Effects of magnesium sulphate on the noradrenaline‐induced cerebral vasoconstrictor and pressor responses in the goat

Objective To examine the ability of magnesium sulphate to counteract the noradrenaline‐induced cerebral vasoconstrictor and pressor responses in goats by using both in vivo and in vitro techniques. Design Cerebral blood flow was measured in vivo by means of an electromagnetic flow probe around the internal maxillary artery. Isometric tension was recorded in vitro from rings of goat middle cerebral artery maintained in an organ bath. Results 1. In vivo. Continuous infusion of noradrenaline (10 μg/min) directly into the cerebral arterial supply elicited sustained decrease in cerebral blood flow (61% [SEM 3] of control values) and increase in cerebral vascular resistance (178% [SEM 9] of control values). Magnesium sulphate, injected directly into the cerebral arterial supply (10–300 mg) or infused intravenously (0.3 g and 3 g during 15 min) at the noradrenaline‐induced steady state, increased cerebral blood flow by decreasing cerebral vascular resistance in a dose‐dependent manner. A similar result was obtained when intravenous magnesium sulphate (3 g/15 min) was tested against the cerebral vasoconstrictor and pressor responses induced by intravenous infusion of noradrenaline (30 ug/min). 2. In vitro. When compared with the response obtained in a control medium (1 mmol/L Mg2+), 10 mmol/L Mg2+significantly inhibited the maximum contraction elicited by noradrenaline (10−8 to 3 × 10−3 mol/L) from 45% [SEM 4] to 26% [SEM 4]. Conclusions Magnesium sulphate reverses the noradrenaline‐induced cerebral vasoconstrictor and pressor responses by a direct inhibitory action of Mg2+ on the actions of noradrenaline in the cerebral and peripheral vascular beds, which leads to a decrease in vascular resistance. These results could explain, at least in part, the beneficial effects of magnesium sulphate in the management of pre‐eclampsia and eclampsia.