THE SPATIAL AND TEMPORAL DISTRIBUTION OF INSULIN-LIKE GROWTH-FACTOR-IFOLLOWING EXPERIMENTAL MYOCARDIAL-INFARCTION IN THE RAT

Citation
Rv. Krishnamurthi et al., THE SPATIAL AND TEMPORAL DISTRIBUTION OF INSULIN-LIKE GROWTH-FACTOR-IFOLLOWING EXPERIMENTAL MYOCARDIAL-INFARCTION IN THE RAT, Cardiovascular pathology, 6(4), 1997, pp. 197-203
Citations number
40
Categorie Soggetti
Pathology,"Cardiac & Cardiovascular System
Journal title
ISSN journal
10548807
Volume
6
Issue
4
Year of publication
1997
Pages
197 - 203
Database
ISI
SICI code
1054-8807(1997)6:4<197:TSATDO>2.0.ZU;2-D
Abstract
Insulin-like growth factor-1 (IGF-1) is believed to be involved in the repair and adaptation that follow ischemic injury to the myocardium. The aim of this study was to elucidate the role of IGF-I by defining t he changes that occur in its distribution following regional myocardia l infarction. The left anterior descending coronary artery was ligated in adult male Wistar rats, and hearts were examined microscopically f rom 6 hours to 20 days later. IGF-I was identified histochemically usi ng the avitin-biotin-peroxidase method with a polyclonal antibody to I GF-1 and was quantified by optical density measurements of standard fi elds in sections of hearts prepared in a single batch. Immunoreactivit y was located in the cytoplasm of viable myocytes, vascular smooth mus cle cells, mast cells, leukocytes, endothelial cells, and fibroblasts. The zone of viable myocardium immediately adjacent to infarcts reacte d significantly more intensely for IGF-1 than all other regions at all stages, with a maximum optical density (617% higher than sham-operate d control myocardium, p<.001) 24 hours after coronary artery ligation. Immunoreactivity in myocardium tissue distant from the infarcts also increased during the first day (382% at 24 hours), but this increase w as not statistically significant thereafter. These temporal and spatia l changes in the distribution and amount of IGF-1 indicate that this f inding is predominantly associated with a localized response to injury by the viable myocytes adjacent to infarcts. (C) 1997 by Elsevier Sci ence Inc.