The Effect of D,L-6,8-Thioctic Acid on the Volume of Cerebral Infarction in Ischemic Rat Model.
- Author:
Hyeong Joong YI
1
;
Sang Gu LEE
;
Woo Taek RHEE
;
Kwang Myung KIM
;
Young Soo KIM
;
Yong KO
Author Information
1. Department of Neurosurgery, Hanyang University Medical College, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Antioxidant;
Reperfusion;
Rat model;
D,L-6,8-Thioctic acid;
Cerebral infarction;
Neuroprotective agents
- MeSH:
Animals;
Brain;
Cerebral Infarction*;
Hemodynamics;
Infarction;
Models, Animal*;
Neurologic Examination;
Neuroprotective Agents;
Rats*;
Rats, Sprague-Dawley;
Reperfusion;
Reperfusion Injury
- From:Journal of Korean Neurosurgical Society
2002;32(4):363-370
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: The authors demonstrate neuroprotective effects of antioxidant in reperfusion injury using ischemic rat model and evaluate the clinical eligibility of this agent to ischemic cerebrovascular diseases. METHODS: Rat model was made according to Longa method. Thirty-six Sprague-Dawley rats were used and were equally divided into three groups;A) treated subcutaneously with D,L-6,8-Thioctic acid 30 minutes before occlusion, B) within one hour after occlusion, and C) with vehicle only. Neurologic examination was performed immediately and 24 hours after reperfusion. Twenty-four hours after reperfusion, brains were extracted and stained with 2% 2,3,5-Triphenyltetrazolim chloride in 2mm-thickness section. Then, fixed sections were digitalized and used for infarct area calculation. RESULTS: There was no significant statistical difference in recorded hemodynamic and physiologic parameters between three groups. The neurologic status taken immediately following reperfusion were A) 2.67+/-0.492, B) 2.75+/-0.452, and C) 2.83+/-0.389, and were improved to A) 1.67+/-0.898, B) 1.92+/-0.900, and C) 2.08+/-0.793 just before sacrificing. However, there was no statistically significant difference between three groups. Mean volume of cerebral infarction was A) 9.5+/-1.67%, B) 10.4+/-1.58%, and C) 11.3+/-1.12% with no significant difference. Any specific correlation between the neurologic status and the mean infarction volume was not observed. CONCLUSION: Any single agent does not seem to reduce the infarction volume holistically, therefore, the incoming therapeutic target should be the development of versatile neuroprotective agents or the selection of preexisting synergistic compounds without compromising patients' safety.
