantation period (PI40, 40%; PI50, 50% of total, days 1-31) or in late gestation (L, 50% total, days 104-postmortem). Control animals were fed 100% nutrient requirements. Fetal organ blood flows were measured at baseline, and during acute fetal hypoglycaemia induced by maternal insulin infusion at 125 dGA. Baseline heart rate was increased in PI40 fetuses. During hypoglycaemia, an initial rise in fetal heart rate was followed by a slower fall. Fetal femoral artery blood flow decreased, and adrenal blood flow and femoral vascular resistance increased in all fetuses during hypoglycaemia. These changes were accompanied by increased fetal plasma adrenaline and cortisol, and reduced plasma insulin levels. The maximum femoral artery blood flow response to hypoglycaemia occurred earlier in PI50 and PI40 compared with control fetuses. The late gestation fetal cardiovascular response to acute hypoglycaemia was consistent with a redistribution of combined ventricular output away from the periphery and towards central organs. One element of the peripheral vascular response was modified by peri-implantation nutrient restriction, indicating that nutritional challenges early in gestation can have an enduring impact on cardiovascular control.
Authors:
Deborah M Burrage; Lucy Braddick; Jane K Cleal; Paula Costello; David E Noakes; Mark A Hanson; Lucy R Green
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-12-22
Journal Detail:
Title:  The Journal of physiology     Volume:  587     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2009 Feb 
Date Detail:
Created Date:  2009-02-02     Completed Date:  2009-05-06     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  611-24     Citation Subset:  IM    
Affiliation:
Institute of Developmental Sciences, Southampton General Hospital, Tremona Road, Southampton, UK.
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MeSH Terms
Descriptor/Qualifier:
Adrenocorticotropic Hormone / blood
Animals
Blood Gas Analysis
Blood Glucose / analysis
Cardiovascular System / embryology,  physiopathology*
Catecholamines / blood
Female
Fetal Nutrition Disorders / blood,  pathology,  physiopathology*
Fetal Weight
Fetus / physiopathology*
Gestational Age
Hemodynamics
Hydrocortisone / blood
Hypoglycemia / blood,  chemically induced,  embryology,  pathology,  physiopathology*
Hypoglycemic Agents / pharmacology
Insulin / blood,  pharmacology
Lactic Acid / blood
Pregnancy
Prenatal Nutritional Physiological Phenomena*
Sheep
Grant Support
ID/Acronym/Agency:
D17858//Biotechnology and Biological Sciences Research Council; //British Heart Foundation
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Catecholamines; 0/Hypoglycemic Agents; 0/Insulin; 50-21-5/Lactic Acid; 50-23-7/Hydrocortisone; 9002-60-2/Adrenocorticotropic Hormone
Comments/Corrections

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