The cerebral endothelium during pregnancy: a potential role in the development of eclampsia.

The authors investigated the influence of pregnancy on cerebral endothelial cell permeability in response to an acute elevation in intravascular pressure that caused forced dilatation of myogenic tone. Third-order branches of the posterior cerebral artery (PCA) were dissected from nonpregnant (NP) and late-pregnant (LP, days 19 to 20) Sprague-Dawley rats and mounted on glass cannulas in an arteriograph chamber that allowed control over intravascular pressure and measurement of both diameter and permeability to fluorescent dextran (3000 Da). Permeability was determined at 75 mm Hg and after a step increase in pressure to 200 mm Hg. The extent of pinocytosis and transcellular transport in response to pressure was evaluated separately in the same groups of animals at 75 and 200 mm Hg using transmission electron microscopy. All arteries developed myogenic tone at 75 mm Hg that was lost when pressure was increased to 200 mm Hg to cause forced dilatation. The increased pressure caused a significant increase in permeability to dextran and enhanced pinocytosis in arteries from LP animals, but not in NP animals whose permeability remained constant at both pressures. These results suggest a pregnancy-specific effect on the cerebral endothelium that may promote enhanced vascular permeability during acute hypertension and may contribute to the edema formation and neurologic complications of eclampsia.