| PrefaceVein autograft is the most commonly used material in the treatment of arterial stenosis and its effect is widely confirmed. However, the incidence of restenosis after vein autografts is very high, which limits its clinical application. It s reported that the incidence of restenosis may be up to 20 -50% , or even higher. Its believed that restenosis can be caused by intimal hyperplasia which is the result of vascular injury, inflammatory reaction and changes of ischemic hemody-namics. The vascular smooth muscle cells also play a major role in the pathogenesis by actions such as proliferation, migration and extracellular matrix deposition. Recent studies have allowed a better understanding of the biology of restenosis. It has been found that " constric-tive remodeling" has the potential to reduce the vessel lumen after vein autografts. Paclitaxel is a recently - discovered anti - tumor drug. Through investigation on its mechanism of anti - tumor effect it was found that paclitaxel can inhibit the proliferation and migration of vascular smooth muscle cell. We intend to study the effect of paclitaxel on the intimal remodeling of vein autogrfts through histomophorlogy and immunohistochemistry method.Materials and Methods1. Animals50 Wistar rats were divided into 10 groups: blank control groups(0, 7, 14 and 28 days) ; mono - dose groups (7, 14 and 28 days) ; bi - dose group (14 and 28 days) and tri - dose group (28 days) .2. Making Animal ModelAn animal model of the autogenous vein graft through transplanting the jugular vein into common carotid artery was established in 50 rats. After anaesthetizing with 10% chloral hydrate (2ml/kg body weight) , using median incision in cervical part, cutting jugular vein by 0. 5 cm, washing with heparin saline, using 11-0 non - injury suturing , end to end anastomosis jugular vein into common carotid arter-y. There are 8 needles in every stoma. Paclitaxel was given from the 2nd day on. Specimens were harvested on the 7th, 14th, and 28th day respectively after operation in blank control groups; on the 7th, 14th, and 28th day respectively in mono -dose groups; on the 14th, and 28th day respectively in bi - dose groups and on the 28th day in tri - dose groups.3. Harvest and Measurement of SpecimenThe specimens were perfusion - fixed 10% buffered formalin and were embedded in paraffin. These specimens were stained with the method of HE and Verhoeff. Thickness of intima was measured by computer graph analysis system. The positive cells of PCNA were detected to indicate the degree and cause of intimal and VSMCs hyper-plasia.4. Statistical AnalysisExperimental data were analyzed with SPSS statistical software. Numericals are presented in the form of Mean + SEM. Analysis of variance and x2 test were used for statistical comparison. Value of P <0. 05 was rejected as null -hypothesis.ResultNormal veins are surfaced by a monolayer of endothelial cell, under which is media comprised of loose connective tissue and smooth muscle cells. Intimal thickness increased on the 7th day, in blank control group its 18. 08 + 1. 31; in mono - dose group its 14. 26 +0. 73. Difference between the two was significant (P <0. 01). On the 14th day intimal thickness was 22. 30 + 1. 70 in blank control group; 18. 30 + 1. 30 and 16. 99 + 1. 44 in mono - dose and bi - dose group respectively. Difference was significant between blank control and intervention groups ( P < 0. 05 ) , difference between mono - dose and single - dose groups, however, was not significant ( P > 0. 05). On the 28th day intimal thickness -was 27. 82 ?3. 45 in blank control group; 23. 56 +1.84, 21.36 +1.90, 19.67 +2.01 in mono -dose, bi - dose and tri - dose group respectively. Difference between blank control and intervention group was significant. Percentage of PCNA positive cells: on the 7th day 39. 37 +7. 60 in blank control group; 34. 67 + 1. 01 in mono - dose group. Difference between the two was significant. On the 14th day the percentage was 30.71 + 1.46, 27. 23 + 1. |
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