계명대학교 의학도서관 Repository

활성산소로 손상된 심장에 대한 교감신경계의 영향

Metadata Downloads
Author(s)
송영성김수경
Keimyung Author(s)
Kim, Soo Kyung
Department
Dept. of Pharmacology (약리학)
Journal Title
순환기
Issued Date
1996
Volume
26
Issue
1
Keyword
Adrenergic blocking agentOxygen free radical
Abstract
Background It is now well
known that oxygen free radicals act as mediators of cellular injury in many cardiovascular diseases. Although some evidences have been presented for an altered number of adrenergic receptors in heart disease, a detailed examination of the interaction of free radicals with cardiac adrenergic receptors has little been carried out.


Methods

This study is therefore undertaken to examine the influences of adrenergic blocking agents(propranolol, prazosin) and cyclooxygenase inhibitor(aspirin) on the cardiac damage by oxygen free radicals. Ischemic condition of the isolated rat heart was made by Langendorff preparation, and then measured superoxide dismutase(SOD), lactate dehydrogenase(LDH) released in the perfusate, and malondialdhyde(MDA) concentration in the cardiac tissue.


Results

We obtained the results that increased SOD activity and tendency of decreased LDH activity by the pretreatment of propranolol, prazosin, and aspirin in cardiac ischemic-reperfusion injury. Those effects were more predominant in adriamycin treated group comparing with not treated group.


Conclusion

Adrenergic blocking agent, propranolol, prazosin, and aspirin seem to have some protective effect on the reperfusion injury of the heart.






Keywords: Adrenergic blocking agent; Oxygen free radical
Alternative Title
Adrenergic Effects on the Cardiac Damage by Oxygen Free Radicals
Keimyung Author(s)(Kor)
김수경
Publisher
School of Medicine
Citation
송영성 and 김수경. (1996). 활성산소로 손상된 심장에 대한 교감신경계의 영향. 순환기, 26(1), 112–123.
Type
Article
ISSN
1225-164X
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/36723
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Pharmacology (약리학)
공개 및 라이선스
  • 공개 구분공개
파일 목록

Items in Repository are protected by copyright, with all rights reserved, unless otherwise indicated.