Toxemia was induced in 13 of 20 pregnant ewes by the stress of a change in environment and food deprivation late in pregnancy. Of the toxemic ewes, eight developed prominent neurological findings with convulsions, motor weakness, and
blindness, whereas five ewes developed
azotemia without neurological signs.
Proteinuria and
azotemia occurred in all but one of the toxemic animals. Seven animals did not develop clinical or laboratory evidence of
toxemia.
Hypertension did not occur with the onset of
toxemia but all toxemic animals showed glomerular changes by light and electron microscopy. These abnormalities, which were similar to those seen in human
preeclampsia, included endothelial cell swelling, focal reduplication of the basement membrane, and fusion of the epithelial cell foot processes. The
toxemia could not be attributed to changes in hematocrit, plasma
glucose, Na, Cl, CO(2), K, Ca,
fibrinogen, arterial pH,
lactate, or
pyruvate concentrations. Cardiac output fell only in ewes with prominent neurological signs. Plasma
renin rose strikingly in animals developing
toxemia, without change in substrate concentration. In contrast to human and other species, sheep uterus and amniotic fluid contained no detectable quantities of
renin. Thus in response to stress the pregnant ewe develops a
toxemia which in the absence of
hypertension has clinical and pathological similarities to human
preeclampsia.