Activity of the dihydropyridine calcium channels following cerebral ischemia.

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Activity of the dihydropyridine calcium channels following cerebral ischemia. / Hogan, M; Gjedde, A; Hakim, A.

In: Arzneimittel-Forschung, Vol. 41, No. 3A, 1991, p. 332-3.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Hogan, M, Gjedde, A & Hakim, A 1991, 'Activity of the dihydropyridine calcium channels following cerebral ischemia.', Arzneimittel-Forschung, vol. 41, no. 3A, pp. 332-3.

APA

Hogan, M., Gjedde, A., & Hakim, A. (1991). Activity of the dihydropyridine calcium channels following cerebral ischemia. Arzneimittel-Forschung, 41(3A), 332-3.

Vancouver

Hogan M, Gjedde A, Hakim A. Activity of the dihydropyridine calcium channels following cerebral ischemia. Arzneimittel-Forschung. 1991;41(3A):332-3.

Author

Hogan, M ; Gjedde, A ; Hakim, A. / Activity of the dihydropyridine calcium channels following cerebral ischemia. In: Arzneimittel-Forschung. 1991 ; Vol. 41, No. 3A. pp. 332-3.

Bibtex

@article{36585fa0b31511debc73000ea68e967b,
title = "Activity of the dihydropyridine calcium channels following cerebral ischemia.",
abstract = "With an in-vivo autoradiographic method the binding of 3H-nimodipine (CAS 66085-59-4) and cerebral blood flow (14C-iodoantipyrine method) were measured in rat brain after occlusion of the middle cerebral and common carotid arteries. The dependence of the binding to neuronal cellular membranes on the duration of ischemia can be interpreted as indicator of the tissue's functional state or its responsiveness to therapy with calcium entry blockers. In the two analyzed structures, dorsolateral caudate and overlying sensorimotor cortex, the appearance of infarction is preceded by an activation of the nimodipine binding sites followed by persistent decline of the binding intensity. Binding to nimodipine may therefore be a useful marker of ischemic but salvageable brain tissue.",
author = "M Hogan and A Gjedde and A Hakim",
year = "1991",
language = "English",
volume = "41",
pages = "332--3",
journal = "Drug Research",
issn = "2194-9379",
publisher = "GeorgThieme Verlag",
number = "3A",

}

RIS

TY - JOUR

T1 - Activity of the dihydropyridine calcium channels following cerebral ischemia.

AU - Hogan, M

AU - Gjedde, A

AU - Hakim, A

PY - 1991

Y1 - 1991

N2 - With an in-vivo autoradiographic method the binding of 3H-nimodipine (CAS 66085-59-4) and cerebral blood flow (14C-iodoantipyrine method) were measured in rat brain after occlusion of the middle cerebral and common carotid arteries. The dependence of the binding to neuronal cellular membranes on the duration of ischemia can be interpreted as indicator of the tissue's functional state or its responsiveness to therapy with calcium entry blockers. In the two analyzed structures, dorsolateral caudate and overlying sensorimotor cortex, the appearance of infarction is preceded by an activation of the nimodipine binding sites followed by persistent decline of the binding intensity. Binding to nimodipine may therefore be a useful marker of ischemic but salvageable brain tissue.

AB - With an in-vivo autoradiographic method the binding of 3H-nimodipine (CAS 66085-59-4) and cerebral blood flow (14C-iodoantipyrine method) were measured in rat brain after occlusion of the middle cerebral and common carotid arteries. The dependence of the binding to neuronal cellular membranes on the duration of ischemia can be interpreted as indicator of the tissue's functional state or its responsiveness to therapy with calcium entry blockers. In the two analyzed structures, dorsolateral caudate and overlying sensorimotor cortex, the appearance of infarction is preceded by an activation of the nimodipine binding sites followed by persistent decline of the binding intensity. Binding to nimodipine may therefore be a useful marker of ischemic but salvageable brain tissue.

M3 - Journal article

C2 - 1650224

VL - 41

SP - 332

EP - 333

JO - Drug Research

JF - Drug Research

SN - 2194-9379

IS - 3A

ER -

ID: 14946159