BACKGROUND: To refine facial transplantation techniques and achieve sound results, it is essential to develop a suitable animal model. Rat is a small animal and has many advantages over other animals that have been used as transplantation models. The purpose of this study was to describe a rat hemifacial transplantation model and to verify its convenience and reproducibility. METHODS: Animals used in this study were Lewis rats (recipients) and Lewis-Brown Norway rats (donors). Nine transplantations were performed, requiring 18 animals. The hemifacial flap that included the ipsilateral ear was harvested based on the unilateral common carotid artery and external jugular vein and was transferred as a single unit. Cyclosporine A therapy was initiated 24 hours after transplantation and lasted for 2 weeks. Signs of rejection responses were evaluated daily. RESULTS: The mean transplantation time was 1 hour 20 minutes. The anatomy of common carotid artery and external jugular vein was consistent, and the vessel size was appropriate for anastomosis. Six of nine allografts remained good viable without vascular problems at the conclusion of study (postoperative 2 weeks). CONCLUSION: The rat hemifacial transplantation model is suitable as a standard transplantation training model.
Allografts ; Animals ; Carotid Artery, Common ; Cyclosporine ; Ear ; Facial Transplantation ; Jugular Veins ; Models, Animal ; Norway ; Rats* ; Vascularized Composite Allotransplantation

BACKGROUND: To refine facial transplantation techniques and achieve sound results, it is essential to develop a suitable animal model. Rat is a small animal and has many advantages over other animals that have been used as transplantation models. The purpose of this study was to describe a rat hemifacial transplantation model and to verify its convenience and reproducibility. METHODS: Animals used in this study were Lewis rats (recipients) and Lewis-Brown Norway rats (donors). Nine transplantations were performed, requiring 18 animals. The hemifacial flap that included the ipsilateral ear was harvested based on the unilateral common carotid artery and external jugular vein and was transferred as a single unit. Cyclosporine A therapy was initiated 24 hours after transplantation and lasted for 2 weeks. Signs of rejection responses were evaluated daily. RESULTS: The mean transplantation time was 1 hour 20 minutes. The anatomy of common carotid artery and external jugular vein was consistent, and the vessel size was appropriate for anastomosis. Six of nine allografts remained good viable without vascular problems at the conclusion of study (postoperative 2 weeks). CONCLUSION: The rat hemifacial transplantation model is suitable as a standard transplantation training model.
Allografts ; Animals ; Carotid Artery, Common ; Cyclosporine ; Ear ; Facial Transplantation ; Jugular Veins ; Models, Animal ; Norway ; Rats* ; Vascularized Composite Allotransplantation

To establish a murine carotid artery transplantation model for the study of the chronic rejection, 80 rats were divided into two groups, an allotransplant (ACI-Lewis) group and an isotransplant (Lewis-Lewis) group (control group). The donor carotid artery and the recipient carotid artery were anastomosed by using a polyethylene cuff (internal diameter: 0.7 mm, length: 3 mm).The pathological changes of carotid artery transplant were observed 14, 28 and 56 days after the transplantation. The results showed that the model was successfully established in 95% of the animals. The chronic rejection-associated arteriosclerosis was induced 28 days after the transplantation. The new chronic rejection model of carotid artery by using cuff technique caused fewer traumas and was easy to make. The pathological changes of the transplant mimicked the chronic rejection-associated arteriosclerosis found in human transplant.
Anastomosis, Surgical/methods ; Arteriosclerosis ; Carotid Artery, Common/*transplantation ; Delayed Graft Function ; Graft Rejection/*pathology ; Models, Animal ; Polyethylene ; Rats, Inbred ACI ; Rats, Inbred Lew

OBJECTIVETo investigate the potential cell sources of neointimal cells in autologous vein graft in rat model.

METHODSVein graft neointimal cell origins were investigated using a model of vein-to-artery interposition modal. Slides were stained with hematoxylin and eosin, immunohistochemical staining was also performed with primary antibodies alpha-smooth actin or CD34.

RESULTSNeointimal thickening was greater at the proximal ends (65.2 +/- 4.6) microm and, to a lesser extent, distal ends (64.7 +/- 5.3) microm, in comparison to the middle of the graft (63.5 +/- 5.6) microm. Vein-originating cells survived and make a contribution to neointimal formation within the vein graft, mostly adjacent to the lumen, suggesting an intimate association with endothelial cells, donor arterial smooth muscle cells or circulating progenitor cells.

CONCLUSIONSVein graft neointimal cells arise predominantly from vein-derived endothelial cells, donor arteria smooth muscle cells or circulating progenitor cells. It suggests clinical relevance of stenosis-inhibiting therapies directed at the vein graft or early system pharmacologic administration.

Anastomosis, Surgical ; Animals ; Carotid Artery, Common ; surgery ; Hyperplasia ; Jugular Veins ; pathology ; transplantation ; Male ; Models, Animal ; Rats ; Rats, Sprague-Dawley ; Transplantation, Autologous ; Tunica Intima ; pathology

Carotid artery puncture is the most common complication of internal jugular vein catheterization. However, arteriovenous fistula between carotid artery and internal jugular vein has been rarely reported. Here we report a patient who developed arteriovenous fistula following inadvertent carotid artery puncture, while undergoing liver transplantation.
Arteriovenous Fistula* ; Carotid Arteries ; Carotid Artery, Common ; Catheterization* ; Catheters* ; Humans ; Jugular Veins* ; Liver Transplantation* ; Liver* ; Punctures

UNLABELLEDOBJECTIVE Crosslink decellularized canine carotid artery allograft by EDC [1-3-(dimethylamino)propyl-3-ethylcarbodiimide methiodide] and evaluate the biocompatibility of it.

METHODSUse the multi-step detergent-enzyme method to construct decellularized canine carotid artery allograft and cross-link it by EDC with the weight ratio of decellularized artery to EDC 1:1 and 1:2. Evaluate the biocompatibility of it by the cytotoxical MTT test and the rat subdermal bury test.

RESULTSDecellularized canine carotid artery cross-linked by EDC has a lower degradation rate treated by collagenase type II, the result of MTT test show that the EDC cross-linked decellularized artery has no cytotoxity and the rat subdermal bury test show that crosslinking greatly enhance the ability of decellularize artery to resist the enzyme degradation and lower the immune reaction. The more the artery was cross-linked , the more effects it has.

CONCLUSIONSDecellularized canine carotid artery cross-linked by EDC has fairly good biocompatibility and ability to resist the collagenase degradation.

Animals ; Biocompatible Materials ; Carbodiimides ; Carotid Artery, Common ; transplantation ; Cross-Linking Reagents ; Dogs ; Female ; Male ; Materials Testing ; Rats ; Rats, Sprague-Dawley ; Tissue Engineering

BACKGROUNDPlacement of an external support has been reported to prevent intimal hyperplasia of vein grafts. However, it is limited by potential complications. In the present study, we investigated the effect of fibrin glue on preventing vein graft failure as perivenous application.

METHODSTwenty-four rabbits were divided into non-supported group (n = 12) and fibrin glue group (n = 12). All animals underwent unilateral jugular vein into common carotid artery interposition grafting and then fibrin glue was applied as perivenous support. Samples of tissues were harvested after 4 weeks.

RESULTSThe vein grafts with fibrin glue demonstrated a statistically significant decrease in proliferating cell nuclear antigen in the medial/intimal region [13.38% (11.26% - 15.11%)] compared with non-supported vein grafts [31.22% (27.15% - 35.98%)] (P < 0.001). Light microscopy showed remarkable attenuation of endothelial cell loss and numerous microvessels in neoadventitia in the fibrin glue group compared with the non-supported group. The smooth muscle cells migrated into adventitia significantly in fibrin glue group, whereas the smooth muscle cells migrated into intima in non-supported group. Conclusion Perivenous support of vein graft with fibrin glue in vivo can attenuate the severe injury encountered in the non-supported vein grafts exposed to artery.

Animals ; Carotid Artery, Common ; surgery ; Cell Movement ; Coronary Artery Bypass ; Fibrin Tissue Adhesive ; pharmacology ; Hyperplasia ; Jugular Veins ; transplantation ; Muscle, Smooth, Vascular ; pathology ; Proliferating Cell Nuclear Antigen ; analysis ; Rabbits ; Tunica Intima ; pathology

OBJECTIVENeonatal hypoxic-ischemic encephalopathy (HIE) harms the lives and health of newborn infants and children severely. Given the absence of effective therapies for HIE, it is important to derive new strategies. Neural stem cells (NSCs) have great potential as a therapeutic tool for the repair of a number of central nervous system disorders that involve cell loss. This study was designed to transplant the neural stem cells derived from human fetal brain (hNSCs) into cerebral ventricle of neonatal rat following hypoxic-ischemic injury and to investigate their survival, migration and differentiation in rat brain.

METHODSCells obtained from the forebrain of a 12-week old fetus were cultured in the presence of epidermal growth factor, basic fibroblast growth factor and leukemia inhibitory factor for 11 days. Animal models were built in 7-day-postnatal Wistar rats, 3-days after hypoxia-ischemia (HI), 5 microl suspension containing 5.0 x 10(5) hNSCs was injected into the left cerebral ventricle of each HIE rat by using stereotactic instrument. No immunosuppression therapy was given to the animals. At 1, 2, 4 weeks and 3 months after transplantation, the rats were sacrificed and brain tissues were harvested and were then examined by H-E staining and immunohistochemical analysis.

RESULTSImplanted cells expressing human nuclear protein (hNP) migrated form the subventricular zone (SVZ) along corpus callosum to the damaged areas, especially to the injured side of cortex and hippocampus. In different areas, the implanted hNSCs differentiated into different cell types which were similar to the host cells. The 85% implanted cells in cortex consisted of hNuc-NF or hNuc-Tublin double positive cells, while in the migratory way, 60% implanted cells differentiated into hNuc-GFAP double positive cells. Compared with the 1-week time point, an increased number of hNP-positive cells were observed at 2-weeks, but the number of these cells greatly decreased at 4-weeks and 3 months.

CONCLUSIONThe implanted hNSCs could extensively survive, migrate in the brain of neonatal rat with HIE and could differentiate into neurons and astrocytes in a regionally specific manner.

Animals ; Animals, Newborn ; Brain ; pathology ; Carotid Artery, Common ; surgery ; Cell Differentiation ; Cell Movement ; Disease Models, Animal ; Fetal Stem Cells ; transplantation ; Humans ; Hypoxia ; complications ; physiopathology ; Hypoxia-Ischemia, Brain ; pathology ; physiopathology ; therapy ; Immunohistochemistry ; Injections, Intraventricular ; methods ; Ligation ; methods ; Neurons ; Nuclear Proteins ; metabolism ; Rats ; Rats, Sprague-Dawley ; Stem Cell Transplantation ; methods ; Survival Analysis ; Time Factors

OBJECTIVETo establish a neonatal rat model of hypoxic-ischemic encephalopathy and clarify the changing features of neural stem cells (NSCs) in episodes of hypoxic-ischemic encephalopathy (HIE) so as to provide experimental and theoretical evidences for treating HIE by applying NSCs at the appropraite time.

METHODSTotally 210 neonatal rats aged 7 d were divided randomly into three groups, normal control group, hypoxic group and hypoxic-ischemic group with 70 rats in each. According to the time of sacrefice, 70 rats of every group were further divided randomly into seven groups including third hour (3 h), the sixth hour (6 h), first day (1 d), third day (3 d), the seventh day (7 d), the fourteenth day (14 d) and the twenty-first day (21 d), with 10 rats in each subgroup. The left common carotid artery of the neonatal rats in hypoxic-ischemic group was ligated and those in the hypoxic group were subjected to inhalation of 8% oxygen for 2.5 h. NSCs from brain tissues of the rats of the three groups were determined with HE staining and immunohistochemical method under light microscope.

RESULTSMost of neonatal rats in hypoxic-ischemic group behaved turning to the left stably 1 h after normal concentration of oxygen was given. In hypoxic-ischemic group, slight brain injury occurred at 3 h, severe brain injury appeared at 1 d, glial cells proliferated at 3 d and 7 d, brain atrophy was found at 14 d and 21 d. NSCs existed in brain tissues of rats in all the three groups. NSCs in normal control and the hypoxic group mainly distributed in hippocampus, subventricular tissues, striatum and cortex. But NSCs in hippocampus located in layers of molecule, cone cell and inner granular cell. NSCs in hypoxic-ischemic group showed obvious regional distribution, less in the regions with pathological changes. At 3 h, 6 h and 14 d, there was no difference in the number of NSCs between hypoxi and hypoxic-ischemic group. At 1 d, 3 d and 7 d, there was a highly significant difference in the number of NSCs between hypoxic and hypoxic-ischemic group. At 21 d, there was a significant difference in the number of NSCs between hypoxic and hypoxic-ischemic group, meanwhile, there was a significant difference in the number of NSCs between control and hypoxic group. At 3 d, there was a very significant difference in the number of NSCs between control and hypoxic-ischemic group. At 7 d and 21 d points, there was a highly significant difference in the number of NSCs between control and hypoxic group.

CONCLUSIONThe neonatal rat model of HIE was successfully established. NSCs increased in earlier period and decreased in later period of HIE, ultimately, NSCs located in the injured regions died one after anotner. Hypoxia induces NSCs' proliferation.

Animals ; Animals, Newborn ; Atrophy ; Brain ; pathology ; Carotid Artery, Common ; surgery ; Disease Models, Animal ; Hypoxia-Ischemia, Brain ; pathology ; Immunohistochemistry ; Ligation ; Multipotent Stem Cells ; pathology ; Neuroglia ; pathology ; Neurons ; pathology ; Rats ; Rats, Sprague-Dawley ; Stem Cell Transplantation ; methods ; Time Factors