Vascular smooth muscle oxygen consumption is reversibly stimulated by serafrom women with preeclampsia

OBJECTIVE: Preeclampsia is a complication of pregnancy that causes maternal vasoconstriction and hypertension. The disease may progress to eclampsia, which is thought to be related to cerebral vasospasm. Although there is evi dence for more than one circulating factor that causes endothelial cell dys function in preeclampsia, little work has focused on the possibility that v ascular smooth muscle function might be directly stimulated by a circulatin g factor. The aim of this study was to determine whether such a factor or f actors could be detected by the vessels. STUDY DESIGN: Excessive vascular smooth muscle oxygen consumption was used as a screen for metabolic stimulation because pathologic arterial constrict ion would require oxidative metabolism to generate adenosine triphosphate. De-endothelialized porcine carotid artery (a well-validated model of human arterial contractile function) was exposed to sera from patients with preec lampsia (1:30 dilution) in a sealed chamber with an oxygen electrode, and t he rate of oxygen consumption by the tissue was measured. Comparisons with the effects of sera from matched normal pregnant patients and from nonpregn ant women were made. RESULTS: Exposure of vascular smooth muscle to sera from women with preecla mpsia for 90 minutes resulted in greater oxygen consumption by the tissue ( 0.66 +/- 0.16 mu mol O-2/min per gram of dry weight) than did exposure to s era of matched pregnant and nonpregnant control subjects (0.34 +/- 0.08 mu mol O-2/min per gram of dry weight, P <.001, and 0.29 +/- 0.03 mu mol O-2/m in per gram of dry weight, P <.001, respectively). This stimulation was com pletely reversed by rinsing. CONCLUSIONS: There is a factor in the circulation of women with preeclampsi a that has the reversible effect an vascular smooth muscle at accelerating oxygen consumption. We discuss the implications of this observation in term s of known aspects of vascular smooth muscle contractile function.