Stroke, Vol 20, 911-917, Copyright © 1989 by American Heart Association
MD Ellison, DE Erb, HA Kontos and JT Povlishock
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.
ARTICLES
Recovery of impaired endothelium-dependent relaxation after fluid- percussion brain injury in cats
Department of Anatomy, Medical College of Virginia, Richmond 23298.
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