Basic fibroblast growth factor increased regional myocardial blood flow and limited infarct size of acutely infarcted myocardium in dogs.

Abstract

Basic fibroblast growth factor (bFGF), a growth factor potent in promoting angiogenesis, has been shown to reduce infarct size in experimentally induced acute myocardial infarction. However, the effect of bFGF on regional myocardial blood flow (Qm) in the acutely infarcted myocardium has not been well clarified. In 20 open-chest dogs, the left anterior descending (LAD) coronary artery was occluded and animals were maintained in this condition for 4 weeks. In eight of these dogs, bFGF (300 microg) was injected into the myocardium supplied by the LAD and the artery was ligated (bFGF group), and in the other 12 dogs, saline was injected (control group). Nonradioactive colored microspheres were used to measure Qm. The amount of viable myocardium as percent of visual field in the microscope and the extent of fibrosis scored histologically from 0 to 5 in the infarcted area 4 weeks after occlusion were measured. In the outer layer, the Qm values immediately after and 4 weeks after occlusion were 26 +/- 2% and 70 +/- 6%, respectively, in the control group, and 46 +/- 5% and 121 +/- 13%, respectively, in the bFGF group. The Qm at both times in the bFGF group was significantly higher than the corresponding control group values (p < 0.01). The Qm at 4 weeks in the inner and the middle layers also significantly increased in the bFGF group. There was more viable myocardium (control vs bFGF group; 41 +/- 5 vs 61 +/- 7%, p < 0.05) and less fibrosis (3.1 +/- 0.2 vs 2.0 +/- 0.4, p < 0.01) at the outer layer in the bFGF group. It was found that bFGF caused a marked increase in Qm, an increase of viable myocardium, and a decrease of fibrosis in the infarcted myocardium in dogs.