Transplantation-induced functional/morphological changes in rat aorta allografts differ from those in arteries of rat kidney allografts

被引:10
作者
Andriambeloson, E [1 ]
Cannet, C [1 ]
Pally, C [1 ]
Klanke, B [1 ]
Bruns, C [1 ]
Zerwes, HG [1 ]
Bigaud, M [1 ]
机构
[1] Novartis Pharma AG, Transplantat Res Global Business Unit, Basel, Switzerland
关键词
aorta allograft; chronic graft arteriosclerosis; kidney allograft; rat; vascular function;
D O I
10.1046/j.1600-6143.2003.00319.x
中图分类号
R61 [外科手术学];
学科分类号
摘要
The functional/morphological changes observed in rat aorta allografts were compared with those seen in the arteries of rat kidney allografts. Untreated allografts (F344-to-LEW) were collected at various times post-transplantation (Tx). Vascular smooth muscle cell (SMC) constriction to phenylephrine (Phe) and endothelial cell (EC)-dependent relaxation to acetylcholine (Ach) were assessed. Neointima formation in graft vessels was assessed by histology. In aorta allografts, the effects of Phe and Ach were irreversibly abolished within 3-2 weeks post-Tx. Neointima formation was consistently detected between 4 and 8 weeks post-Tx. In kidney allografts, sign of vasculopathy was seen in 10, 30 and 40% of resistance arteries at 8, 16 and 33 weeks post-Tx, respectively. In the main renal artery, substantial neointima formation was not apparent before 33 weeks post-Tx, the vasoconstrictor effect of Phe was fully maintained until then, and Ach-induced vasorelaxation was irreversibly reduced by approximately 70% from week 2 post-Tx onwards. These results indicate that the post-Tx functional/ morphological changes seen in aorta allografts do not reflect those seen in arteries of kidney allografts. Hence, renal arteries from rat kidney allografts can be considered as a more relevant model to study the cascade of events leading to Tx-induced CGA in solid organ allografts.
引用
收藏
页码:188 / 195
页数:8
相关论文
共 33 条
[1]  
Akyurek LM, 1996, TRANSPLANTATION, V62, P1526
[2]  
Akyurek LM, 1996, AM J PATHOL, V149, P1981
[3]   Transplantation-induced endothelial dysfunction as studied in rat aorta allografts [J].
Andriambeloson, E ;
Pally, C ;
Hengerer, B ;
Cannet, C ;
Nikolova, Z ;
Bruns, C ;
Zerwes, HG ;
Bigaud, M .
TRANSPLANTATION, 2001, 72 (12) :1881-1889
[4]   Endothelial dysfunction and denudation in rat aortic allografts [J].
Andriambeloson, E ;
Bigaud, M ;
Schraa, EO ;
Kobel, T ;
Lobstein, V ;
Pally, C ;
Zerwes, HG .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2001, 21 (01) :67-73
[5]   Complete loss of functional smooth muscle cells precedes vascular remodeling in rat aorta allografts [J].
Bigaud, M ;
Schraa, EO ;
Andriambeloson, E ;
Lobstein, V ;
Pally, C ;
Kobel, T ;
Bruns, C ;
Zerwes, HG .
TRANSPLANTATION, 1999, 68 (11) :1701-1707
[6]   PREDICTION OF CREATININE CLEARANCE FROM SERUM CREATININE [J].
COCKCROFT, DW ;
GAULT, MH .
NEPHRON, 1976, 16 (01) :31-41
[7]   Early endothelial dysfunction predicts the development of transplant coronary artery disease at 1 year posttransplant [J].
Davis, SF ;
Yeung, AC ;
Meredith, IT ;
Charbonneau, F ;
Ganz, P ;
Selwyn, AP ;
Anderson, TJ .
CIRCULATION, 1996, 93 (03) :457-462
[8]   Characterization of endothelial factors involved in the vasodilatory effect of simvastatin in aorta and small mesenteric artery of the rat [J].
de Sotomayor, MA ;
Herrera, MD ;
Marhuenda, E ;
Andriantsitohaina, R .
BRITISH JOURNAL OF PHARMACOLOGY, 2000, 131 (06) :1179-1187
[9]   PROGRESSIVE ALBUMINURIA AND GLOMERULOSCLEROSIS IN A RAT MODEL OF CHRONIC RENAL-ALLOGRAFT REJECTION [J].
DIAMOND, JR ;
TILNEY, NL ;
FRYE, J ;
DING, G ;
MCELROY, J ;
PESEKDIAMOND, I ;
YANG, H .
TRANSPLANTATION, 1992, 54 (04) :710-716
[10]   RESPONSES OF CORONARY-ARTERIES OF CARDIAC TRANSPLANT PATIENTS TO ACETYLCHOLINE [J].
FISH, RD ;
NABEL, EG ;
SELWYN, AP ;
LUDMER, PL ;
MUDGE, GH ;
KIRSHENBAUM, JM ;
SCHOEN, FJ ;
ALEXANDER, RW ;
GANZ, P .
JOURNAL OF CLINICAL INVESTIGATION, 1988, 81 (01) :21-31