AJP - Regulatory, Integrative and Comparative Physiology, Vol 257, Issue 4 705-R710, Copyright © 1989 by American Physiological Society

ARTICLES

Effect of beta-adrenergic blockade on lung liquid secretion during fetal asphyxia

S. B. Hooper and R. Harding
Department of Physiology, Monash University, Melbourne, Victoria, Australia.

The hypothesis tested in this study was that beta-adrenergic stimulation is responsible for the inhibition of fetal lung liquid production during moderate fetal asphyxia. In chronically catheterized fetal sheep, net lung liquid production rates were measured over three consecutive periods: a control period, a period of reduced uterine blood flow (RUBF) or epinephrine infusion, and periods of RUBF or epinephrine infusion in the presence of the beta-adrenergic receptor antagonist propranolol. The net production rate of fetal lung liquid was decreased from a mean control value of 7.7 +/- 1.0 to 1.5 +/- 0.4 ml/h (P less than 0.001) by RUBF; the administration of propranolol had no further effect on these liquid production rates (1.1 +/- 0.5 ml/h). In other experiments epinephrine infusion reduced the net production rate of fetal lung liquid from a mean control value of 7.2 +/- 1.4 to 1.7 +/- 1.8 ml/h (P less than 0.025); the addition of propranolol reversed this inhibition (secretion rate 6.1 +/- 1.4 ml/h, P less than 0.005). We conclude that the inhibition of fetal lung liquid production induced by moderate fetal asphyxia does not solely result from catecholamine stimulation of pulmonary beta-receptors.

This article has been cited by other articles:

				A. Lines, S. B. Hooper, and R. Harding Lung liquid production rates and volumes do not decrease before labor in healthy fetal sheep J Appl Physiol, March 1, 1997; 82(3): 927 - 932. [Abstract] [Full Text] [PDF]