Traumatic brain injury does not alter cerebral artery
contractility.
Bukoski, Richard D., Shi Nan Wang, Ka Bian, and Douglas S. Dewitt.
Section of Hypertension and Vascular Research, Departments of
Internal Medicine and Physiology & Biophysics and Charles R.
Allen Research Laboratories, Department of Anesthesiology, University
of Texas Medical Branch
APStracts 3:0418H, 1996.
Previous studies have demonstrated that traumatic brain injury (TBI)
significantly reduces cerebral blood flow (CBF) determined in vivo
and reduces vascular reactivity in the pial circu lation measured
with cranial window preparations. We have now tested the hypothesis
that TBI induces these changes by impairing intrinsic contractile
activity of cerebral arteries. 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 force generation measured. Moderate (n=5)
and severe (n=3) trauma had no effect on the magnitude of serotonin
or K+-induced force generation or sensitivity to serotonin in
arteries isolated within 10 min of 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 which was similar in both groups.
Blockade of cyclooxygenase with 1_M indomethacin had no effect on
serotonin-induced force generated by vessels of moderate trauma and
sham treated rats. Acetylcholine induced an endothelium-dependent
relaxation of posterior and middle cerebral arteries; and the
magnitude of the response was unaffected by moderate TBI. To
determine whether prolonged in situ exposure of vessels to the
traumatized cerebral milieu could reveal an alteration in intrinsic
contractility, posterior cerebral arteries were isolated 30 min after
TBI; and again no differences in the tension or relaxation responses
were observed. It is concluded that midline fluid percussion TBI did
not affect contraction or relaxation of proximal middle or posterior
cerebral arteries in rats.
Received 18 June 1996; accepted in final form 17 September 1996.
APS Manuscript Number H533-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996