SERUM TROPONIN-T, MALONDIALDEHYDE AND NITRITE IN MYOCARDIAL INFARCTION-REPERFUSION

Citation
J. Antani et al., SERUM TROPONIN-T, MALONDIALDEHYDE AND NITRITE IN MYOCARDIAL INFARCTION-REPERFUSION, Medical science research, 24(8), 1996, pp. 545-547
Citations number
23
Categorie Soggetti
Medicine, Research & Experimental
Journal title
ISSN journal
02698951
Volume
24
Issue
8
Year of publication
1996
Pages
545 - 547
Database
ISI
SICI code
0269-8951(1996)24:8<545:STMANI>2.0.ZU;2-8
Abstract
To understand whether there was any fresh myocardial damage at reperfu sion, serum malondialdehyde (MDA, an index of Lipid peroxidative damag e caused by oxygen-foe radicals), serum troponin-T levels (to recognis e the myocardial damage) and serum nitrite levels (as an index of nitr ic oxide generation) were studied in 10 acute myocardial infarction pa tients for 10 h following administration of TV streptokinase (1.5 mill ion units in saline in 30 min). These parameters were compared with th ose studied over the same period in similar patients without streptoki nase treatment and with healthy controls. The appearance of frequent a nd significant arrythmias was noted within 2 h in all the patients who received streptokinase and was taken as an index of successful thromb olysis. In these patients, serum troponin-T had increased by 6-fold at the end of 2 h and 12 fold at the end of 10 h, along with a significa nt rise in serum MDA levels at both these times. Serum nitrite levels increased only at the end of 10 h. There were only marginal elevations in the levels of serum troponin-T and MDA, without any significant ch ange in serum nitrite in patients who did not receive thrombolytic the rapy, at the times mentioned above. These results suggest the occurren ce of fresh myocardial damage at the time of reperfusion and subsequen tly by the uninhibited, infiltrated neutrophils, consequent to the end othelial damage. The increased serum nitrite levels were thought to be due to the nitric oxide produced by the induced nitric oxide synthase in the neutrophils. This might promote vasodilation and inhibition of platelet aggregation, preventing reocclusion.