Effects of Calcium Channel Antagonist Flunarizine on Parvalbumin-and Calbindin-immunoreactive Structures in Experimental Spinal Cord Ischemia.
10.11637/kjpa.1998.11.1.49
- Author:
Ki Hyun CHO
1
;
Myeong Kyu KIM
;
Yo Sik KIM
;
Sei Jong KIM
;
Kwang Il NAM
;
Jong Keun KIM
;
Choon Sang BAE
Author Information
1. Department of Neurology, Chonnam University Medical School, Kwangju 501 -190, Korea.
- Publication Type:Original Article
- Keywords:
flunarizine;
Ca 2+ channel antagonist;
parvalbumin;
calbindin. spinal cord ischemia;
immunocytochemistry;
cytochrome oxidase
- MeSH:
Adult;
Animals;
Aorta;
Aorta, Abdominal;
Calbindins;
Calcium Channels*;
Calcium*;
Catheters;
Central Nervous System;
Electron Transport Complex IV;
Extremities;
Flunarizine*;
Humans;
Immunohistochemistry;
Ischemia;
Male;
Neurons;
Perfusion;
Rabbits;
Reperfusion;
Spinal Cord;
Spinal Cord Injuries;
Spinal Cord Ischemia*;
Stroke
- From:Korean Journal of Physical Anthropology
1998;11(1):49-59
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The aortic occlusion spinal stroke model was utilized to examine the neurological and histological effects of flunarizine, a Ca 2+ channel antagonist, in central nervous system ischemia. Spinal cord ischemia was induced in rabbits by infrarenal aortic occlusion with angiographic balloon catheter for 20 minutes. Adult male albino rabbits of local breed were randomly assigned to one of three groups (6 in each group): flunarizine (0.3 mg/kg iv, dissolved in vehicle of 1ml of 40% ethanol) during occlusion of aorta; flunarizine at 30 min after reperfusion; and the vehicle only. At 48 hours after ischemia the hind limb motor function was assessed according to an ordinal grading scale from 0 to 5. Then the animals were sacrificed and fixed with transcardiac perfusion, and the spinal cord were studied for the activity of cytochrome oxidase (CO) and for expression of parvalbumin (PV) and calbindin. Highly reproducible spinal cord injury was produced after 20 min occlusion of infrarenal abdominal aorta. The animals treated with flunarizine either during occlusion or after reperfusion showed significant reductions in hind -limb motor dysfunction. But both flunarizine -treated groups did not differ significantly. Spinal gray matter of the flunarizine -treated animals either during occlusion or after reperfusion retained more CO activities and expressed less PV -and calbindin -immunoreactivities than that of the control. PV -and calbindin -immunoreactive neurons in control group was noted mainly in lamina I -III. Thus, flunarizine administration during occlusion or early after reperfusion reduces the ischemic injury in the spinal cord.
