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Effects And Echanism Of Chitosan's Stent On Restenosis After Rabbit Carotid Artery Balloon Injury

Posted on:2002-08-15Degree:DoctorType:Dissertation
Country:ChinaCandidate:D X WangFull Text:PDF
GTID:1104360032451557Subject:Cardiovascular medicine profession
Abstract/Summary:PDF Full Text Request
Percutaneous transluminal coronary angioplsty(PTCA) is the milestone of treatment for coronary heart disease. However, its major limitation is the development of restenosis, which occurs in 30-50% of patients within six months. Recent research reveals that proliferation of vascular smooth muscle cells (VSMC) is a key event in the pathogenesis of restenosis and that injury of vascular endothelial cells(VCE) is a starting factor. Growth factors and oncogene play an important role in the VSMC proliferation. An important therapeutic aim at restenosis is to inhibit VSMC proliferation and to promote VEC proliferation. The search for an appropriate agent which inhibits VSMC proliferation and promote VEC proliferation will contribute to better treatment of restenosis. Chitosan has been shown to inhibit fibroblast growth and promote epidermal cells growth. It could be assumed that chitosan might inhibit VSMC proliferation and promote VEC proliferation, both of which are important in preventing and treating restenosis. The present study aimed at demonstrating the above mentioned hyoithesis. This paper consists of the following five parts: 1. Effects of chitosan on proliferation of rabbit cultrued VSMC and VEC We used: cell culture and count method to study the efects of chitosan on cell number stimulated by newborn bull serum (NBS) in cultured rabbit VSMC and VEC. Results reveal Chitosan (0. 2μg/ml-2000μg/ml) inhibited VSMC proliferation and promoted VEC proliferation stimulated by NBS. 2. Effects of chitosan on rabbit VSMC oncogene c-myc mRNA expression. 7 We adopted Northern blot skill to examine the effects of chitosan on rabbit cultrued VSMC c-myc mRNA expression stimulated by NBS (20%). Outcome found the oncogene c-myc mRNA expression was increased in rabbit cultured VSMC at 24h after NBS exposure. These effects were inhibited by chitosan (2OOOμg/ml). 3. Effects of chitosan on adhesion of monocytes to endothelial cells. Chitosan inhibited endothlial cells adhesiveness to monocytes with a doseependent manner. 4.Effects of chitosan on [Ca+]i [H-]i of VSMC Recent research has proved that rising of intracelluar [Ca2+]i concentration and pH caused growth factor is cell proliferation essential condition. The experiment used fluorescent probe marking method to observe effects of NBS on VSMC[Ca2+] i and [H+]i and intervention action of ehitosan on theirs. Outcome confirmed VSMC [Ca+] concentration and intracelluar pH stimulated by NBS contained multirowth factors rose obviously; After acceding to Chitosan [Ca+]i concentration and intracelluar pH receded evidencely. 5. Effects of chitosan stent on restenosis after rabbit carotid artery balloon injury 40 rabbits are separated into five groupsEcontrol group, atherosclerosis(AS)group, restenosis(RS)group, Pravacholonopril group and chitosan?s stent group]. Then examinated serum lipid, femoral arterial cannulatio photograph film and pathological section after they have been feeded by high serum lipid respectively for five weeks, ten weeks and twenty weeks. Results found that every group serum lipid are obviously higher than control group. Serum lipid of Pravachol+Monopril group is lower than other experimental groups, but higher than control grou...
Keywords/Search Tags:angioplasty, atherosclerosis, restenosis, smooth muscle cells, endothelial cells, monocyte, gene expression, oncogene, adhesion, chitosan, stent, rabbit
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