The effects of long-term infusions of angiotensin II into the pregnant ewe on uterine blood flow and on the fetus.

Abstract

The effects of intravenous (i.v.) infusions of 62.5 microg/h of angiotensin II (Ang II) on maternal arterial pressure (MMAP), cardiac output (CO), and uteroplacental blood flow (UPF) were studied in 11 chronically catheterized pregnant ewes and their fetuses. Over the first 4 h of infusion, MMAP (p < 0.01) increased and CO decreased (p < 0.05). UPF and fetal PO2, PCO2, and pH were unchanged. After 16-24 h, MMAP increased further (p < 0.05-p < 0.005); UPF decreased (p < 0.05), and vascular resistance increased (p < 0.05). Fetal arterial PO2 decreased and PCO2 increased (p < 0.001; p < 0.05). There were correlations between fetal arterial PO2 and UPF (r = 0.6; p < 0.00005; n = 81), pH and UPF (r = 0.39; p < 0.0003; n = 81) and a negative correlation between PCO2 and UPF (r = -0.5; p < 0.00005; n = 81). Infusions of 33 microg/h of noradrenaline initially caused a decrease in UPF. In the longer term, UPF was unchanged, as was UVR. There were no changes in fetal blood gases or pH, but there was a correlation between fetal arterial PO2 and UPF (r = 0.48; p < 0.01; n = 27). The short-term effects of Ang II and noradrenaline on UPF and UVR are similar to effects reported previously. The finding that long-term infusions of Ang II caused a reduction in UPF and compromised fetal gas exchange was unexpected. Thus the protective effect of reduced vascular reactivity of the uteroplacental circulation to Ang II is only a transient phenomenon.