Nimodipine binding in focal cerebral ischemia.

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Nimodipine binding in focal cerebral ischemia. / Hogan, M; Gjedde, A; Hakim, A M.

In: Stroke, Vol. 21, No. 12 Suppl, 1990, p. IV78-80.

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

Harvard

Hogan, M, Gjedde, A & Hakim, AM 1990, 'Nimodipine binding in focal cerebral ischemia.', Stroke, vol. 21, no. 12 Suppl, pp. IV78-80.

APA

Hogan, M., Gjedde, A., & Hakim, A. M. (1990). Nimodipine binding in focal cerebral ischemia. Stroke, 21(12 Suppl), IV78-80.

Vancouver

Hogan M, Gjedde A, Hakim AM. Nimodipine binding in focal cerebral ischemia. Stroke. 1990;21(12 Suppl):IV78-80.

Author

Hogan, M ; Gjedde, A ; Hakim, A M. / Nimodipine binding in focal cerebral ischemia. In: Stroke. 1990 ; Vol. 21, No. 12 Suppl. pp. IV78-80.

Bibtex

@article{13d49e80b31511debc73000ea68e967b,
title = "Nimodipine binding in focal cerebral ischemia.",
abstract = "We investigated the binding properties of the voltage-sensitive calcium channel antagonist nimodipine in a rat model of focal cerebral ischemia. Male Sprague-Dawley rats weighing 250 g underwent occlusion of both the proximal middle cerebral artery and the ipsilateral common carotid artery. 3H-nimodipine (130 Ci/mmol) was infused intravenously and circulated for 30 minutes before the rats were killed at 5 minutes, 4, 24, and 48 hours after occlusion. The brains were removed and examined by autoradiography. We observed a focal increase of nimodipine binding in severely ischemic regions at 5 minutes after occlusion, which also appeared in regions with presumed penumbral blood flow levels at 4 hours after occlusion. We hypothesize that nimodipine binds to activated calcium channels in ischemic tissue. This increased binding depends on the duration and severity of cerebral ischemia. Sequential measurements of nimodipine binding may allow the identification of regions with potentially reversible effects of ischemia and the monitoring of their response to therapy.",
author = "M Hogan and A Gjedde and Hakim, {A M}",
year = "1990",
language = "English",
volume = "21",
pages = "IV78--80",
journal = "Stroke",
issn = "0039-2499",
publisher = "Lippincott Williams & Wilkins",
number = "12 Suppl",

}

RIS

TY - JOUR

T1 - Nimodipine binding in focal cerebral ischemia.

AU - Hogan, M

AU - Gjedde, A

AU - Hakim, A M

PY - 1990

Y1 - 1990

N2 - We investigated the binding properties of the voltage-sensitive calcium channel antagonist nimodipine in a rat model of focal cerebral ischemia. Male Sprague-Dawley rats weighing 250 g underwent occlusion of both the proximal middle cerebral artery and the ipsilateral common carotid artery. 3H-nimodipine (130 Ci/mmol) was infused intravenously and circulated for 30 minutes before the rats were killed at 5 minutes, 4, 24, and 48 hours after occlusion. The brains were removed and examined by autoradiography. We observed a focal increase of nimodipine binding in severely ischemic regions at 5 minutes after occlusion, which also appeared in regions with presumed penumbral blood flow levels at 4 hours after occlusion. We hypothesize that nimodipine binds to activated calcium channels in ischemic tissue. This increased binding depends on the duration and severity of cerebral ischemia. Sequential measurements of nimodipine binding may allow the identification of regions with potentially reversible effects of ischemia and the monitoring of their response to therapy.

AB - We investigated the binding properties of the voltage-sensitive calcium channel antagonist nimodipine in a rat model of focal cerebral ischemia. Male Sprague-Dawley rats weighing 250 g underwent occlusion of both the proximal middle cerebral artery and the ipsilateral common carotid artery. 3H-nimodipine (130 Ci/mmol) was infused intravenously and circulated for 30 minutes before the rats were killed at 5 minutes, 4, 24, and 48 hours after occlusion. The brains were removed and examined by autoradiography. We observed a focal increase of nimodipine binding in severely ischemic regions at 5 minutes after occlusion, which also appeared in regions with presumed penumbral blood flow levels at 4 hours after occlusion. We hypothesize that nimodipine binds to activated calcium channels in ischemic tissue. This increased binding depends on the duration and severity of cerebral ischemia. Sequential measurements of nimodipine binding may allow the identification of regions with potentially reversible effects of ischemia and the monitoring of their response to therapy.

M3 - Journal article

C2 - 2175462

VL - 21

SP - IV78-80

JO - Stroke

JF - Stroke

SN - 0039-2499

IS - 12 Suppl

ER -

ID: 14944295