|
|
||||||||
The Annals of Thoracic Surgery, Vol 58, 170-175, Copyright © 1994 by The Society of Thoracic Surgeons
KB Kim, HH Chung, MS Kim and JR Rho
It is known that reperfusion of the ischemic myocardium may intensify
damage and increase the extent of myocardial necrosis. Oxygen free radicals
and their metabolites have been implicated as possible elements in
myocardial ischemia-reperfusion injury. In this study in cyanotic patients
undergoing open heart operation for tetralogy of Fallot, the myocardial
tissue activities of catalase, superoxide dismutase, glutathione
peroxidase, and lactate dehydrogenase were determined together with the
tissue contents of malondialdehyde, oxidized glutathione, and total
glutathione using the spectrophotometric assay method. The tissue
activities of catalase, superoxide dismutase, and glutathione peroxidase
increased significantly after myocardial reperfusion (p < 0.05) when
compared with the tissue activities of the control group (myocardial tissue
taken immediately after aortic cross-clamping). The tissue content of
malondialdehyde increased significantly after reperfusion (p < 0.05),
but the tissue activity of lactate dehydrogenase and the ratio of oxidized
glutathione to total glutathione showed an insignificant difference after
reperfusion. These data suggest that peroxidation of the cardiac lipids was
triggered by the reperfusion of the hypoxic heart, but the myocardial
cellular damage was not significant enough to decrease the myocardial
lactate dehydrogenase and total glutathione levels. These results also
suggest that oxygen free radicals may play an important role in in-vivo
myocardial reperfusion stress, but endogenous self-defensive enzyme systems
to protect the cell against the cytotoxic oxygen metabolites also were
triggered, and the resulting myocardial cellular damage was insignificant.
ARTICLES
Changes in the antioxidative defensive system during open heart operations in humans
Department of Thoracic and Cardiovascular Surgery, College of Medicine, Seoul National University, Korea.
This article has been cited by other articles:
![]() |
N. R. Sodha, R. T. Clements, J. Feng, Y. Liu, C. Bianchi, E. M. Horvath, C. Szabo, and F. W. Sellke The effects of therapeutic sulfide on myocardial apoptosis in response to ischemia-reperfusion injury Eur. J. Cardiothorac. Surg., May 1, 2008; 33(5): 906 - 913. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. B. Sharma, J. Sun, L. L. Howard, A. G. Williams Jr., and R. T. Mallet Oxidative stress reversibly inactivates myocardial enzymes during cardiac arrest Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H198 - H206. [Abstract] [Full Text] [PDF] |
||||
![]() |
Q.-D. Wang, J. Pernow, P.-O. Sjoquist, and L. Ryden Pharmacological possibilities for protection against myocardial reperfusion injury Cardiovasc Res, July 1, 2002; 55(1): 25 - 37. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Rahman, B. Ustunda, O. Burma, I. H. Ozercan, A. Cekirdekci, and M. K. Bayar Does aprotinin reduce lung reperfusion damage after cardiopulmonary bypass? Eur. J. Cardiothorac. Surg., November 1, 2000; 18(5): 583 - 588. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Nagashima, G. Nollert, U. Stock, J. Sperling, S. Hatsuoka, D. Shum-Tim, K. Takeuchi, A. Nedder, and J. E. Mayer Jr Cardiac performance after deep hypothermic circulatory arrest in chronically cyanotic neonatal lambs J. Thorac. Cardiovasc. Surg., August 1, 2000; 120(2): 238 - 246. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. L. Park and B. R. Lucchesi Mechanisms of myocardial reperfusion injury Ann. Thorac. Surg., November 1, 1999; 68(5): 1905 - 1912. [Abstract] [Full Text] [PDF] |
||||
| 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 |