IMPORTANCE OF PLATELETS IN MYOCARDIAL INJURY AFTER REPERFUSION IN THEPRESENCE OF RESIDUAL CORONARY STENOSIS IN DOGS

Citation
G. Rousseau et al., IMPORTANCE OF PLATELETS IN MYOCARDIAL INJURY AFTER REPERFUSION IN THEPRESENCE OF RESIDUAL CORONARY STENOSIS IN DOGS, The American heart journal, 125(6), 1993, pp. 1553-1563
Citations number
43
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00028703
Volume
125
Issue
6
Year of publication
1993
Pages
1553 - 1563
Database
ISI
SICI code
0002-8703(1993)125:6<1553:IOPIMI>2.0.ZU;2-#
Abstract
Residual coronary stenosis is common after successful thrombolysis for acute infarction. We investigated the role of platelets and the influ ence of a residual critical stenosis during early reperfusion in survi val of reperfused myocardium. The left anterior descending coronary ar tery was occluded for 90 minutes and reperfused for 6 hours in 5 group s of dogs, 3 with a residual critical stenosis (groups 1 through 3) an d 2 without (groups 4 and 5). Thrombocytopenia was produced by an anti serum in groups 2, 3, and 5; group 3 was also made neutropenic by anot her antiserum. Platelets (groups 1 and 4) and neutrophils (groups 1, 2 , 4, and 5) labeled with indium 111 were reinjected at occlusion. Coll ateral flow was estimated with radioactive microspheres and was statis tically similar among groups. Infarct size (percentage of area at risk ), revealed by triphenyltetrazolium, was more severe (49.4% +/- 4.0%; p < 0.05) with stenosis (group 1) than without stenosis (group 4: 29.5 % +/- 4.6%). Platelet depletion reduced infarct size in group 2 (28.6% +/- 6.3%; p < 0.05 vs group 1) with stenosis, but not in group 5 with out stenosis (24.5% +/- 6.2% vs group 4: 29.5% +/- 4.6%). Neutropenia (group 3) did not decrease infarct size in thrombocytopenic dogs. Neut rophil accumulations in reperfused myocardium were similar among group s, but platelets accumulated in greater numbers in reperfused infarcts with stenosis (group 1: 338,581 +/- 52,857/gm; p < 0.05) than without stenosis (group 4: 153,445 +/- 23,949/gm). Therefore a critical steno sis at reperfusion compromises myocardial salvage and increases infarc t size by means of a platelet-mediated mechanism.