AJP - Heart and Circulatory Physiology, Vol 258, Issue 4 1159-H1163, Copyright © 1990 by American Physiological Society
Atrial tachycardia causes hydrops in fetal lambs
A. L. Gest, T. N. Hansen, A. A. Moise and C. J. Hartley
Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030.
The purpose of this project was to study mechanisms responsible for edema
formation in fetuses with hydrops. We produced hydrops fetalis in 28 fetal
sheep [gestational age of 125 +/- 5 days (mean +/- SD)] by pacing their
atria at 300-320 beats/min for 68 +/- 40 (SD) h. All fetuses developed
peripheral edema and ascites [volume of ascitic fluid was 134 +/- 75 (SD)
ml; total protein concentration was 3.10 +/- 0.6 (SD) g/dl, and total
albumin concentration was 1.68 +/- 0.3 (SD) g/dl]. Pacing did not affect
aortic pressure but increased venous pressure from 4 +/- 1 to 8 +/- 1 (SE)
Torr. Pacing did not affect pH, arterial partial pressure of O2 (PaO2), or
Na+ but increased PaCO2 from 53 +/- 1 to 55 +/- 1 (SE) Torr and K+ from 3.9
+/- 0.1 to 4.3 +/- 0.1 (SE) meq/l. Hematocrit increased from 29 +/- 1 to 32
+/- 1 (SE)% acutely with pacing but returned to base line by the last day
of the experiment. Plasma protein concentration decreased slightly from 3.7
+/- 0.1 to 3.5 +/- 0.1 (SE) g/dl by the last day of the experiment; plasma
albumin concentration did not change. Plasma volume decreased acutely from
271 +/- 19 to 238 +/- 16 (SE) ml and then remained decreased throughout the
experiment. Red blood cell mass and the turnover time for albumin were not
affected by pacing. We found no consistent relationship between edema
formation and changes in arterial blood gas tensions, plasma protein
concentrations, or the turnover time for albumin.2
