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Titolo:
Mice overexpressing extracellular superoxide dismutase have increased resistance to global cerebral ischemia
Autore:
Sheng, H; Kudo, M; Mackensen, GB; Pearlstein, RD; Crapo, JD; Warner, DS;
Indirizzi:
Duke Univ, Med Ctr, Dept Anesthesiol, Durham, NC 27710 USA Duke Univ Durham NC USA 27710 Ctr, Dept Anesthesiol, Durham, NC 27710 USA Duke Univ, Med Ctr, Dept Surg, Durham, NC 27710 USA Duke Univ Durham NC USA 27710 v, Med Ctr, Dept Surg, Durham, NC 27710 USA Yamagata Univ, Dept Anesthesiol & Resuscitat, Yamagata 990, Japan YamagataUniv Yamagata Japan 990 esiol & Resuscitat, Yamagata 990, Japan Tech Univ Munich, Klinikum Rechts Isar, Dept Anesthesiol, D-8000 Munich, Germany Tech Univ Munich Munich Germany D-8000 esthesiol, D-8000 Munich, Germany Natl Jewish Ctr Immunol & Resp Med, Dept Med, Denver, CO 80206 USA Natl Jewish Ctr Immunol & Resp Med Denver CO USA 80206 nver, CO 80206 USA
Titolo Testata:
EXPERIMENTAL NEUROLOGY
fascicolo: 2, volume: 163, anno: 2000,
pagine: 392 - 398
SICI:
0014-4886(200006)163:2<392:MOESDH>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; HUMAN CELL-LINES; FOREBRAIN ISCHEMIA; NITRIC-OXIDE; POLYMORPHONUCLEAR LEUKOCYTES; BRAIN INJURY; BLOOD-FLOW; RAT; MOUSE; DEFICIENCY;
Keywords:
extracellular superoxide dismutase; brain; ischemia; cerebral blood how; mouse; transgenic;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Sheng, H Duke Univ, Med Ctr, Dept Anesthesiol, Durham, NC 27710 USA Duke Univ Durham NC USA 27710 Anesthesiol, Durham, NC 27710 USA
Citazione:
H. Sheng et al., "Mice overexpressing extracellular superoxide dismutase have increased resistance to global cerebral ischemia", EXP NEUROL, 163(2), 2000, pp. 392-398

Abstract

Transgenic mice, which exhibit a fivefold increase in brain parenchymal extracellular superoxide dismutase (EC-SOD) activity, were used to investigate the role of EC-SOD in global ischemic brain injury. Halothane-anesthetized normothermic wild-type (n = 22) and transgenic (n = 20) mice underwent 10min of near-complete forebrain ischemia induced by bilateral carotid artery occlusion and systemic hypotension (mean arterial pressure = 30 mm Hg). After 3 days of recovery, the brains were histologically examined. Other mice underwent autoradiographic determination of regional CBF 10 min prior to,during, and 30 min after forebrain ischemia. Histologic injury in the cortex and caudoputamen was minimal in both groups. The percentage of dead hippocampal CA1 neurons was reduced in the EC-SOD transgenic group (wild type =44 +/- 28%; EC-SOD transgenic = 23 +/- 21%, mean +/- SD, P = 0.015). CBF was similar between groups prior to ischemia. The intraischemic blood how was severely reduced in forebrain structures and was similar between groups. Blood flow at 30 min postischemia had recovered to 50-60% of baseline values in both groups. These results indicate that EC-SOD can play an important role in defining the magnitude of selective neuronal necrosis resulting from near-complete forebrain ischemia. This implicates involvement of extracellular superoxide anions in the pathologic response to global cerebral ischemia. (C) 2000 Academic Press.

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Documento generato il 09/04/20 alle ore 00:22:51