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Abstract
Objective: Among the pathogenetic factors of pregnancy-induced hypertension (PIH), oxidative damage seems to play a pivotal role. The aim of this study is to investigate if the oxidative status in patients with PIH could induce the altered platelet reactivity responsible for the abnormal uteroplacental microcirculation.
Methods: Twenty pregnant women with PIH were admitted to our study. The presence of a mild hypertensive disorder was defined on the basis of blood pressure, proteinuria, and serum uric acid levels. Fifteen normotensive pregnant women and 15 nonpregnant women represented the control groups. The serum lipemic profile, including apoproteins, was measured to confirm that all subjects were normolipemic and, consequently, to avoid the influence of these parameters on platelet reactivity. Malondialdehyde (MDA), as an index of lipid peroxidation and cyclooxygenase pathway activation, was determined in plasma and in unstimulated and thrombin-stimulated platelets. Measurements of platelet membrane microviscosity were performed by means of fluorescence polarization, to determine the extent and rate of platelet reactivity.
Main Outcome Measures: MDA concentration in plasma and platelet membrane microviscosity served as predetermined measures of lipid peroxidation and enhanced platelet reactivity.
Results: Plasma MDA values were significantly higher in hypertensive pregnant patients than in nonhypertensive pregnant and nonpregnant women. A reduced fluidity of the platelet membrane and a reduced activity of the in vitro cyclooxygenase pathway were also evident.
Conclusions: The trend toward an oxidative status in hypertensive pregnant women, confirmed by the significant elevation in plasma MDA values, could be responsible for the lower platelet membrane fluidity in these patients, which may explain the enhanced in vivo platelet reactivity.