Kupferminc M J, Mullen T A, Russell T L, Silver R K
Department of Obstetrics and Gynecology, Northwestern University Medical School, Evanston, Illinois 60201, USA.
J Soc Gynecol Investig. 1996 Mar-Apr;3(2):89-92. doi: 10.1016/1071-5576(95)00052-6.
We evaluated the hypothesis that circulating factors in preeclampsia promote direct endothelial cell injury using an in vitro index of cytotoxicity.
Subconfluent umbilical vein endothelial cell monolayers were established and radiolabeled with chromium (51Cr), then randomly exposed for 24 hours in triplicate to 20% sera from nonlaboring patients with severe preeclampsia (n = 5) or mild preeclampsia and normotensive controls (n = 5). Additional experiments were performed by exposing endothelial monolayers to sera for 3 and 48 hours, and under hypoxic conditions (1% oxygen). Cytotoxicity was defined by the percentage of 51Cr release, expressed as the ratio of radioactivity in the supernatant to the maximum cell-associated radioactivity.
Mean 51Cr release was similar in all experiments comparing preeclamptic and normal sera. Although consistently greater 51Cr release was noted in hypoxic as compared with normoxic incubations, no differences in cytotoxicity were identified among severe preeclampsia, mild preeclampsia, and normal sera in hypoxia.
Sera from patients with preeclampsia do not appear to be cytotoxic to vascular endothelium in this in vitro model.
