Recovery of impaired endothelium-dependent relaxation after fluid-percussion brain injury in cats.

Abstract

The effect of a moderate level of fluid-percussion brain injury on acetylcholine-induced cerebral arteriolar vasodilation was examined for 12 hours after trauma in anesthetized cats equipped with cranial windows. The cats were then perfused with aldehydes, and the pial arteries were prepared for electron microscopy. Immediately after brain injury, the normal vasodilator response to topical application of acetylcholine was converted to vasoconstriction. By 4 hours after trauma, the ability of small pial arterioles (diameters less than 100 microns) to dilate after acetylcholine application had returned to the pretrauma level and was observed to be normal at both 8 and 12 hours after trauma (p less than 0.05). The vasodilator response of large caliber arterioles (diameters greater than or equal to 100 microns) at 4, 8, and 12 hours after injury was reduced relative to the pretrauma response but was significantly improved relative to their response at 30 minutes after trauma (p less than 0.05). Moreover, the response of large vessels at 4, 8, and 12 hours in injured animals was equal to that observed in noninjured control animals assessed at 4, 8, and 12 hours after window implantation. At 12 hours after injury, the ultrastuctural characteristics of both large and small vessels resembled their preinjury state. These data suggest that the impairment of acetylcholine-induced endothelium-dependent relaxation observed in cats after fluid-percussion brain injury is not irreversible but returns to normal (small arterioles) or exhibits significant recovery (large arterioles) within 4 hours after injury.