Alterations in blood vessels during gastric injury and protection.

Recent investigations suggest that the mucosal vascular endothelium is not a passive bystander, and that alterations within the blood vessel wall actively participate in the pathogenesis of gastric mucosal injury. We review here our data on rapidly developing vascular injury as detected by monastral blue deposition and increased vascular permeability measured by Evan's blue extravasation in dose- and time-dependent experiments with ethanol, HCl, and NaOH in the rat. In addition, using in vivo microscopy and laser-Doppler velocimetry, we demonstrate circulatory stasis in the superficial capillaries within about 1 min after topical application of damaging agents, and a gradual decrease in blood flow that correlates with the extent of hemorrhagic erosions. Prostaglandins or sulfhydryl agents prevented the circulatory standstill and the development of hemorrhagic mucosal lesions. We conclude that microvascular damage, increased vascular permeability, and capillary stasis precede the development of hemorrhagic mucosal lesions.