INJURY IN A TRANSIENTLY OCCLUDED CORONARY-ARTERY INCREASES MYOCARDIALNECROSIS - EFFECT OF ASPIRIN

Citation
Ja. Barrabes et al., INJURY IN A TRANSIENTLY OCCLUDED CORONARY-ARTERY INCREASES MYOCARDIALNECROSIS - EFFECT OF ASPIRIN, Pflugers Archiv, 432(4), 1996, pp. 663-670
Citations number
34
Categorie Soggetti
Physiology
Journal title
ISSN journal
00316768
Volume
432
Issue
4
Year of publication
1996
Pages
663 - 670
Database
ISI
SICI code
0031-6768(1996)432:4<663:IIATOC>2.0.ZU;2-D
Abstract
This study tested the hypothesis that intimal injury in a transiently occluded coronary artery limits myocardial salvage, The effect of inti mal injury on reactive hyperaemia was investigated in 17 pigs submitte d to a 30-min occlusion of the left anterior descending coronary arter y (LAD), not resulting in myocardial infarction. Catheter-induced inti mal damage increased local platelet deposition (Tc-99m) and reduced hy peraemia, but did not modify myocardial platelet or polymorphonuclear leucocyte content (myeloperoxidase activity) after 6 h reperfusion. To investigate the influence of intimal injury on the extent of myocardi al necrosis secondary to a more prolonged coronary occlusion, and the role of platelets on this influence, 52 pigs were submitted to a doubl e randomization (2x2 factorial design) to 250 mg i.v. aspirin vs. plac ebo and to coronary intimal injury vs. no coronary damage before a 48- min occlusion of the LAD and 6 h of reperfusion. After excluding 12 an imals with reocclusion, coronary intimal injury was associated with la rger infarcts (triphenyltetrazolium reaction) in animals receiving pla cebo (36.2+/-7.0% of the area at risk in animals with intimal injury v s. 10.81+/-3.9% in animals without coronary injury, P=0,006) but not i n those receiving aspirin (20.3+/-6.5 vs. 21.7+/-6.5% of the area at r isk in animals with and without intimal injury respectively). These re sults suggest that coronary intimal injury in the reperfused artery ma y have adverse effects on myocardial salvage by mechanisms other than reocclusion or embolization of platelet aggregates.