Stroke, Vol 23, 1154-1162, Copyright © 1992 by American Heart Association
M Debdi, J Seylaz and R Sercombe
BACKGROUND AND PURPOSE: Subarachnoid hemorrhage frequently leads to
long-term cerebral artery narrowing called vasospasm. Very early changes in
cerebral arteries have not been studied extensively and may be critical for
the later pathological developments. We therefore determined what changes
in the reactivity of cerebral arteries could be observed after 10 minutes'
or 24 hours' contact with subarachnoid blood. METHODS: Ten minutes or 24
hours after the injection of blood or physiological solution (sham
hemorrhage) into the cisterna magna of anesthetized rabbits or no injection
(control rabbits), segments of the middle cerebral, basilar, and vertebral
arteries were removed for conventional in vitro tension measurements.
Concentration-response curves to four endogenous constrictors likely to be
released after hemorrhage were obtained, and the maximum relaxation to
acetylcholine was determined. RESULTS: There were no significant
differences between the sham hemorrhage and control groups. Compared with
control rabbits, treated animals showed increased reactivity to uridine
triphosphate in the basilar and vertebral arteries at 10 minutes but not at
24 hours, whereas reactivity was increased in the middle cerebral artery
only at 24 hours. Reactivity to serotonin was greatly increased in all
arteries at both latencies (up to 2.7 times). Reactivity to noradrenaline
was unchanged in the basilar and vertebral arteries at 10 minutes;
reactivity in both the basilar and middle cerebral arteries was increased
at 24 hours, which is compatible with denervation supersensitivity. There
were only minor changes in the reactivity to histamine, and only at 10
minutes. Relaxation to acetylcholine was increased for the middle cerebral
artery at 10 minutes but otherwise was not significantly changed.
CONCLUSIONS: Reactivity to uridine triphosphate, serotonin, and
noradrenaline greatly increases by 10 minutes to 24 hours after
subarachnoid hemorrhage, and this increase is not owing to the mechanical
effects of intracranial hypertension, nor is it related to impaired
endothelium-dependent relaxation. It is suggested that these and other
spasmogens cause excessive muscular calcium loading with a very rapid onset
after subarachnoid hemorrhage.
ARTICLES
Early changes in rabbit cerebral artery reactivity after subarachnoid hemorrhage
Centre National de la Recherche Scientifique U.A. 641, Universite Paris VII, France.
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