ANGIOPEPTIN INHIBITS INTIMAL HYPERPLASIA AFTER ANGIOPLASTY IN PORCINE CORONARY-ARTERIES

被引:77
作者
SANTOIAN, EC
SCHNEIDER, JE
GRAVANIS, MB
FOEGH, M
TARAZONA, N
CIPOLLA, GD
KING, SB
机构
[1] EMORY UNIV,SCH MED,DEPT MED,DIV CARDIOL,ANDREAS GRUENTZIG CARDIOVASC CTR,ATLANTA,GA 30322
[2] EMORY UNIV,SCH MED,DEPT RADIOL,ATLANTA,GA 30322
[3] EMORY UNIV,SCH MED,DEPT PATHOL,ATLANTA,GA 30322
[4] GEORGETOWN UNIV,MED CTR,SCH MED,DEPT SURG,WASHINGTON,DC 20007
关键词
ANGIOPEPTIN; ANGIOPLASTY;
D O I
10.1161/01.CIR.88.1.11
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background. Restenosis is mediated by uncontrolled neointimal growth at the site of coronary angioplasty. Angiopeptin is an octapeptide analogue of somatostatin that has been shown to decrease the experimental intimal hyperplasia associated with vascular injury in rats and rabbits. The study purpose was to determine if angiopeptin inhibits the development of intimal hyperplasia in normolipemic swine coronary arteries after overstretch-balloon injury. Methods and Results. Overstretch-balloon injury was performed in normolipemic swine coronary arteries using a 3.5-mm angioplasty balloon. Treated animals received angiopeptin (50 mug/kg) 1 hour before and at the time of balloon injury. Angiopeptin was administered at 100 (mug/kg)/day SQ in two divided doses for 14 days. Animals were killed at 14 and 28 days (2 weeks after cessation of angiopeptin) after balloon injury. Treatment animals were compared with control animals receiving balloon injury alone. Angiopeptin significantly limited the experimental intimal hyperplasia estimated by the maximal intimal thickness and residual lumen (lumen area/lumen area+intimal area) compared with controls. Conclusions. Angiopeptin inhibits the development of intimal hyperplasia in swine coronary arteries after balloon injury. The beneficial effect was detectable 2 weeks after cessation of angiopeptin therapy.
引用
收藏
页码:11 / 14
页数:4
相关论文
共 14 条
[1]   STIMULATION OF A MEMBRANE TYROSINE PHOSPHATASE-ACTIVITY BY SOMATOSTATIN ANALOGS IN RAT PANCREATIC ACINAR-CELLS [J].
COLAS, B ;
CAMBILLAU, C ;
BUSCAIL, L ;
ZEGGARI, M ;
ESTEVE, JP ;
LAUTRE, V ;
THOMAS, F ;
VAYSSE, N ;
SUSINI, C .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1992, 207 (03) :1017-1024
[2]  
CONTE JV, 1989, TRANSPLANT P, V21, P3686
[3]   A DILEMMA FOR THE 1990S - CHOOSING APPROPRIATE EXPERIMENTAL ANIMAL-MODEL FOR THE PREVENTION OF RESTENOSIS [J].
FERRELL, M ;
FUSTER, V ;
GOLD, HK ;
CHESEBRO, JH .
CIRCULATION, 1992, 85 (04) :1630-1631
[4]   INHIBITION OF CORONARY-ARTERY TRANSPLANT ATHEROSCLEROSIS IN RABBITS WITH ANGIOPEPTIN, AN OCTAPEPTIDE [J].
FOEGH, ML ;
KHIRABADI, BS ;
CHAMBERS, E ;
AMAMOO, S ;
RAMWELL, PW .
ATHEROSCLEROSIS, 1989, 78 (2-3) :229-236
[5]   A PARADIGM FOR RESTENOSIS BASED ON CELL BIOLOGY - CLUES FOR THE DEVELOPMENT OF NEW PREVENTIVE THERAPIES [J].
FORRESTER, JS ;
FISHBEIN, M ;
HELFANT, R ;
FAGIN, J .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1991, 17 (03) :758-769
[6]  
FRENCH J. E., 1965, ANN N Y ACAD SCI, V127, P780, DOI 10.1111/j.1749-6632.1965.tb49444.x
[7]   ARTERIOSCLEROSIS IN NORMAL AND VONWILLEBRAND PIGS - LONG-TERM PROSPECTIVE-STUDY AND AORTIC TRANSPLANTATION STUDY [J].
FUSTER, V ;
FASS, DN ;
KAYE, MP ;
JOSA, M ;
ZINSMEISTER, AR ;
BOWIE, EJW .
CIRCULATION RESEARCH, 1982, 51 (05) :587-593
[8]   CORONARY INTIMAL PROLIFERATION AFTER BALLOON INJURY AND STENTING IN SWINE - AN ANIMAL-MODEL OF RESTENOSIS [J].
KARAS, SP ;
GRAVANIS, MB ;
SANTOIAN, EC ;
ROBINSON, KA ;
ANDERBERG, KA ;
KING, SB .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1992, 20 (02) :467-474
[9]   INHIBITION OF MYOINTIMAL PROLIFERATION OF THE RAT CAROTID-ARTERY BY THE PEPTIDES, ANGIOPEPTIN AND BIM-23034 [J].
LUNDERGAN, C ;
FOEGH, ML ;
VARGAS, R ;
EUFEMIO, M ;
BORMES, GW ;
KOT, PA ;
RAMWELL, PW .
ATHEROSCLEROSIS, 1989, 80 (01) :49-55
[10]   G-PROTEIN ACTIVATION OF A HORMONE-STIMULATED PHOSPHATASE IN HUMAN TUMOR-CELLS [J].
PAN, MG ;
FLORIO, T ;
STORK, PJS .
SCIENCE, 1992, 256 (5060) :1215-1217