Basic fibroblast growth factor caused no change in collateral flow or infarct size of acutely-infarcted myocardium in rats.

The extent to which local administration of basic fibroblast growth factor (bFGF) increased regional myocardial blood flow (Qm) to acutely-infarcted areas of the heart, thereby mediating myocardial salvage, was examined in this study. Myocardial infarction was induced in two groups of rats by ligation of the left coronary artery. The bFGF group (n = 16) received 100 microg bFGF in physiological saline by intramyocardial injection into the infarcted area, while the control group (n = 7) received only saline. The rats were then maintained for four weeks. Among the controls, Qm decreased in the infarcted areas to 6.5+/-6.7% of that in the noninfarcted areas immediately after coronary ligation, then increased to 11.5+/-8.6% during the four-week maintenance period. In the bFGF group, Qm immediately decreased to 17.5+/-14.7% following ligation and remained stable thereafter (18.3+/-9.1%). There were no significant differences between the bFGF and control groups with respect to Qm, the number of viable myocardial cells or the extent of myocardial fibrosis. In this study we failed to show any significant effect of bFGF on coronary angiogenesis in acutely-ischemic myocardium in rats. Application of bFGF using different dosage, different routes of administration, measuring new capillaries morphologically will be needed to confirm the present negative results.