Stroke, Vol 17, 483-487, Copyright © 1986 by American Heart Association
LH Pitts, AR Young, J McCulloch and E MacKenzie
We studied the direct vascular effects of dimethyl sulfoxide (DMSO) in
isolated middle cerebral arteries and on pial arteriolar caliber after
subarachnoid perivascular microinjection in chloralose-anesthetized cats,
and on brain retraction in cats given DMSO intravenously. DMSO did not
constrict isolated cerebral arteries at any of the concentrations studied
(10(-10) to 4 X 10(-1) M). In middle cerebral arteries precontracted with
potassium, 5-hydroxytryptamine, prostaglandin F2 alpha, or with
mechanically raised tone, DMSO at concentrations of 10(-10) to 10(-2) M had
no significant effects; at concentrations greater than 10(-2) M, DMSO
consistently relaxed the arteries, probably because of the hyperosmolarity
of the bathing solution. Microapplication of DMSO (10(-6) to 10(-2) M)
around pial arterioles on the cortical surface did not change arteriolar
caliber significantly. Higher concentrations of DMSO (1%) increased
arteriolar caliber by 56 +/- 4% (p less than 0.001), probably as a
consequence of solution hypertonicity. DMSO did not modify in vivo
cerebrovascular responses to alterations in perivascular potassium ion
concentrations. Intravenous administration of DMSO did cause obvious brain
shrinkage. These data provide no support for the view that direct cerebral
vascular effects play a major role in the clinical efficacy of DMSO, but
are consistent with the hypothesis that DMSO's ability to lower
intracranial pressure derives from its osmotic effect on cerebral issue.
ARTICLES
Vasomotor effects of dimethyl sulfoxide on cat cerebral arteries in vitro and in vivo
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