Growth factors and myointimal hyperplasia in experimental aortic allografts.
OBJECTIVE
To analyse the role of growth factors (platelet derived growth factor, PDGF; basic fibroblast growth factor, bFGF; interleukin 1, IL-1) in the genesis of myointimal hyperplasia in arterial allografts.


METHODS
Two groups of experiments were performed: isografts and allografts. The isograft group consisted of 15 inbred Lewis rats in which a 1 cm long segment of aorta was inserted as an abdominal aortic interposition graft. The aortic segments were obtained from syngenic Lewis rats. The allograft group consisted of 15 inbred Lewis rats, in which a 1 cm long segment of aorta was interposed at the abdominal aorta level. The aortic segments were obtained from allogenic Brown-Norway rats.


METHODS
The animals were killed 4 weeks after surgery and were analysed by morphometric analysis (n = 3 for each group). In addition, production of PDGF, bFGF and IL-1 by aortic segments (n = 12 for each group) in organ culture was assessed.


RESULTS
Allografts had more myointimal hyperplasia, than isografts (p < 0.05). PDGF and bFGF production, generally considered to be the cause of myointimal hyperplasia, was not increased in allografts. IL-1 production was higher in allografts (p < 0.001).


CONCLUSIONS
Myointimal hyperplasia in aortic allografts is dependent on growth factors produced by the graft itself. These growth factors are different from PDGF and bFGF that generally have been implicated in the genesis of naturally occurring myointimal hyperplasia and atherosclerosis. IL-1 may have a principal role in the genesis of myointimal hyperplasia in arterial allografts.
Randone
B
B
Department of Surgery, University of Rome, La Sapienza, Italy.
Sterpetti
A V
AV
Stipa
F
F
Proietti
P
P
Aromatario
C
C
Guglielmi
M B
MB
Palestini
M
M
Santoro-D'Angelo
L
L
Cavallaro
A
A
Cucina
A
A
D016475:3T3 Cells / Q000378:metabolism / Q000473:pathology; D000818:Animals; D001011:Aorta / Q000637:transplantation*; D001012:Aorta, Abdominal / Q000473:pathology / Q000503:physiopathology / Q000601:surgery*; D004714:Endometrial Hyperplasia / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006133:Growth Substances / Q000502:physiology*; D007375:Interleukin-1 / Q000096:biosynthesis; D051379:Mice; D008934:Mitogens / Q000096:biosynthesis; D051381:Rats; D011917:Rats, Inbred Lew; D017539:Tunica Intima / Q000473:pathology* / Q000503:physiopathology; D014654:Vascular Patency
D006133:Growth Substances; D007375:Interleukin-1; D008934:Mitogens