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Brain Injury pp 71–97Cite as

Molecular and Cellular Mechanisms of Traumatic Cerebral Vascular Injury

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Part of the book series: Molecular and Cellular Biology of Critical Care Medicine ((MCCM,volume 2))

Abstract

Traumatic brain injury (TBI) is a major health care problem resulting in 50,000 deaths and nearly 50 billion dollars in medical expenses and lost productivity annually in the United States alone (Sosin et al. 1995). The physiologic deficit most likely responsible for this higher mortality is inadequate cerebral blood flow (CBF). Cerebral ischemia is caused by complex interactions between reduced blood pressure, impaired cerebral vasodilatory responsiveness, cerebral swelling and elevated intracranial pressure (ICP). Prompt treatment of hypotension in head-injured patients is essential because even mild hypotension (systolic blood pressure 10–29 mm Hg below normal) has been associated with increased mortality (Chesnut et al. 1993). Although appropriate maintenance of cerebral perfusion pressure is critical for the effective treatment of head-injured patients, an important additional therapeutic strategy would be to restore the vasodilatory and vasoconstrictory properties of the cerebral vasculature that are intended to protect the brain by maintaining as constant and ideal an environment as possible.

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  1. The University of Texas Medical Branch, Galveston, TX, USA

    Douglas S. DeWitt & Donald S. Prough

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  1. Pediatric Critical Care Medicine, Children’s Hospital of Pittsburgh, Pittsburgh, PA, 15213, USA

    Robert S. B. Clark M.D.

  2. Safar Center for Resuscitation Research, Pittsburgh, PA, USA

    Patrick Kochanek M.D.

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DeWitt, D.S., Prough, D.S. (2001). Molecular and Cellular Mechanisms of Traumatic Cerebral Vascular Injury. In: Clark, R.S.B., Kochanek, P. (eds) Brain Injury. Molecular and Cellular Biology of Critical Care Medicine, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1721-4_4

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