PRODUCTION OF OXYGEN-FREE RADICALS DURING MYOCARDIAL-INFARCTION TREATED BY THROMBOLYSIS - ANALYSIS OF GLUTATHIONE-PEROXIDASE, SUPEROXIDE-DISMUTASE AND MALONDIALDEHYDE

Citation
T. Beard et al., PRODUCTION OF OXYGEN-FREE RADICALS DURING MYOCARDIAL-INFARCTION TREATED BY THROMBOLYSIS - ANALYSIS OF GLUTATHIONE-PEROXIDASE, SUPEROXIDE-DISMUTASE AND MALONDIALDEHYDE, Archives des maladies du coeur et des vaisseaux, 87(10), 1994, pp. 1289-1296
Citations number
48
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
00039683
Volume
87
Issue
10
Year of publication
1994
Pages
1289 - 1296
Database
ISI
SICI code
0003-9683(1994)87:10<1289:POORDM>2.0.ZU;2-1
Abstract
Many enzyme systems such as glutathione peroxidase (GPx) or superoxide dismutase (SOD) neutralise the oxygen derived free radicals produced during myocardial reperfusion by thrombolysis. Erythrocytic SOD, plasm a and erythrocytic GPx and their cofactor selenium, substances reactin g with thiobarbituric acid (TBARS) were analysed by repeated sampling between T0 and 48 hours in 24 patients treated by thrombolysis for acu te myocardial infarction. Angiographic control was undertaken systemat ically between 60 and 180 minutes after initiating thrombolytic therap y : 18 patients had a patent vessel and 6 patients had an occluded ves sel recanalised in 5 cases by angioplasty. Biological analysis was per formed in the 23 patients successfully revascularised by thrombolysis, eventually completed by angioplasty. The plasma GPx decreased non-sig nificantly between T0 and 2 hours from 246.8 +/- 53.3 to 233 +/- 39 U/ ml with a significant increase between 2 and 48 hours from 233 +/- 39. 2 to 294 +/- 76 U/ml, whereas the erythrocytic GPx rose significantly and constantly between T0 and 48 hours from 34.8 +/- 7.1 to 37.6 +/- 7 .5 U/gHb with significant consumption of selenium between TO and 4 hou rs from 81.2 +/- 14 to 68.5 +/- 12.6 mu g/l. The erythrocytic SOD incr eased significantly between T0 and 48 hours from 318.9 +/- 40.8 to 337 +/- 59 U/gHb. Finally, the analysis of plasma TBARS showed a non-sign ificant rise between T0 and 30 minutes from 1.59 +/- 0.30 to 1.71 +/- 1.43 mm/l with a return to the basic line values after about 2 hours. These results show a significant increase in the activity of enzymes p rotecting against the liberation of oxygen free radicals, such as eryt hrocyte or plasma GPx and erythrocyte SOD between T0 and 48 hours with consumption of selenium, cofactor of GPx, and an increase in circulat ing lipid peroxydes in acute myocardial infarction heated by thromboly sis. They also illustrate the oxidative stress which occurs in this si tuation.