TRAUMATIC BRAIN INJURY DOES NOT ALTER CEREBRAL-ARTERY CONTRACTILITY

Previous studies have shown that traumatic brain injury (TBI) signific antly reduces cerebral blood flow determined in vivo and reduces vascu lar reactivity in the pial circulation measured with cranial window pr eparations. We have now tested the hypothesis that TBI induces these c hanges by impairing intrinsic contractile activity of cerebral arterie s. Anesthetized rats underwent moderate (2.2 atm) and severe (3.0 atm) midline fluid percussion TBI or sham injury following which posterior cerebral or middle cerebral arteries were isolated and isometric forc e generation was measured. Moderate (n = 5) and severe (n = 3) trauma had no effect on the magnitude of serotonin- or K+-induced force gener ation or sensitivity to serotonin in arteries isolated within 10 min o f TBI. Functional disruption of the endothelium of posterior cerebral arteries isolated 10 min after moderate trauma or sham injury caused a reduction in the active tension response to serotonin that was simila r in both groups. Blockade of cyclooxygenase with 5 PM indomethacin ha d no effect on serotonin-induced force generated by vessels with moder ate trauma or in sham-treated rats. Acetyl choline induced an endothel ium-dependent relaxation of posterior and middle cerebral arteries; th e magnitude of the response was unaffected by moderate TBI. To determi ne whether prolonged in situ exposure of vessels to the traumatized ce rebral milieu could reveal an alteration in intrinsic contractility, p osterior cerebral arteries were isolated 30 min after TBI; again, no d ifferences in the tension or relaxation responses were observed. It is concluded that midline fluid percussion TBI did not affect contractio n or relaxation of proximal middle or posterior cerebral arteries in r ats.