Functional, morphological, and metabolic abnormalities of the cerebral microcirculation after concussive brain injury in cats.

Abstract

Experimental concussive brain injury was induced by a fluid percussion device in anesthetized cats equipped with a cranial window for the observation of the pial microcirculation of the parietal cortex. Brain injury resulted in transient but pronounced increases in arterial blood pressure and in sustained arteriolar vasodilation associated with reduced or absent responsiveness to the vasoconstrictor effect of arterial hypocapnia and with reduced or absent ability of the vessels to undergo autoregulatory vasodilation in response to reductions in arterial blood pressure. Such vessels had reduced resting O2 consumption in vitro. EM examination of the same vessels that were studied physiologically disclosed discrete endothelial lesions consisting of vacuolization or crater formation. Occasionally there was extensive destruction and necrosis of the endothelial cells. There was little or no morphological evidence of vascular smooth muscle damage. There was a close association between endothelial lesions and vessel dilation and unresponsiveness, suggesting a causal relationship. In cats in which the transient post-traumatic hypertensive episode was prevented, the vessels retained their normal caliber, remained normally responsive and had no endothelial lesions. Apparently vascular lesions in the pialmicrocirculation following this type of brain injury are due to the rise in arterial pressure.