Our objective is to establish the role of glutamine (GLN) nutrition during stressed pregnancies. We hypothesize that dietary GLN deprivation in pregnant rats treated with the endotoxin lipopolysaccharide (LPS) results in higher maternal morbidity and fetal mortality. Sprague-Dawley rats were treated with 3 doses of LPS (either 0.5 or 1.0 mg/kg, intraperitoneally) on days 17 through 19 of pregnancy and dams were sacrificed on day 20 of pregnancy. The control group (GLN+) received a diet containing 4% GLN by weight while the treatment group (GLN-) received an isonitrogenous, isocaloric diet without glutamine. To determine whether GLN- dams compensate for the lack of dietary GLN by increasing endogenous synthesis of GLN, we measured glutamine synthetase (GS) activities in the liver, lung, placenta, and kidney. Weights of each of these organs were also recorded. Results: Fetuses from 6 GLN- dams had significantly more dead pups (37 of 73) than those from 7 GLN+ dams (21 of 65; p < 0.05, Chi-square analysis). GLN- dams tended to gain less weight prior to the beginning of LPS treatment and tended to lose more weight as a result of treatment with LPS. There were no differences in the weights of the liver, placenta, and kidney; however lungs from GLN- dams were heavier than lungs from GLN+ dams (1.69g ± 0.13g vs. 1.52 ± 0.15g, p < 0.05). This suggests that dietary GLN can ameliorate pulmonary edema known to be induced by LPS. There were no differences in organ-specific GS activities between the treatment groups, suggesting that there were no compensatory responses by GS during LPS stress. These data demonstrate the importance of GLN nutrition for fetal survival as well as maternal health and suggest that glutamine may be a conditionally essential nutrient during stressed pregnancy.