Dimethyl sulfoxide effects on platelet aggregation and vascular reactivity in pial microcirculation

DMSO is a hydroxyl radical scavenger that inhibits platelet aggregation in vivo in injured microvessels, and that also inhibits the dilation displayed by pial arterioles following a local injury. The injurious stimulus is a result of local excitation of circulating sodium fluorescein by an appropriate light source. It is likely that this excitation results in the generation of hydroxyl radicals, which are the immediately injurious agent. This postulate is supported not only by the inhibitory effect of DMSO but also by the inhibitory effect of glycerol, another hydroxyl scavenger. Both the hypothesis that DMSO inhibits hydroxyl-mediated dilation, and the hypothesis that free radicals can dilate pial arterioles, are further supported by direct evidence from studies employing local application of xanthine oxidase plus acetaldehyde. This well established radical-generating system dilated pial arterioles. The dilation was inhibited by the local application of superoxide dismutase and also by local application of catalase, as well as by intraperitoneal administration of DMSO. Since DMSO failed to inhibit the dilation produced by increases of inspired CO2, we believe that the inhibitory effect of DMSO on the other dilating stimuli in these studies was due to the hydroxyl scavenging properties of this drug, rather than to other nonspecific effects.