Stroke, Vol 22, 922-927, Copyright © 1991 by American Heart Association
Z Ram, M Sadeh, I Shacked, A Sahar and M Hadani
We induced experimental delayed cerebral vasospasm by the intracisternal
injection of greater than 0.5 ml blood in 30 rats. Seventy-two hours later
the basilar artery was exposed via the transclival approach and
photographed at high-power magnification through an operating microscope.
We then evaluated the effect of topical (n = 30) and intravenous (n = 20)
magnesium sulfate on the spastic artery by computerized image analysis. A
greater than 50% reduction in baseline diameter of the basilar artery was
observed in the rats subjected to subarachnoid hemorrhage compared with the
10 controls (p less than 0.0001). Intravenous magnesium sulfate dilated the
spastic artery to approximately 75% of the baseline diameter in control
rats (p less than 0.0001). Topical magnesium sulfate caused dramatic
dilation of the basilar artery in both the control and the subarachnoid
hemorrhage groups to near 150% of the baseline diameter in the controls (p
less than 0.001). All rats receiving intravenous magnesium sulfate reached
therapeutic plasma levels of the ion. Hemodynamic effects were mild and
immediately reversible upon cessation of magnesium sulfate administration.
We suggest that magnesium has a role in the treatment of subarachnoid
hemorrhage-induced vasospasm in humans.
ARTICLES
Magnesium sulfate reverses experimental delayed cerebral vasospasm after subarachnoid hemorrhage in rats
Department of Neurosurgery, Chaim Sheba Medical Center, Sackler School of Medicine, Tel-Hashomer, Israel.
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