Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
POSTTRAUMATIC HYPOTHERMIA IN THE TREATMENT OF AXONAL DAMAGE IN AN ANIMAL-MODEL OF TRAUMATIC AXONAL INJURY
Autore:
KOIZUMI H; POVLISHOCK JT;
Indirizzi:
VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT ANAT,POB 980709 RICHMOND VA 23298 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT ANAT RICHMOND VA 23298 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DIV NEUROSURG RICHMOND VA 23298 YAMAGUCHI UNIV,SCH MED,DEPT NEUROSURG YAMAGUCHI JAPAN
Titolo Testata:
Journal of neurosurgery
fascicolo: 2, volume: 89, anno: 1998,
pagine: 303 - 309
SICI:
0022-3085(1998)89:2<303:PHITTO>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID PRECURSOR PROTEIN; CONTROLLED CORTICAL IMPACT; DIFFUSE BRAIN INJURY; MODERATE HYPOTHERMIA; HEAD-INJURY; THERAPEUTIC HYPOTHERMIA; GLUTAMATE RELEASE; MILD HYPOTHERMIA; RATS; PROTECTION;
Keywords:
TRAUMATIC BRAIN INJURY; AXONAL INJURY; BETA-AMYLOID PRECURSOR PROTEIN IMMUNOHISTOCHEMISTRY; RAT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
47
Recensione:
Indirizzi per estratti:
Citazione:
H. Koizumi e J.T. Povlishock, "POSTTRAUMATIC HYPOTHERMIA IN THE TREATMENT OF AXONAL DAMAGE IN AN ANIMAL-MODEL OF TRAUMATIC AXONAL INJURY", Journal of neurosurgery, 89(2), 1998, pp. 303-309

Abstract

Object. Many investigators have demonstrated the protective effects of hypothermia following traumatic brain injury (TBI) in both animals and humans. Typically,:his protection has been evaluated in relation tothe preservation of neurons and/or the blunting of behavioral abnormalities. However, little consideration has been given to any potential protection afforded in regard to TBI-induced axonal injury, a feature of human TBI. In this study, the authors evaluated the protective effects of hypothermia on axonal injury after TBT in rats. Methods. Male Sprague-Dawley rats weighing 380 to 400 g were subjected to experimental TBI induced by an impact-acceleration device. These rats were subjected to hypothermia either before or after injury, with their temporalis muscle and rectal temperatures maintained at 32 degrees C for 1 hour. After this I-hour period of hypothermia, rewarming to normothermic levels was accomplished over a 90-minute period. Twenty-four hours later, the animals were killed and semiserial sagittal sections of the brain were reacted for visualization of the amyloid precursor protein (APP), a marker of axonal injury. The density of APP-marked damaged axonswithin the corticospinal tract at the pontomedullary junction was calculated for each animal. In all hypothermic animals, a significant reduction in APP-marked damaged axonal density was found. In animals treated with preinjury, immediate postinjury, and delayed hypothermia, thedensity of damaged axons was dramatically reduced in comparison with the untreated controls (p < 0.05). Conclusions. The authors infer fromthese findings that early as well as delayed posttraumatic hypothermia results in substantial protection in TBI, at least in terms of the injured axons.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/04/20 alle ore 11:00:39