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Titolo:
Exacerbation of traumatically induced axonal injury by rapid posthypothermic rewarming and attenuation of axonal change by cyclosporin A
Autore:
Suehiro, E; Povlishock, JT;
Indirizzi:
Virginia Commonwealth Univ, Med Coll Virginia, Dept Anat, Richmond, VA 23298 USA Virginia Commonwealth Univ Richmond VA USA 23298 , Richmond, VA 23298 USA Yamaguchi Univ, Sch Med, Dept Neurosurg, Yamaguchi, Japan Yamaguchi Univ Yamaguchi Japan ch Med, Dept Neurosurg, Yamaguchi, Japan
Titolo Testata:
JOURNAL OF NEUROSURGERY
fascicolo: 3, volume: 94, anno: 2001,
pagine: 493 - 498
SICI:
0022-3085(200103)94:3<493:EOTIAI>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID PRECURSOR PROTEIN; DIFFUSE BRAIN INJURY; POSTTRAUMATIC HYPOTHERMIA; HEAD-INJURY; INTRACRANIAL HYPERTENSION; THERAPEUTIC HYPOTHERMIA; MODERATE HYPOTHERMIA; MILD HYPOTHERMIA; DAMAGE; MODEL;
Keywords:
traumatic brain injury; hypothermia; cyclosporin A; axonal injury; rat;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Povlishock, JT Virginia Commonwealth Univ, Med Coll Virginia, Dept Anat, Virginia Campus,POB 980709, Richmond, VA 23298 USA Virginia Commonwealth Univ Virginia Campus,POB 980709 Richmond VA USA 23298
Citazione:
E. Suehiro e J.T. Povlishock, "Exacerbation of traumatically induced axonal injury by rapid posthypothermic rewarming and attenuation of axonal change by cyclosporin A", J NEUROSURG, 94(3), 2001, pp. 493-498

Abstract

Object. Although considerable attention has been focused on the use of posttraumatic hypothermia, little consideration has been given to the issue ofposthypothermic rewarming and its potentially damaging consequences. In this communication, the authors examine the issue of rapid posthypothermic rewarming compared with gradual rewarming while exploring the potential utility of cyclosporin A (CsA) administration for attenuatings any rapid rewarming-induced axonal change. Methods. Male Sprague-Dawley rats were subjected to impact-acceleration injury and then their body temperature was lowered to 32 degreesC for 1 hour postinjury. After hypothermia, rewarming to normothermic levels was accomplished either within a 20-minute period (rapid rewarming) or over a 90-minute period (slow rewarming). Some animals in the rapid rewarming group received intrathecal infusion of either CsA or its vehicle, whereas the rats in the slow rewarming group received vehicle alone. Both the CsA and its vehicle were administered immediately before initiation of rewarming. Twenty-fourhours postinjury the animals' brains were processed for visualization of amyloid precursor protein (APP), a marker of traumatic axonal injury. The APP-positive axonal density in the gradual ly rewarmed group receiving vehicle was statistically significantly reduced in comparison with the rapidly rewarmed, vehicle-treated group. For the group undergoing rapid rewarming andtreatment with CsA, a statistically significant reduction was also found in the density of the APP profiles compared with the rapidly rewarmed, vehicle-treated group. Conclusions. The results of this study show that rapid rewarming exacerbates traumatically induced axonal injury, which can be significantly attenuated by administering CsA.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 13:15:17