JTCS Speed Up Your Browser
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zhen, R.
Right arrow Articles by Xiaoqing, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhen, R.
Right arrow Articles by Xiaoqing, Y.

J Thorac Cardiovasc Surg 1994;108:126-133
© 1994 Mosby, Inc.

CARDIOPULMONARY BYPASS,
MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Mechanisms of brain injury with deep hypothermic circulatory arrest and protective effects of coenzyme Q10

Ren Zhen, MD, Ding Wenxiang, MD, Su Zhaokang, MD, Gu Xinling, MD, Huang Huiming, MD, Liu Jingfeng, MD, Yan Qing, MB, Zhang Weizhong, MB, Yu Xiaoqing, EB


Shanghai, People's Republic of China

From the Department of Pediatric Cardiothoracic Surgery, Xinhua Hospital, Shanghai Second Medical University, Shanghai, People's Republic of China.

Received for publication Aug. 4, 1993. Accepted for publication Dec. 14, 1993. Address for reprints: Ren Zhen, MD, Department of Cardiothoracic Surgery, Nanjing Children's Hospital, Nanjing 210008, People's Republic of China.

Abstract

Sixteen dogs, divided randomly into a control group and coenzyme Q10 group (10mg/kg, intraperitoneally before the operation), underwent deep hypothermic circulatory arrest with cardiopulmonary bypass, as is done clinically. At four time points cerebral cortex and cerebrospinal fluid specimens were collected to study free radical formation, energy metabolism, and ultrastructure. During cardiopulmonary bypass cerebral electron spin resonance spectra and malondialdehyde contents were progressively higher than before bypass, especially at the 60 minutes of circulatory arrest and 30 minutes of reperfusion (p1 < 0.01, p2 < 0.05). In the coenzyme Q10 group at the latter two time points, they had increased less than in the control group at same time points (p1 < 0.02, p2 < 0.005). Adenosine triphosphate content in the cortex during bypass decreased gradually from the prebypass level (p1 < 0.02, p2 = p3 < 0.001), while lactate in cerebrospinal fluid increased (p1 < 0.05, p2 = p3 < 0.001). In the coenzyme Q10 group, adenosine triphosphate at the latter two time points was greater than that in the control group (p1 = p2 < 0.05), while the lactate changes were not significantly different from control at each time point (all p > 0.05). Ultrastructure of the cortex was normal before bypass and almost normal during bypass, but it was obviously abnormal at 60 minutes of circulatory arrest and more seriously abnormal at 30 minutes of reperfusion. In the coenzyme Q10 group the abnormality was obviously reduced. The results suggest that oxygen-derived free radicals and abnormal energy metabolism might play critical roles in brain ischemia/reperfusion injury. Coenzyme Q10 could protect the brain by improving cerebral metabolism. (J THORACCARDIOVASCSURG1994;108:126-33)






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS
Copyright © 1994 by The American Association for Thoracic Surgery.