Premium
Effects of magnesium sulphate on the noradrenaline‐induced cerebral vasoconstrictor and pressor responses in the goat
Author(s) -
Perales Alfredo J.,
Torregrosa German,
Salom Juan B.,
Barbera Maria D.,
Jover Teresa,
Alborch Enrique
Publication year - 1997
Publication title -
bjog: an international journal of obstetrics and gynaecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.157
H-Index - 164
eISSN - 1471-0528
pISSN - 1470-0328
DOI - 10.1111/j.1471-0528.1997.tb14348.x
Subject(s) - in vivo , isometric exercise , cerebral blood flow , cerebral arteries , cerebral circulation , vascular resistance , magnesium , norepinephrine , medicine , chemistry , endocrinology , hemodynamics , anesthesia , biology , dopamine , microbiology and biotechnology , organic chemistry
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 Mg 2+ ), 10 mmol/L Mg 2+ 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 Mg 2+ 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.