We induced experimental concussive brain injury 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 oxygen consumption in vitro. Electron microscopic examination of the same vessels that were studied physiologically disclosed the presence of discrete endothelial lesions consisting of either 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 the presence of 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. The results show that the vascular lesions in the pial microcirculation following this type of brain injury are due to the rise in arterial pressure.