Citation

Toth P, Szarka N, Farkas E, Ezer E, Czeiter E, Amrein K, Ungvari Z, Hartings JA, Büki A, Koller A. Am. J. Physiol. Heart. Circ. Physiol. 2016; 311(5): H1118-H1131.

Affiliation

Department of Physiology, New York Medical College, Valhalla, New York.

Copyright

(Copyright © 2016, American Physiological Society)

DOI

10.1152/ajpheart.00267.2016

PMID

27614225

Abstract

Traumatic brain injury (TBI) is a major health problem worldwide. In addition to its high mortality (35-40%), survivors are left with cognitive, behavioral, and communicative disabilities. While little can be done to reverse initial primary brain damage caused by trauma, the secondary injury of cerebral tissue due to cerebromicrovascular alterations and dysregulation of cerebral blood flow (CBF) is potentially preventable. This review focuses on functional, cellular, and molecular changes of autoregulatory function of CBF (with special focus on cerebrovascular myogenic response) that occur in cerebral circulation after TBI and explores the links between autoregulatory dysfunction, impaired myogenic response, microvascular impairment, and the development of secondary brain damage. We further provide a synthesized translational view of molecular and cellular mechanisms involved in cortical spreading depolarization-related neurovascular dysfunction, which could be targeted for the prevention or amelioration of TBI-induced secondary brain damage.

Copyright © 2016 the American Physiological Society.

Language: en