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Am J Physiol Regul Integr Comp Physiol. 2001 Apr;280(4):R1045-51.

Nonimmune hydrops fetalis and activation of the renin-angiotensin system after asphyxia in preterm fetal sheep.

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  • 1School of Physiology and Pharmacology, The University of New South Wales, Sydney, New South Wales 2052, Australia. E.Lumbers@unsw.edu.au

Abstract

This study examined the hypothesis that the development of hydrops fetalis after asphyxia in the 0.6 gestation sheep fetus would be associated with activation of the fetal renin-angiotensin system (RAS). Fetuses were randomly assigned to either sham occlusion (n = 7) or to 30 min of asphyxia induced by complete umbilical cord occlusion for 30 min (n = 8). Asphyxia led to severe bradycardia and hypotension that resolved after release of occlusion. After occlusion, plasma renin concentration was significantly increased in the asphyxia group compared with controls (P < 0.005) after 3 min (16.3 +/- 5.3 vs. 4.1 +/- 1.3 ng. ml(-1). h(-1)), and 72 h (30.6 +/- 6.3 vs. 3.7 +/- 1.2 ng. ml(-1). h(-1)). Renal renin concentrations and mRNA levels were significantly greater in the asphyxia group after 72 h of recovery. All fetuses in the asphyxia group showed generalized tissue edema, ascites, and pleural effusions after 72 h of recovery. In conclusion, asphyxia in the preterm fetus caused sustained activation of the RAS, which was associated with hydrops fetalis.

PMID:
11247826
[PubMed - indexed for MEDLINE]
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