Aprotinin Preserves Cellular Junctions and Reduces Myocardial Edema After Regional Ischemia and Cardioplegic Arrest
Author(s) -
Tanveer Khan,
Cesario Bianchi,
Eugênio Gonçalves de Araújo,
Pierre Voisine,
Shuhua Xu,
Jun Feng,
Jian Li,
Frank W. Sellke
Publication year - 2005
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.104.526053
Subject(s) - aprotinin , medicine , anesthesia , ischemia , cardiopulmonary bypass , thrombin , edema , pharmacology , cardiology , platelet
Cardiac surgery with cardiopulmonary bypass (CPB) and cardioplegic arrest has been associated with myocardial edema attributable to vascular permeability, which is regulated in part by thrombin-induced alterations in cellular junctions. Aprotinin has been demonstrated to prevent activation of the thrombin protease-activated receptor, and we hypothesized that aprotinin preserves myocardial cellular junctions and prevents myocardial edema in a porcine model of regional ischemia and cardioplegic arrest.
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