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Objective To investigate the advantages and disadvantages of two different approaches (i.e.internal jugular vein and subclavian vein) when used for the implantation of central venus access ports (CVAP).Methods We retrospectively analyzed 620 patients who underwent the implantation of CVAP via the approach of internal jugular vein (n =222) or subclavian vein (n =398) and compared the success rate on first attempt as well as the incidences of peroperative and long-term complications.Results The implantation of CVAP was successfully performed in all the 620 patients,with the success rate on first attempt being 97.24％ (387/398) in the subclavian vein group and 89.19％ (198/222) in the internal jugular vein group (U =0.171,P ＜ 0.01).The incidences of perioperative/long-term complications were 0.90％ (2/222) /1.80％ (4/222) in the internal jugular vein group and 1.26％ (5/398) /2.01％ (8/398) in the subclavian vein group,showing no significant differences (all P ＞ 0.05).Conclusions The implantation of CVAP via either the internal jugular vein approach or subclavian vein approach is safe and reliable.Few complications will occur if performed properly.
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[ABSTRACT]AIM:ToevaluatetheeffectsofantisenseTGF-β1oligodeoxynucleotide(ASTGF-β1)ontheex-pression of TGF-β1 , deposition of extracellular matrix ( ECM) and the neointima formation in the arteries after balloon inju-ry.METHODS:The unmodified and phosphorothioate-modified AS TGF-β1 which containing 15 bases and surrounding the initiation codon region (ATG) of rat TGF-β1 complementary DNA (cDNA) were designed.At the same time, sense TGF-β1 oligodeoxynucleotide ( S TGF-β1 ) with the base sequence complement to AS TGF-β1 was synthesized as a control . The oligodeoxynucleotides were introduced into in vivo and in vitro experiments , respectively .RESULTS:The AS TGF-β1 significantly inhibited the protein expression of TGF-β1 in a concentration-dependent manner , and S TGF-β1 did not have the same effect.Furthermore, no effect of the AS TGF-β1 on the mRNA expression of TGF-β1 in injured VSMCs was ob-served.Moreover, for the injured VSMCs, AS TGF-β1 significantly and concentration-dependently inhibited the basal DNA synthesis.Both AS TGF-β1 and S TGF-β1 did not exhibit dose-dependent effects on DNA synthesis in uninjured VSMCs . Fibronectin ( FN) mRNA expression in injured VSMCs was significantly decreased by AS TGF-β1 in a concentration (0.01~1 μmol/L)-dependent manner .AS TGF-β1 significantly increased the mRNA expression of contractile marker SM 22α, and decreased the mRNA expression of synthetic markers osteopontin and matrix Gla , especially at the concentration of 0.01μmol/L and 0.1 μmol/L.After treatment with AS TGF-β1 (90 μg· kg-1 · d-1 ) for 28 d, the neointima formation was significantly inhibited , and the area ratio of intima/media was markedly decreased by 68% compared with untreated group , but S TGF-β1 had no effect on neointimal formation .CONCLUSION:The AS TGF-β1 specifically inhibits the pro-tein expression of TGF-β1 in the VSMCs derived from injured arteries .Moreover , it significantly inhibits DNA synthesis and cell proliferation, and decreases the expression of FN .Therefore, AS TGF-β1 dramatically attenuates neointima formation after balloon njury .The effects of AS TGF-β1 on the injured VSMCs may be associated with its reverse effects on the altera-tion of VSMC phenotype after balloon injury .
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AIM: To investigate the effects of fluvastatin on intimal hyperplasia following balloon injury of rabbit iliac artery. METHODS: The iliac arteries of twelve white New Zealand rabbits were injured with an inflated balloon catheter, six rabbits were given fluvastatin 8 mg?kg~-1 ?d~-1 by gavage, the others served as controls. Serum concentrations of endothelin, thromboxane A_2 and prostacyclin were measured by radioimmunoassay at time points before, 3 hours and 3 days after balloon injury. After 28 days, ratio of intima-to-media area (I/M) of the injured arteries were calculated using a computer image analysis system and the alteration of TGF-?_1 and extracellular matrix (FN, LN) were quantified with immunohistochemistry. RESULTS: ① Serum endothelin-1 and thromboxane A_2 significantly increased after injury, whereas serum prostacyclin markedly decreased. The alterations were completely reversed by the treatment with fluvastatin. ② The expression of TGF-?_1 and deposition of ECM in intimal were much lower than that in the untreatment animals. ③ Intimal hyperplasia after balloon injury was significantly attenuated by fluvastatin treatment. CONCLUSION: The inhibitory effects of fluvastatin on intimal hyperplasia after balloon injury may attribute to its inhibiting thrombosis and deposition of ECM. [