REINJURY OF ARTERIAL LESIONS INDUCES INTIMAL SMOOTH-MUSCLE CELL REPLICATION THAT IS NOT CONTROLLED BY FIBROBLAST GROWTH-FACTOR-2

In this study we have examined the response of rat carotid arteries wi th intimal lesions to an angioplasty injury. Rat carotid arteries were subjected to injury with a 2F Fogarty catheter (first injury), and 28 days later the same arteries were subjected to reinjury with a 1.5-mm -diameter coronary dilation catheter (second injury) or a sham operati on. After the second injury, the injured arterial surfaces were covere d by a platelet monolayer, with occasional small thrombi. The size of the intimal area was significantly increased 28 days after the second injury, although the luminal area was not changed at this time. Intima l and medial cell replication, measured by 5-bromo-2'-deoxyuridine lab eling, was significantly increased at 2 days after the second injury b ut was markedly reduced by 7 days. Addition of fibroblast growth facto r-2 (FGF2, 60 mu g IV) did not increase smooth muscle cell (SMC) repli cation in arteries subjected to the second injury, and replication was not inhibited with an antibody against FGF2 (120 mg IV). Both these r eagents, however, did significantly affect SMC replication in normal c arotid arteries subjected to Fogarty catheter injury. In a similar man ner, heparin (888 UPS units/kg body wt IV) did not inhibit cell replic ation after second injury, although it did suppress SMC replication af ter a single injury. One conclusion is that rat intimal cells in vivo are different from medial SMCs and that other, as-yet-unknown, factors are important for their proliferation.