Received August 15, 2007
Revised September 24, 2007
Accepted after revision October 2, 2007

¹ University of Vermont

^* To whom correspondence should be addressed. E-mail: marilyn.cipolla{at}uvm.edu.

	Abstract

Eclampsia is associated with increased blood-brain barrier (BBB) permeability and cerebral oedema formation. Magnesium sulphate is used to treat eclampsia despite an unclear mechanism of action. This study was to determine the effect of magnesium sulphate on in vivo BBB permeability and cerebral oedema formation during acute hypertension and on brain aquaporin-4 (AQP4) protein expression. An in vivo model of hypertensive encephalopathy was used in late-pregnant (LP) rats following magnesium treatment, 270 mg/kg I.P. injection every 4 hours for 24 hours. BBB permeability was determined by in situ brain perfusion of Evan's blue (EB) and sodium fluorescein (NaFl), and dye clearance determined by fluorescence spectrophotometry. Cerebral oedema was determined following acute hypertension by measuring brain water content. The effect of magnesium treatment on AQP4 expression was determined by Western blot. Acute hypertension with autoregulatory breakthrough increased BBB permeability to EB in both brain regions studied (P<0.05). Magnesium attenuated BBB permeability to EB during acute hypertension by 41% in the posterior cerebrum (P<0.05), but had no effect in the anterior cerebrum (P>0.05.). Magnesium treatment did not change NaFl permeability, cerebral oedema formation, or AQP4 expression. In summary, BBB permeability to Evan's blue was increased by acute hypertension in LP rats that was attenuated by treatment with magnesium sulphate. The greatest effect on BBB permeability to EB was in the posterior cerebrum, an area particularly susceptible to oedema formation during eclampsia.

Key Words: Blood-brain barrier, Hypertension, Pregnancy