Seongyup Kim

Histological changes of the unligated vein wall adjacent to the central venous catheter after open cutdown in rats

BACKGROUND The sequelae of a central venous cutdown usually include venous deformity causing venous stenosis or stricture. However, the cellular mechanisms causing these deformities have not been elucidated. METHODS Silicone 2.7-Fr catheters were placed via the right external jugular vein of 16 rats with the cutdown method. After fixation with formalin at scheduled intervals (1week, 2weeks, 4weeks, and 8weeks; 4 rats in each group), the vein segment with the catheter in situ was harvested. Histological changes in the vein wall were studied and serially compared with light microscopy; standard hematoxylin-eosin staining, Massons trichrome staining, van Giesons elastin stain, and immunohistochemical stain against α-actin. RESULTS Pericatheter sleeve formation, circumferential smooth muscle cell proliferation and infiltration into the pericatheter sleeve by direct contact were noted in all 4 rats of 1-week model; this indicated the initiation of neointimal hyperplasia. The neointimal hyperplasia was located inside the elastin layer. At 2weeks, the SMCs stained faintly but the components of the vein wall were largely replaced by collagen. The proliferation and infiltration of SMCs stabilized at 4weeks and no SMCs were stained around the catheter. At 8weeks, luminal narrowing was noted and the venous wall was composed mainly of collagen. CONCLUSIONS Circumferential neointimal hyperplasia occurred after surgical cutdown of the external jugular vein in a rat model and was caused by SMC activation, proliferation, and infiltration into the pericatheter sleeve.

Inhibitory effect of sustained perivascular delivery of paclitaxel on neointimal hyperplasia in the jugular vein after open cutdown central venous catheter placement in rats

Purpose Inhibitory effect of paclitaxel on neointimal hyperplasia after open cutdown has not been elucidated. Methods For the control group (n = 16), silicone 2.7-Fr catheters were placed via the right external jugular vein with the cutdown method. For the treatment group (n = 16), a mixture of 0.65 mg of paclitaxel and 1 mL of fibrin glue was infiltrated around the exposed vein after cutdown. After scheduled intervals (1, 2, 4, and 8 weeks), the vein segment was harvested and morphometric analysis was performed on cross-sections. Results Proliferation of smooth muscle cell (SMC) was strongly suppressed in the treatment group, and the ratio of neointima to vein wall was significantly reduced in the treatment group (8 weeks; 0.63 ± 0.08 vs. 0.2 ± 0.08, P < 0.05). Luminal patency was significantly more preserved in the treatment group, and the luminal area was significantly wider in the paclitaxel-treated group compared to the control group (8 weeks; 1.91 ± 0.43 mm2 vs. 5.1 ± 0.43 mm2, P < 0.05). Mean SMC counts measured at 1 and 2 weeks after cutdown were significantly lower in the treatment group (2 weeks; 115 ± 22 vs. 62 ± 22). Paclitaxel was undetectable in systemic circulation (<10 ng/mL). Conclusion Sustained perivascular delivery of paclitaxel with fibrin glue was effective in inhibiting neointimal hyperplasia in rat jugular vein after open cutdown.