Mechanisms of brain injury after global cerebral ischemia

被引：276

作者：

Harukuni, I

Bhardwaj, A

机构：

[1] Johns Hopkins Univ, Sch Med, Neurosci Crit Care Div, Dept Neurol,Johns Hopkins Hosp, Baltimore, MD 21287 USA

[2] Johns Hopkins Univ, Sch Med, Div Cardiac Anesthesiol,Johns Hopkins Hosp, Dept Anesthesiol & Crit Care Med, Baltimore, MD 21287 USA

[3] Johns Hopkins Univ, Sch Med, Neurosci Crit Care Div,Johns Hopkins Hosp, Dept Anesthesiol & Crit Care Med, Baltimore, MD 21287 USA

来源：

NEUROLOGIC CLINICS | 2006年 / 24卷 / 01期

关键词：

D O I：

10.1016/j.ncl.2005.10.004

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Global cerebral ischemia occurs commonly in patients who have a variety of clinical conditions including cardiac arrest, shock, and asphyxia and in patients undergoing complex cardiac surgery. Irrespective of the etiology of cerebral ischemia, cellular and molecular processes trigger a cascade of events that culminates in a "final common pathway," resulting in ischemic neuronal injury. Identification of these injury mediators and pathways in a variety of experimental animal models of global cerebral ischemia has led to investigation of target-specific cytoprotective strategies that are critical to clinical brain injury outcome.

引用

页码：1 / +

页数：22

共 135 条

[1] GLUTAMATE-INDUCED NEURONAL DEATH - A SUCCESSION OF NECROSIS OR APOPTOSIS DEPENDING ON MITOCHONDRIAL-FUNCTION [J].

ANKARCRONA, M ;

DYPBUKT, JM ;

BONFOCO, E ;

ZHIVOTOVSKY, B ;

ORRENIUS, S ;

LIPTON, SA ;

NICOTERA, P .

NEURON, 1995, 15 (04) :961-973

[2]

ARNOWSKI J, 1993, J CEREB BLOOD FLOW M, V13, P550

[3]

ARTRU AA, 1981, ANESTH ANALG, V60, P41

[4]

Auer RN, 2001, ANN NY ACAD SCI, V939, P271

[5] Persistent poststroke hyperglycemia is independently associated with infarct expansion and worse clinical outcome [J].

Baird, TA ;

Parsons, MW ;

Phanh, T ;

Butcher, KS ;

Desmond, PM ;

Tress, BM ;

Colman, PG ;

Chambers, BR ;

Davis, SM .

STROKE, 2003, 34 (09) :2208-2214

[6] Ischemic preconditioning and brain tolerance - Temporal histological and functional outcomes, protein synthesis requirement, and interleukin-1 receptor antagonist and early gene expression [J].

Barone, FC ;

White, RF ;

Spera, PA ;

Ellison, J ;

Currie, RW ;

Wang, XK ;

Feuerstein, GZ .

STROKE, 1998, 29 (09) :1937-1950

[7] EVALUATION OF DELAYED TREATMENT OF FOCAL CEREBRAL-ISCHEMIA WITH 3 SELECTIVE KAPPA-OPIOID AGONISTS IN CATS [J].

BASKIN, DS ;

WIDMAYER, MA ;

BROWNING, JL ;

HEIZER, ML ;

SCHMIDT, WK .

STROKE, 1994, 25 (10) :2047-2053

[8] ELEVATION OF THE EXTRACELLULAR CONCENTRATIONS OF GLUTAMATE AND ASPARTATE IN RAT HIPPOCAMPUS DURING TRANSIENT CEREBRAL-ISCHEMIA MONITORED BY INTRACEREBRAL MICRODIALYSIS [J].

BENVENISTE, H ;

DREJER, J ;

SCHOUSBOE, A ;

DIEMER, NH .

JOURNAL OF NEUROCHEMISTRY, 1984, 43 (05) :1369-1374

[9] INITIATION OF PROTEIN-SYNTHESIS AND HEAT-SHOCK PROTEIN-72 EXPRESSION IN THE RAT-BRAIN FOLLOWING SEVERE INSULIN-INDUCED HYPOGLYCEMIA [J].

BERGSTEDT, K ;

HU, BR ;

WIELOCH, T .

ACTA NEUROPATHOLOGICA, 1993, 86 (02) :145-153

[10] Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia [J].

Bernard, SA ;

Gray, TW ;

Buist, MD ;

Jones, BM ;

Silvester, W ;

Gutteridge, G ;

Smith, K .

NEW ENGLAND JOURNAL OF MEDICINE, 2002, 346 (08) :557-563

← 1 2 3 4 5 6 7 8 9 10 →