title: Cerebral blood flow decreased by adrenergic stimulation of cerebral vessels in anesthetized newborn pigs with traumatic brain injury.
abstract: Changes in cerebral blood flow (CBF), pial arteriolar diameter, and arterial blood pressure, gases, and pH were examined before and for 3 hours after fluid-percussion brain injury in alpha-chloralose-anesthetized piglets. The brain injury was induced by a percussion of 2.28 +/- 0.06 atm applied for 23.7 +/- 0.5 msec to the right parietal cortex. Regional CBF was measured with radiolabeled microspheres, and changes in pial arteriolar diameter were monitored in the left parietal cortex using closed cranial windows. Immediately following brain injury, mean blood pressure transiently (for approximately 10 minutes) either increased or decreased and then exhibited a prolonged decrease in all of the animals. The brains showed changes consistent with traumatic brain injury such as subarachnoid hemorrhage, contusions, or reactive axonal swelling; none showed histological evidence of a global alternative pathogenetic mechanism such as hypoxic ischemic damage. While CBF of uninjured control animals did not change over a 3-hour observation period, after brain injury blood flow decreased 30% +/- 1% below the baseline level within 10 minutes and remained there for 2 to 3 hours posttrauma. After adrenergic blockade, CBF did not decrease at any time during the 3-hour period in either the uninjured control or the injured animals. Concomitant with the decreased blood flow after brain injury, pial arteriolar diameter decreased 14% below the preinjury level. However, in piglets treated with adrenoceptor antagonists, uninjured control and brain-injured animals did not show a decrease in pial arteriolar diameter. The present results support the hypothesis that increased sympathetic outflow to the cephalic vasculature following the fluid-percussion brain injury causes cerebral vasoconstriction decreasing pial arteriolar diameter and regional CBF.
authors.affiliation: Department of Physiology and Biophysics, University of Tennessee, Memphis.
authors.forename: M
authors.initials: M
authors.lastname: Shibata
authors.forename: S
authors.initials: S
authors.lastname: Einhaus
authors.forename: J B
authors.initials: JB
authors.lastname: Schweitzer
authors.forename: S
authors.initials: S
authors.lastname: Zuckerman
authors.forename: C W
authors.initials: CW
authors.lastname: Leffler
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000818:Animals; D000831:Animals, Newborn; D001160:Arterioles / Q000187:drug effects / Q000473:pathology; D001794:Blood Pressure / Q000187:drug effects; D001930:Brain Injuries / Q000473:pathology / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D005260:Female; D006863:Hydrogen-Ion Concentration; D008297:Male; D010841:Pia Mater / Q000098:blood supply; D011224:Prazosin / Q000494:pharmacology; D013552:Swine; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D000317:Adrenergic alpha-Antagonists; D015016:Yohimbine; D011224:Prazosin