In vivo binding of nimodipine in the brain: II. Binding kinetics in focal cerebral ischemia.

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

Standard

In vivo binding of nimodipine in the brain: II. Binding kinetics in focal cerebral ischemia. / Hogan, M J; Gjedde, A; Hakim, A M.

In: Journal of Cerebral Blood Flow and Metabolism, Vol. 11, No. 5, 1991, p. 771-8.

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

Harvard

Hogan, MJ, Gjedde, A & Hakim, AM 1991, 'In vivo binding of nimodipine in the brain: II. Binding kinetics in focal cerebral ischemia.', Journal of Cerebral Blood Flow and Metabolism, vol. 11, no. 5, pp. 771-8.

APA

Hogan, M. J., Gjedde, A., & Hakim, A. M. (1991). In vivo binding of nimodipine in the brain: II. Binding kinetics in focal cerebral ischemia. Journal of Cerebral Blood Flow and Metabolism, 11(5), 771-8.

Vancouver

Hogan MJ, Gjedde A, Hakim AM. In vivo binding of nimodipine in the brain: II. Binding kinetics in focal cerebral ischemia. Journal of Cerebral Blood Flow and Metabolism. 1991;11(5):771-8.

Author

Hogan, M J ; Gjedde, A ; Hakim, A M. / In vivo binding of nimodipine in the brain: II. Binding kinetics in focal cerebral ischemia. In: Journal of Cerebral Blood Flow and Metabolism. 1991 ; Vol. 11, No. 5. pp. 771-8.

Bibtex

@article{06cd0c40b31511debc73000ea68e967b,
title = "In vivo binding of nimodipine in the brain: II. Binding kinetics in focal cerebral ischemia.",
abstract = "We report the binding characteristics of [3H]nimodipine to normal and ischemic brain in vivo. We used the 1,4-dihydropyridine, nimodipine, to label the L-type voltage-sensitive calcium channel in focal cerebral ischemia after occlusion of both the middle cerebral and ipsilateral common carotid arteries in rats. Varying concentrations of [3H]nimodipine were infused 3.5 h after the onset of ischemia and circulated for 30 min before the brain was obtained for autoradiography and determination of regional nimodipine content. In separate sets of experiments, the metabolites of nimodipine were determined and the conditions for equilibrium of nimodipine distribution were established. Increased nimodipine uptake was observed in ischemic regions. This increased binding was saturable and specific with an affinity constant, KD, of 0.45 nM and a maximal regional binding capacity, Bmax, ranging from 3.1 to 10.9 pmol/g. Only binding to ischemic tissue was specific and saturable whereas that in nonischemic tissue was nonspecific. In vivo binding of nimodipine may be used to identify cell membrane depolarization and calcium channel activation in focal cerebral ischemia.",
author = "Hogan, {M J} and A Gjedde and Hakim, {A M}",
year = "1991",
language = "English",
volume = "11",
pages = "771--8",
journal = "Journal of Cerebral Blood Flow and Metabolism",
issn = "0271-678X",
publisher = "SAGE Publications",
number = "5",

}

RIS

TY - JOUR

T1 - In vivo binding of nimodipine in the brain: II. Binding kinetics in focal cerebral ischemia.

AU - Hogan, M J

AU - Gjedde, A

AU - Hakim, A M

PY - 1991

Y1 - 1991

N2 - We report the binding characteristics of [3H]nimodipine to normal and ischemic brain in vivo. We used the 1,4-dihydropyridine, nimodipine, to label the L-type voltage-sensitive calcium channel in focal cerebral ischemia after occlusion of both the middle cerebral and ipsilateral common carotid arteries in rats. Varying concentrations of [3H]nimodipine were infused 3.5 h after the onset of ischemia and circulated for 30 min before the brain was obtained for autoradiography and determination of regional nimodipine content. In separate sets of experiments, the metabolites of nimodipine were determined and the conditions for equilibrium of nimodipine distribution were established. Increased nimodipine uptake was observed in ischemic regions. This increased binding was saturable and specific with an affinity constant, KD, of 0.45 nM and a maximal regional binding capacity, Bmax, ranging from 3.1 to 10.9 pmol/g. Only binding to ischemic tissue was specific and saturable whereas that in nonischemic tissue was nonspecific. In vivo binding of nimodipine may be used to identify cell membrane depolarization and calcium channel activation in focal cerebral ischemia.

AB - We report the binding characteristics of [3H]nimodipine to normal and ischemic brain in vivo. We used the 1,4-dihydropyridine, nimodipine, to label the L-type voltage-sensitive calcium channel in focal cerebral ischemia after occlusion of both the middle cerebral and ipsilateral common carotid arteries in rats. Varying concentrations of [3H]nimodipine were infused 3.5 h after the onset of ischemia and circulated for 30 min before the brain was obtained for autoradiography and determination of regional nimodipine content. In separate sets of experiments, the metabolites of nimodipine were determined and the conditions for equilibrium of nimodipine distribution were established. Increased nimodipine uptake was observed in ischemic regions. This increased binding was saturable and specific with an affinity constant, KD, of 0.45 nM and a maximal regional binding capacity, Bmax, ranging from 3.1 to 10.9 pmol/g. Only binding to ischemic tissue was specific and saturable whereas that in nonischemic tissue was nonspecific. In vivo binding of nimodipine may be used to identify cell membrane depolarization and calcium channel activation in focal cerebral ischemia.

M3 - Journal article

C2 - 1874809

VL - 11

SP - 771

EP - 778

JO - Journal of Cerebral Blood Flow and Metabolism

JF - Journal of Cerebral Blood Flow and Metabolism

SN - 0271-678X

IS - 5

ER -

ID: 14943559