Citation

Armstead WM, Riley J, Vavilala MS. J. Neurotrauma 2016; 34(8): 1666-1675.

Affiliation

University of Washington, Anesthesiology , 325 Ninth Ave , Box 359724 , Seattle, Washington, United States , 98104 ; vavilala@u.washington.edu.

Copyright

(Copyright © 2016, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2016.4770

PMID

27912253

Abstract

Traumatic brain injury (TBI) is the leading cause of injury related death in children, with boys and children under 4 years having particularly poor outcomes. Cerebral autoregulation is often impaired after TBI, contributing to poor outcome. Cerebral perfusion pressure can be normalized by use of vasoactive agents. The c-Jun-terminal kinase (JNK) isoform of mitogen activated protein kinase (MAPK) produces hemodynamic impairment after TBI, but less is known about its role in histopathology. We investigated whether epinephrine (EPI) age and sex dependently protected cerebral autoregulation and limited histopathology after TBI and the role of JNK in that outcome. Lateral FPI was produced in anesthetized pigs. Pial artery reactivity was measured via a closed cranial window. Phosphorylated JNK MAPK was quantified by ELISA.

RESULTS show that EPI preserves autoregulation , prevents histopathology, and blocks phosphorylated JNK upregulation in newborn males and females and juvenile females but not juvenile males after TBI. These data indicate that EPI preserves cerebral autoregulation and limits histopathology after TBI through blockade of JNK in an age and sex dependent manner.

Language: en