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