• B P Mathew, D S DeWitt, R M Bryan, R D Bukoski, and D S Prough.
• Charles R. Allen Research Laboratories, Department of Anesthesiology, University of Texas Medical Branch, Galveston 77555-0830, USA.
• J. Neurotrauma. 1999 Dec 1;16(12):1177-86.

AbstractTraumatic brain injury (TBI) reduces cerebral vascular pressure autoregulation in experimental animals and in patients. In order to understand better the mechanisms of impaired autoregulation, we measured myogenic responses to changes in intraluminal pressure in vitro in pressurized, rodent middle cerebral arteries (MCAs) harvested after TBI. In an approved study, male Sprague-Dawley rats (275-400 g) were anesthetized, intubated, ventilated with 2.0% isoflurane in O2/air, and prepared for fluid percussion TBI. The isoflurane concentration was reduced to 1.5%, and rats (n = 6 per group) were randomly assigned to receive sham TBI followed by decapitation 5 or 30 min later or moderate TBI (2.0 atm) followed by decapitation 5 or 30 min later. After decapitation, MCA segments were removed, mounted on an arteriograph, and pressurized. MCA diameters were measured as transmural pressure was sequentially reduced. MCA diameters remained constant or increased in the sham groups as intraluminal pressure was reduced from 100 to 40 mm Hg. In both TBI groups, diameter decreased with each reduction in pressure. In summary, MCAs removed from uninjured, isoflurane-anesthetized rats had normal vasodilatory responses to decreased intraluminal pressure. In contrast, after TBI, myogenic vasodilatory responses were significantly reduced within 5 min of TBI and the impaired myogenic responses persisted for at least 30 min after TBI.

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