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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.

Vasomotor effects of dimethyl sulfoxide on cat cerebral arteries in vitro and in vivo.