The late gestation fetal cardiovascular response to hypoglycaemia is modified by prior peri-implantation undernutrition in sheep.
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.
Burrage
Deborah M
DM
Institute of Developmental Sciences, Southampton General Hospital, Tremona Road, Southampton, UK.
Braddick
Lucy
L
Cleal
Jane K
JK
Costello
Paula
P
Noakes
David E
DE
Hanson
Mark A
MA
Green
Lucy R
LR
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D001784:Blood Gas Analysis; D001786:Blood Glucose / Q000032:analysis; D002319:Cardiovascular System / Q000196:embryology / Q000503:physiopathology*; D002395:Catecholamines / Q000097:blood; D005260:Female; D048070:Fetal Nutrition Disorders / Q000097:blood / Q000473:pathology / Q000503:physiopathology*; D020567:Fetal Weight; D005333:Fetus / Q000503:physiopathology*; D005865:Gestational Age; D006439:Hemodynamics; D006854:Hydrocortisone / Q000097:blood; D007003:Hypoglycemia / Q000097:blood / Q000139:chemically induced / Q000196:embryology / Q000473:pathology / Q000503:physiopathology*; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007328:Insulin / Q000097:blood / Q000494:pharmacology; D019344:Lactic Acid / Q000097:blood; D011247:Pregnancy; D039401:Prenatal Nutritional Physiological Phenomena; D012756:Sheep
D001786:Blood Glucose; D002395:Catecholamines; D007004:Hypoglycemic Agents; D007328:Insulin; D019344:Lactic Acid; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone