title: Prevention of the normal expansion of maternal plasma volume: a model for chronic fetal hypoxaemia.
abstract: The effects of inadequate expansion of maternal blood volume on uterine blood flow, fetal oxygen levels and vasoactive mediators during the third trimester were studied in 8 pregnant sheep. Results were compared to those obtained during 15 normal pregnancies. Prevention of the normal (20 ml/day) increase in maternal plasma volume was achieved by repeated haemorrhage and injections of furosemide. These treatments also reduced the rise in blood flow to the pregnant uterine horn that normally occurs during this period of gestation: at term flow was only 508 +/- 61 (SEM) compared to 838 +/- 83 ml/min in the control group (P greater than 0.01). This reduction in uterine blood flow caused a gradual fall in fetal PaO2, and rise in fetal levels of plasma renin activity, vasopressin, catecholamines and angiotensin II without change in pHa or base excess. Four to 5 days prior to delivery, the difference from control in PaO2 was -3.9 +/- 0.5 mmHg, plasma renin activity +2.9 +/- 1.7 ng/ml.h, vasopressin +4.2 +/- 1.1 pg/ml, catecholamines +957 +/- 145.3 pg/ml and angiotensin II +243 +/- 108.2 pg/ml. Furthermore, the fall in PaO2 and rise in vasoactive mediators that normally occur 3-5 days prior to the onset of labour was either absent (PaO2 and plasma renin activity) or blunted. Thus when expansion of blood volume during pregnancy is inadequate, blood flow to the uterus is adversely affected. This leads to various degrees of chronic fetal hypoxaemia and stimulation of vasoactive mediator systems. However, the normal stimulation of vasoactive mediator systems that occurs 3-5 days before delivery appears to be blunted. Experimental prevention of blood volume expansion during pregnancy produces an excellent model for the study of chronic mild fetal hypoxaemia.
authors.affiliation: Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.
authors.forename: S S
authors.initials: SS
authors.lastname: Daniel
authors.forename: S
authors.initials: S
authors.lastname: James
authors.forename: R I
authors.initials: RI
authors.lastname: Stark
authors.forename: P J
authors.initials: PJ
authors.lastname: Tropper
mesh_terms: D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001794:Blood Pressure; D001815:Bloodletting; D002395:Catecholamines / Q000097:blood; D004195:Disease Models, Animal; D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D005311:Fetal Hypoxia / Q000209:etiology* / Q000503:physiopathology; D005665:Furosemide / Q000494:pharmacology; D006340:Heart Rate, Fetal; D006863:Hydrogen-Ion Concentration; D010100:Oxygen / Q000097:blood; D010953:Plasma Volume / Q000187:drug effects / Q000502:physiology*; D011247:Pregnancy; D012039:Regional Blood Flow; D012083:Renin / Q000097:blood; D012756:Sheep; D014599:Uterus / Q000098:blood supply; D014667:Vasopressins / Q000097:blood
chemical_list: D002395:Catecholamines; D014667:Vasopressins; D000804:Angiotensin II; D005665:Furosemide; D012083:Renin; D010100:Oxygen