허혈 및 저산소 전조건화가 신생 백서의 저산소-허혈 뇌손상에 미치는 보호 효과: 수소 자기 공명 분광법을 이용한 연구

Background: A brief episode of cerebral ischemia confers transient ischemic tolerance to a subsequent ischemic challenge. We examined the effect of ischemic and hypoxic preconditioning in the neonatal rat. Methods: Seven-day old Sprague-Dawley rat pups were divided into three groups:control (n = 53)...

Full description

Saved in:
Bibliographic Details
Published inKorean journal of anesthesiology pp. 188 - 197
Main Authors 정성문, 정화성, 최재문, 방지연, 임근호, 박평환
Format Journal Article
LanguageKorean
Published 대한마취통증의학회 01.02.2006
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Background: A brief episode of cerebral ischemia confers transient ischemic tolerance to a subsequent ischemic challenge. We examined the effect of ischemic and hypoxic preconditioning in the neonatal rat. Methods: Seven-day old Sprague-Dawley rat pups were divided into three groups:control (n = 53), ischemic preconditioning (n = 51), and hypoxic preconditioning (n = 48). For ischemic preconditioning, the right common carotid artery was occluded for 10 min. Rats in the hypoxic preconditioning group were kept under hypoxic (8% oxygen/92% nitrogen) conditions for 4h. Twenty-four hours after the preconditioning, rats from all groups were exposed to the right common carotid artery ligature, followed by 2.5 h of hypoxia. Lipid/N-acetyl aspartate (Lip/NAA) and lipid/creatine (Lip/Cr) ratios from 1H MR spectroscopy and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) were evaluated as measures of apoptosis 1 and 7 days after hypoxic-ischemic injury. Results: In the ischemic and hypoxic preconditioning groups, the Lip/NAA and Lip/Cr ratios and the numbers of TUNEL- positive cells were significantly lower than those in the control group (P < 0.05), but there were no significant differences between the two preconditioning groups. Conclusions: These results suggest that ischemic and hypoxic preconditioning in the neonatal rat attenuate the apoptosis that is caused by hypoxic-ischemic brain injury. (Korean J Anesthesiol 2006; 50: 188~97) KCI Citation Count: 0
Bibliography:G704-000679.2006.50.2.021
ISSN:2005-6419
2005-7563