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

This study examined the hypothesis that the development of hydrops fetalis after asphyxia in the 0.6 gestation sheep fetus would be associated with ac tivation 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 s evere 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 signi ficantly 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 f etus caused sustained activation of the RAS, which was associated with hydr ops fetalis.