Objective To study the feasibility of transplanting human saphanous vein endothelial cells to luminal surface of blood vessel prosthesis and to play a theoretical foundation for the clinical application of autologous endothelial cell transplantation. Methods Human saphanous vein endothelial cells were harvested with 0.1% collagenase and cultivated in vitro for 13.08±1.24 days. The cultures were confirmed as endothelial cells with the fourescent linked anti-Ⅷ antigen antibodies. The content of both 6-keto-PGF1α and Von Willebrand factor (vWF) in the supernatant were detected with ELISA and radioimmunoassay. The multiplied cells were lined in vitro onto the luminal surface of expanded polytetraflouroethylene (ePTFE) grafts precoated with fibrin glue and fibronectin, then cultivated again for 9 days. Results 11.46±2.69×１０６ of available endothelial cells could be regularly obtained, the number of endothelial cells increased 147.93±88.68 times when culture were terminated. All the cells diploid cells with a purity of 99%. The content of both 6-keto-PGF1α and vWF in the media showed no significant difference between the primary and subculture passages. The luminal surface of grafts was covered completely by a spindlelike endothelial monolayer and an even fibrin glue matrix could be seen underneath. Conclusion Endothelial cells derived from human saphanous veins might be feasible to be transplanted onto the luminal surface of ePTFE and present a potential clinical application.
Objective To understand the value of pre-coating in artificial vessel endothelialization. Methods Literature concerning precoating in artificial vessel endothelialization was extensively reviewed. Results Pre-coating included chemical coatings(collagen, fibronectin, laminin, poly-l-lysin, gelatin andextracellular matrix), pre-clotting(plasma, blood, serum and fibrin glue), chemical bonding (heparin, RGD and lectins) and surface modification. Most of them could enhance the adhesion of the endothelial cells. Conclusion Pre-coating couldimprove endothelialization, but further research is needed to search for the appropriate concentration and incubation time.
OBJECTIVE: To investigate the clinical effects of revascularization in lower extremity for severe ischemia. METHODS: Fifty-six lower limbs with severe ischemia in 49 patients were evaluated retrospectively, who underwent surgical intervention from January of 1995 to December of 2000. By arteriography, the actual anatomic distributions of occlusive disease included infrarenal aorta-bicommon iliac arteries, abdominal aorta-bicommon iliac arteries, iliac artery, and femoral artery or femoropopliteal artery. The indication for surgery was disabling claudication, rest pain and gangrene. Fourteen limbs in 12 cases received arterialization of femoral venous system by artificial venous-arterial fistula. Artificial vascular grafts were implanted in 33 limbs of 28 cases, endarterectomy and patch profundaplasty were performed in 5 limbs of 5 cases, and primary amputation was carried out in 4 cases. RESULTS: During 38 months follow-up in average, 4 limbs were amputated within 52 revascularizated limbs, and accumulated amputation rate was 14.3%. Patency rate was 68.4% in arterial revascularization limbs (26/38 limbs), and limb survival rate was 94.7%(36/38 limbs) by procedure of artificial vascular grafts, endarterectomy and patch profundaplasty. Limb survival rate in procedure of artificial venous-arterial fistula was 85.7%(12/14 limbs). CONCLUSION: In treatment of severe lower extremity ischemia, the effective revascularization can be achieved by artificial vascular bypass, endarterectomy and patch profundaplasty, or arterialization of femoral venous system. Options in the surgical management should depend on individual. Arteriography is essential for revascularization and properly planning a practicable surgical approach.
The autograft and non-autograft cannot meet the needs of clinical vascular surgery. Since there are possibilities of thrombus formation in artificial vascular grafts, the methods for deposing the graft using physical and chemical ways or simply seeding with endothelial cells cannot produce satisfactory grafts for vascular operations until now. In order to increase the anticoagulative capacity of artificial vascular graft, it is rational to use genetic engineering methods modifying the endothelial cells to make it express anticoagulative factors stably. Although seeding artificial graft with the genetically engineered endothelial cells can possibly produce a satisfactory graft for vascular surgery, some problems still need to be solved.
ObjectiveTo investigate whether the recombinant human growth hormone (rhGH) can promote endothelialization, inhibit vascular intimal hyperplasia, and improve long-term patency rate by the treatment of rhGH after vascular prostheses bypass. MethodsBetween August 2007 and January 2009, 94 patients with lower extremity arteriosclerotic occlusive disease were treated. Among them, 32 patients (34 limbs) who met the selection criteria were enrolled in this study. All cases were randomly divided into study group (16 cases, 18 limbs) and control group (16 cases, 16 limbs). There was no significant difference (P>0.05) in gender, age, disease time, location of lesions, the Trans-Atlantic Inter-Society Consensus (TASC) grade, and basic diseases between 2 groups. The patients with superficial femoral artery disease received above-knee femoro-popliteal prostheses bypass. The patients who had combined abdominal-iliac artery disease received concurrent abdominal-femoral and femoro-popliteal prostheses bypass. Subcutaneous injection of 9 U rhGH was given every night for 7 days in study group, and saline was applied in control group. Ultrasonography was taken after 2 weeks and 3 months of operation to observe the patency and measure the wall thickness of vascular prostheses. ResultsAfter operation, 1 patient of control group died of renal failure caused by acute thrombosis. After 2 weeks, ultrasonography showed no obvious intimal hyperplasia in 2 groups; the wall thickness was (0.13±0.02) cm in study group and (0.15±0.03) cm in control group, showing no significant difference (t=-1.720, P=0.108). After 3 months, the wall thickness was (0.17±0.06) cm in study group and was (0.26±0.09) cm in control group, showing significant difference (t=-2.240, P=0.045). All cases were followed up 36-60 months (mean, 56.4 months). The 5-year primary patency rate was 52.5% in study group and 35.7% in control group, showing no significant difference (χ2=1.470, P=0.225). ConclusionThe rhGH can improve endothelialization in vascular prostheses and can inhibit postoperative vascular intimal hyperplasia in clinical application.
Objective To evaluate surgical treatment of infected femoral artery pseudoaneurysm. Methods The data on surgical treatment of 45 patients with infected femoral artery pseudoaneurysm admitted from January 2003 to June 2008 were analyzed retrospectively. Fourty-three patients underwent operative treatment including excision of infected femoral artery pseudoaneurysm, exhaustive debridement and bypass graft with vascular prosthesis. Two patients were unavoidable to undergo removing of infected femoral artery pseudoaneurysm and ligating the proximal and distal artery of pseudoaneurysm because of severe infection and large volume. Results The patients were followed up from 3 to 12 months (mean 7.82 months). The limbs of all the patients underwent bypass graft with vascular prosthesis were salvaged successfully, patients of which had secondary wound healing and had not intermittent lameness. One of two patients performed ligation of artery was salvaged successfully but had severe intermittent lameness, another patient underwent high amputation above knee because of ischemic gangrene. Conclusion For infected femoral artery pseudoaneurysm, the operative treatment including excision of infected femoral artery pseudoaneurysm, exhaustive debridement and bypass graft with vascular prosthesis is effective and safe.
OBJECTIVE To investigate the clinical application of artificial blood vessel graft for arteriovenous fistulization. METHODS From October 1995 to August 1998, 23 cases with renal failure received PTEF artificial vessels grafting for arteriovenous fistulization in the forearm. The PTFE artificial vessel was 6 mm in diameter, and 40 cm in length. Artificial vessel "U"-shaped loop was formed from elbow incision to wrist incision, and perfused by 20 ml heparin saline. The two ends of artificial vessel were end-to-side anastomosed with superficial cubital vein and cubital artery respectively. RESULTS All of arteriovenous fistulas were successfully formed, and could be performed hemodialysis periodically. The artificial vessels could be punctured repeatedly, and had sufficient volume of blood flow. It had no rejection, no formation of false aneurysm, and no ischemia in arm or exacerbated reflux to heart. CONCLUSION The artificial vessel grafting for arteriovenous fistulization is a safe and convenient technique in clinical practice, especially when there is no autogenous vessels for arteriovenous fistula.
Objective To explore whether 125I-vascular endothel ial growth factor (VEGF)-coated artificial vascular patch accelerate the vessel endothel ial ization and inhibit thrombosis. Methods Ten adult male New Zealand rabbits (weighing 2.5-3.0 kg) were allocated into experimental group (n=5) and control group (n=5). In experimental group, the right common jugular vein was exposed for vascular clamping between proximal location and distal location, and then a 10 mm × 5 mm 125I-VEGF-coated artificial vascular patch was implanted into the right common jugular vein and sutured with 8-0 thread.In control group, the artificial vascular patch was implanted. After 2 weeks, the vein specimens were collected to measure the residues of 125I-VEGF by γ-ray counter. HE staining and immunohistochemical staining for smooth muscle actin (SMA) and CD34 were performed. The vascular endothel ial cells were counted and the intimal thickness was measured. Results The γ-ray counter showed the residues of 125I-VEGF in experimental group was (427.5 ± 194.9) CPM after 2 weeks, equivalent to 2.0% ± 0.8% of the preoperative value. Thrombosis formed in 2 rabbits of control group; no thrombosis formed in experimental group. There was significant difference in the intimal thickness [(41.1 ± 6.6) μm vs (49.0 ± 6.9) μm, P lt; 0.05]; but no significant difference in the vascular endothel ial cells count between experimental group and control group (60.0 ± 6.8 vs 58.0 ± 5.7, P gt; 0.05). Conclusion 125I-VEGF-coated artificial vascular patch can reduce thrombosis and inhibit intimal prol iferation at the acute phase. A consecutive l ine of endothel ial cells can form after implantation of patch in the rabbit jugular vein, however, the function of endothel ial cells may be premature.