Cerebral Blood Flow, Metabolism, and Head Trauma 2013
DOI: 10.1007/978-1-4614-4148-9_2
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Situating Cerebral Blood Flow in the Pathotrajectory of Head Trauma

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Cited by 3 publications
(2 citation statements)
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“…27 Molecular models focus around endothelin-1 protein and its effect on endothelin receptor A. CSF and serum obtained in patients who have sustained a TBI show increased levels of endothelin-1, supporting its involvement in TBI and subsequent vasospasm in these patients. 8 PTV results in diminished blood flow to areas of the brain, producing DCI and manifesting in new-onset neurological deterioration occurring after initial brain injury. 21 Westermaier et al found neurological evaluation to be the most accurate method for discovering vasospasm or infarction following aSAH.…”
Section: Pathophysiologymentioning
confidence: 99%
“…27 Molecular models focus around endothelin-1 protein and its effect on endothelin receptor A. CSF and serum obtained in patients who have sustained a TBI show increased levels of endothelin-1, supporting its involvement in TBI and subsequent vasospasm in these patients. 8 PTV results in diminished blood flow to areas of the brain, producing DCI and manifesting in new-onset neurological deterioration occurring after initial brain injury. 21 Westermaier et al found neurological evaluation to be the most accurate method for discovering vasospasm or infarction following aSAH.…”
Section: Pathophysiologymentioning
confidence: 99%
“…Secondary processes also contribute to vessel narrowing and spasm. These include the chronic depolarization of vascular smooth muscle due to reduced potassium channel activity, the breakdown of blood products resulting in endothelin release and reduced availability of nitric oxide, free radical formation, cyclic GMP depletion of vascular smooth muscle, and potentiation of prostaglandin-induced vasoconstriction [ 41 , 42 , 43 ]. Whether VSP becomes symptomatic depends on several clinical factors.…”
Section: Pathophysiologymentioning
confidence: 99%