The Effect of Nitric Oxide Synthase Inhibition in Reperfusion Injury of Rat Brain.
- Author:
Tai Hyung CHO
1
;
Jung Yul PARK
;
Heung Seob CHUNG
;
Youn Kwan PARK
;
Ki Chan LEE
;
Hoon Kap LEE
Author Information
1. Department of Neurosurgery, College of Medicine, Korea University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Nitric oxide synthase;
Reperfusion injury;
L-NAME;
L-arginine;
Caudate
- MeSH:
Adult;
Animals;
Arginine;
Blood Pressure;
Brain Ischemia;
Brain*;
Central Nervous System;
Cerebral Cortex;
Excitatory Amino Acids;
Humans;
Hydrogen;
Ischemia;
Models, Animal;
Neurons;
Neuroprotective Agents;
NG-Nitroarginine Methyl Ester;
Nitric Oxide Synthase*;
Nitric Oxide*;
Rats*;
Rats, Sprague-Dawley;
Reperfusion Injury*;
Reperfusion*
- From:Journal of Korean Neurosurgical Society
1996;25(11):2155-2164
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Excitatory amino acids play a crucial role in the initiation of various pathophysiological events that ultimately lead to neuronal death during cerebral ischemia. Nitric oxide(NO) is an important messenger molecule which has been implicated in various physiological functions in periphery as well as central nervous system. This study was designed to examine the neuroprotective effects of NO synthase inhibitor in a rat model of focal cerebral ischemia. Halothane-anesthetized, mechanically ventilated adult Sprague-Dawley rats underwent one hour of right middle cerebral artery(MCA) occlusion and three hours of reperfusion after they were randomly assigned to receive either intravenous Nw-nitro-L-arginine methyl ester(L-NAME:10mg/kg, n=10 in each group) before and during the ischemic procedure or L-NAME plus L-arginine(300mg, n=10) and control group which received the equal volume of diluent(saline 3 mg/kg/hr, n=10). Continuous monitoring of blood pressure was made and serial cerebral blood flow(CBF) measurements were performed by hydrogen clearence and ischemic injury volume was calculated by 2,3,5-triphenyl tetrazolium chloride(TTC) staining. CBF decreased to the nearly same extent as the initial MCA occlusion and progressively recovered during ischemia. There were no difference between those groups that received L-NAME and those that did not. Injured volume of ischemic brains in L-NAME treated groups before and during MCA occlusion(mean 55+/-16%) were smaller than saline(81+/-9%) or L-NAME with L-Arginine treated groups(83+/-24%) in caudate area but there were no differences in the cerebral cortex area(p<0.05). These data indicated that inhibition of NO synthase by L-NAME protected the transient focal ischemic injury in caudate region and were not correlated to the CBF or blood pressure changes.
