Adaptation of Cerebral Circulation to Brain Arteriovenous Malformations Increases Feeding Artery Pressure and Decreases Regional Hypotension

ABSTRACT PURPOSE To determine how the adaptation of extranidal cerebral vessels affects feeding artery pressure, draining vein pressure, and regional hypotension due to the presence of brain arteriovenous malformations (BAVMs). CONCEPT BAVMs cause high flows in feeding arteries and draining veins and can induce profound hypotension in the neighboring vasculature. Despite the large difference in flow, endothelial shear stress (τ) observed in vessels ipsilateral to the BAVM is similar to τ in vessels contralateral to the BAVM, suggesting that the conductance vessels successfully adapt to keep τ constant. However, because BAVMs are discovered only after they are well developed, the natural history of the adaptation process in extranidal vessels is unknown. RATIONALE Currently, no way exists to determine experimentally the effects of adaptation of extranidal vessels in human patients. Therefore, a mathematical model of the cerebral vasculature is used to study adaptation in response to BAVMs. By comparing pressures and flows calculated before and after adaptation, the effect of adaptation of the conductance vessels on regional hemodynamics can be evaluated. DISCUSSION Structural adaptation of the extranidal circulation seems not only to reset τ, but also to ameliorate regional hypotension induced by BAVMs. However, this compensatory mechanism also increases feeding artery pressure and thus may increase the risk of hemorrhagic stroke.

Contributions of ischemia and reperfusion to mucosal lesion formation

Two theories have been proposed to account for the mucosal injury associated with intestinal ischemia, hypoxia-countercurrent exchange, and oxygen free radicals. The countercurrent mechanism suggests that mucosal injury should occur predominately during the ischemic period, whereas the oxygen free radical hypothesis predicts that the majority of mucosal injury results from reperfusion of ischemic tissue. Histological specimens obtained during the ischemic period and following reperfusion allowed a systematic evaluation of the time course of development of mucosal lesions in a regional ischemia model. Reperfusion after 3 h of regional hypotension reduced mean mucosal thickness from 1,022.2 +/- 6.3 to 503.6 +/- 10.0 microns. The decrease in mucosal thickness was largely due to a reduction in villus height, inasmuch as the reduction in crypt depth was statistically insignificant. A significantly smaller change in mucosal thickness was observed when the bowel was subjected to 3 h ischemia without reperfusion. The mucosal injury produced by 3 h ischemia and 1 h reperfusion was more severe than that produced by 4 h ischemia without reperfusion. The results of this study suggest that most of the tissue damage produced by the widely employed regional hypotension model occurs at the time of reperfusion.