EFFECT OF MODERATE ENDOTHELIAL DAMAGE ON THE INVIVO REACTIVITY OF PIAL-ARTERIES TO NOREPINEPHRINE AND SEROTONIN

Most of the information on the role of the endothelium for the vascular reactivity comes from in vitro experiments on noncerebral vessels. Few studies address the contribution of the endothelium to the cerebrovascular reactions in vivo. In the present study, arterial cerebral air embolism was employed to induce endothelial damage in anesthetized cats. The endothelial injury was verified by scanning electron microscopy: air embolism induced obvious damage to the endothelial layer, consisting of flattening, superficial peeling and/or fissures within and between endothelial cells. Cell debris and small platelet and erythrocyte aggregations were also observed. The present study concerns the effect of endothelial damage on the reactivity to the vasoconstrictor substances serotonin (10(-10)-10(-4) M) and norepinephrine (10(-9)-10(-3) M) in vivo. The reactions of the same pial arteries to these substances were tested using the microapplication method before and after air embolism. In contrast to the abolition of the vasodilatation to carbachol found in a previous study, the constriction of pial arteries to serotonin and norepinephrine was preserved after air embolism, although it was diminished in the case of norepinephrine. These results are consistent with the hypothesis that the endothelium may be less important for vasoconstriction than for vasodilatation in cerebral vessels.