NEURONAL PROTECTIVE EFFECTS OF CALCIUM-ANTAGONISTS IN CEREBRAL-ISCHEMIA

被引：45

作者：

RAMI, A

KRIEGLSTEIN, J

机构：

[1] Institut für Pharmakologie und Toxikologie, Philipps-Universität, 35037 Marburg

来源：

LIFE SCIENCES | 1994年 / 55卷 / 25-26期

关键词：

CEREBRAL ISCHEMIA; CALCIUM ANTAGONISTS; NEUROPROTECTION;

D O I：

10.1016/0024-3205(94)00391-2

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

We investigated the effects of calcium antagonists against ischemic injury in vivo and against excitotoxic damage in vitro. In vivo nimodipine protected significantly the CA1 hippocampal neurons from neurodegeneration after transient global ischemia in rats without changing the local cerebral blood flow. Furnidipine reduced the area of ischemia after permanent MCA-occlusion in mice. The results in vitro using the Ca2+-sensitive dye fura-2 showed that nimodipine reduced in a dose-dependent manner the elevation of [Ca2+](i) in hippocampal neurons induced by K+-stimulation. The present in vitro and in vivo data show that calcium antagonists are potent agents in protecting neurons against the deleterious consequences of an excitotoxic or ischemic insult.

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页码：2105 / 2113

页数：9

相关论文

共 36 条

[1] EFFECTS OF FLUNARIZINE ON POSTISCHEMIC BLOOD-FLOW, ENERGY-METABOLISM AND NEURONAL DAMAGE IN THE RAT-BRAIN [J].

BECK, T ;

NUGLISCH, J ;

SAUER, D ;

BIELENBERG, GW ;

MENNEL, HD ;

ROSSBERG, C ;

KRIEGLSTEIN, J .

EUROPEAN JOURNAL OF PHARMACOLOGY, 1988, 158 (03) :271-274

[2] DIHYDROPYRIDINE RECEPTOR IN RAT-BRAIN LABELED WITH [H-3]-LABELED NIMODIPINE [J].

BELLEMANN, P ;

SCHADE, A ;

TOWART, R .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1983, 80 (08) :2356-2360

[3] EPINEPHRINE ENHANCES CA-2+ CURRENT-REGULATED CA-2+ RELEASE AND CA-2+ REUPTAKE IN RAT VENTRICULAR MYOCYTES [J].

CALLEWAERT, G ;

CLEEMANN, L ;

MORAD, M .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (06) :2009-2013

[4]

Dennis C, 1939, P SOC EXP BIOL MED, V40, P559

[5] HISTOPATHOLOGICAL AND HEMODYNAMIC CONSEQUENCES OF COMPLETE VERSUS INCOMPLETE ISCHEMIA IN THE RAT [J].

DIETRICH, WD ;

BUSTO, R ;

YOSHIDA, S ;

GINSBERG, MD .

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1987, 7 (03) :300-308

[6] STUDIES ON THE LINKAGE OF ENERGY-METABOLISM AND NEURONAL-ACTIVITY IN THE ISOLATED PERFUSED RAT-BRAIN [J].

DIRKS, B ;

HANKE, J ;

KRIEGLSTEIN, J ;

STOCK, R ;

WICKOP, G .

JOURNAL OF NEUROCHEMISTRY, 1980, 35 (02) :311-317

[7] NIMODIPINE POSTTREATMENT DOES NOT INCREASE BLOOD-FLOW IN RATS WITH FOCAL CORTICAL ISCHEMIA [J].

DIRNAGL, U ;

JACEWICZ, M ;

PULSINELLI, W .

STROKE, 1990, 21 (09) :1357-1361

[8] CEREBRAL CARBOHYDRATE METABOLISM DURING ACUTE HYPOXIA AND RECOVERY [J].

DUFFY, TE ;

NELSON, SR ;

LOWRY, OH .

JOURNAL OF NEUROCHEMISTRY, 1972, 19 (04) :959-&

[9] THE EFFECT OF THE CALCIUM-ANTAGONIST NIMODIPINE ON THE GERBIL MODEL OF EXPERIMENTAL CEREBRAL-ISCHEMIA [J].

FUJISAWA, A ;

MATSUMOTO, M ;

MATSUYAMA, T ;

UEDA, H ;

WANAKA, A ;

YONEDA, S ;

KIMURA, K ;

KAMADA, T .

STROKE, 1986, 17 (04) :748-752

[10] BACKGROUND REVIEW AND CURRENT CONCEPTS OF REPERFUSION INJURY [J].

HALLENBECK, JM ;

DUTKA, AJ .

ARCHIVES OF NEUROLOGY, 1990, 47 (11) :1245-1254

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