• Derek Nusbaum, Jonathan Clark, Kenneth Brady, Kathleen Kibler, Jeffrey Sutton, and Ronald Blaine Easley.
• Neurol. Res. 2014 Dec 1;36(12):1063-71.

ObjectivesRecent studies suggest that elevated intracranial pressure (ICP), created by hydrocephalus, can alter the lower limit of cerebrovascular autoregulation (LLA). Our objective in the present study was to determine if ICP elevation from cerebral venous outflow obstruction would result in comparable alterations in the LLA.MethodsAnesthetized juvenile pigs were assigned to one of two groups: naïve ICP (n  =  15) or high ICP (>20 mmHg; n  =  20). To elevate ICP through venous obstruction, a modified 5F esophageal balloon catheter was inserted via the right external jugular vein into the superior vena cava (SVC) and inflated to maintain an ICP of >20 mmHg. To calculate the LLA, gradual hypotension was induced by continuous hemorrhage from a catheter in the femoral vein. The LLA was determined by monitoring cortical laser Doppler flux (LDF).ResultsThe naïve and high ICP groups had LLAs of 45 mmHg (95% CI: 41-49 mmHg) and 71 mmHg (95% CI: 66-77 mmHg) respectively by LDF. The LLA was significantly different between the two groups and correlated significantly with ICP.DiscussionElevated ICP from cephalic venous engorgement leads to an increase in the LLA. These findings suggest that pathologic processes resulting in cephalic venous outflow obstruction and intracranial venous congestion can acutely elevate ICP and may place the brain at risk for impaired cerebrovascular autoregulation.

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