Aneurysm, False/etiology* ; Carotid Artery Injuries/therapy* ; Carotid Artery, Internal ; Embolization, Therapeutic ; Epistaxis/etiology* ; Humans

PURPOSE: To explore the diagnosis and treatment of traumatic external carotid branch pseudoaneurysms. METHODS: Eleven cases of traumatic external carotid artery branch pseudoaneurysms were admitted in our hospital. Digital subtraction angiography was performed in all patients. It revealed that the pseudoaneurysms originated from the internal maxillary artery in 5 cases, superficial temporal artery in 5 cases and occipital artery in 1 case. Five cases of internal maxillary artery pseudoaneurysms and 2 cases of superficial temporal artery pseudoaneurysms were treated by embolization; the other 3 cases were surgically resected. RESULTS: Complete cessation of nasal bleeding was achieved in all the 5 pseudoaneurysms of internal maxillary artery after the endovascular therapies. Scalp bleeding stopped and scalp defect healed up in 2 patients with superficial temporal artery pseudoaneurysms treated by interventional therapy. All patients were followed up for 0.5-2.0 years without recurrence of nosebleed and scalp lump. CONCLUSION For patients with repeated severe epistaxis after craniocerebral injury, digital subtraction angiography should be performed as soon as possible to confirm traumatic pseudoaneurysm. Endovascular therapy is an effective method for traumatic internal maxillary artery pseudoaneurysms. For patients with scalp injuries and pulsatile lumps, further examinations including digital subtraction angiography should be performed to confirm the diagnosis. Surgical treatment or endovascular therapy for scalp traumatic pseudoaneurysm is effective.
Aneurysm, False/therapy* ; Angiography, Digital Subtraction ; Carotid Artery Injuries/therapy* ; Carotid Artery, External/diagnostic imaging* ; Embolization, Therapeutic ; Humans

OBJECTIVETo investigate the effect and potential mechanisms of rutaecarpine (Rut) in a rat artery balloon-injury model.

METHODSThe intimal hyperplasia model was established by rubbing the endothelia with a balloon catheter in the common carotid artery (CCA) of rats. Fifty rats were randomly divided into five groups, ie. sham, model, Rut (25, 50 and 75 mg/kg) with 10 rats of each group. The rats were treated with or without Rut (25, 50, 75 mg/kg) by intragastric administration for 14 consecutive days following injury. The morphological changes of the intima were evaluated by hematoxylin-eosin staining. The expressions of proliferating cell nuclear antigen (PCNA) and smooth muscle (SM) α-actin in the ateries were assayed by immunohistochemical staining. The mRNA expressions of c-myc, extracellular signal-regulated kinase 2 (ERK2), MAPK phosphatase-1 (MKP-1) and endothelial nitric oxide synthase (eNOS) were determined by real-time reverse transcription-polymerase chain reaction. The protein expressions of MKP-1 and phosphorylated ERK2 (p-ERK2) were examined by Western blotting. The plasma contents of nitric oxide (NO) and cyclic guanosine 3',5'-monophosphate (cGMP) were also determined.

RESULTSCompared with the model group, Rut treatment significantly decreased intimal thickening and ameliorated endothelial injury (P<0.05 or P<0.01). The positive expression rate of PCNA was decreased, while the expression rate of SM α-actin obviously increased in the vascular wall after Rut (50 and 75 mg/kg) administration (P<0.05 or P<0.01). Furthermore, the mRNA expressions of c-myc, ERK2 and PCNA were downregulated while the expressions of eNOS and MKP-1 were upregulated (P<0.05 or P<0.01). The protein expressions of MKP-1 and the phosphorylation of ERK2 were upregulated and downregulated after Rut (50 and 75 mg/kg) administration (P<0.05 or P<0.01), respectively. In addition, Rut dramatically reversed balloon injury-induced decrease of NO and cGMP in the plasma (P<0.05 or P<0.01).

CONCLUSIONRut could inhibit the balloon injury-induced carotid intimal hyperplasia in rats, possibly mediated by promotion of NO production and inhibiting ERK2 signal transduction pathways.

Actins ; metabolism ; Animals ; Carotid Arteries ; drug effects ; metabolism ; pathology ; Carotid Artery Injuries ; drug therapy ; genetics ; pathology ; Cyclic GMP ; blood ; Disease Models, Animal ; Gene Expression Regulation ; drug effects ; Hyperplasia ; Indole Alkaloids ; pharmacology ; therapeutic use ; Male ; Nitric Oxide ; blood ; Phosphorylation ; drug effects ; Proliferating Cell Nuclear Antigen ; metabolism ; Quinazolines ; pharmacology ; therapeutic use ; RNA, Messenger ; genetics ; metabolism ; Rats, Sprague-Dawley ; Tunica Intima ; drug effects ; pathology

The aims of the present study were to determine the effects of heparin-derived oligosaccharides (HDOs) on vascular intimal hyperplasia (IH) in balloon-injured carotid artery and to elucidate the underlying mechanisms of action. An animal model was established by rubbing the endothelia within the common carotid artery (CCA) in male rabbits. The rabbits were fed a high-cholesterol diet. Arterial IH was determined by histopathological changes to the CCA. Serum lipids were detected using an automated biochemical analysis. Expressions of mRNAs for vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), vascular cell adhesion molecule-1 (VCAM-1), monocyte chemoattractant protein-1 (MCP-1), scavenger receptor class B type I (SR-BI), and ATP-binding cassette transporter A1 (ABCA-1) were analyzed using reverse transcription polymerase chain reaction assays. Expressions of VEGF, VCAM-1, MCP-1, SR-BI and ABCA-1 proteins were analyzed by Western blotting. Enzyme-linked immunosorbent assays were used to quantify expression levels of VEGF and bFGF. Our results showed that administration of HDO significantly inhibited CCA histopathology and restenosis induced by balloon injury. The treatment with HDOs significantly decreased the mRNA and protein expression levels of VEGF, bFGF, VCAM-1, MCP-1, and SR-BI in the arterial wall; however, ABCA-1 expression level was elevated. HDO treatment led to a reduction in serum lipids (total cholesterol, triglycerides, high-density and low-density lipoproteins). Our results from the rabbit model indicated that HDOs could ameliorate IH and underlying mechanism might involve VEGF, bFGF, VCAM-1, MCP-1, SR-BI, and ABCA-1.
ATP Binding Cassette Transporter 1 ; analysis ; Animals ; Carotid Artery Injuries ; drug therapy ; pathology ; Chemokine CCL2 ; analysis ; Heparin ; therapeutic use ; Hyperplasia ; Male ; Oligosaccharides ; therapeutic use ; Rabbits ; Tunica Intima ; pathology ; Vascular Cell Adhesion Molecule-1 ; analysis ; Vascular Endothelial Growth Factor A ; analysis

Common carotid artery (CCA) dissection is a rare emergency condition. Early diagnosis of these cases is important to prevent the ischemic emergencies. We presented a CCA dissection case, who was admitted to the hospital after taken out from under rubble with satisfactory outcome.
Carotid Artery Injuries ; diagnosis ; therapy ; Carotid Artery, Common ; Humans ; Male ; Middle Aged

OBJECTIVEThis study was aimed to investigate the effects of carbon monoxide releasing molecule (CORM-2), a novel carbon monoxide carrier, on the reendothelialization of carotid artery in rat endothelial denudation model.

METHODSMale rats subjected to carotid artery balloon injury were treated with CORM-2, inactive CORM-2 (iCORM-2) or dimethyl sulfoxide (DMSO). The reendothelialization capacity was evaluated by Evans Blue dye and the immunostaining with anti-CD31 antibody. The number of circulating endothelial progenitor cells (EPCs) was detected by flow cytometry. The proliferation, migration, and adhesion of human umbilical vein endothelial cells (HUVECs) were assessed by using [3H]thymidine, Boyden chamber and human fibronectin respectively. The expressions of protein were detected by using western blot analysis.

RESULTSCORM-2 remarkably accelerated the re-endothelialization 5 d later and inhibited neointima formation 28 d later. In addition, the number of peripheral EPCs significantly increased in CORM-2-treated rats than that in iCORM-2 or DMSO-treated rats after 5 d later. In vitro experiments, CORM-2 significantly enhanced the proliferation, migration and adhesion of HUVECs. The levels of Akt, eNOS phosphorylation, and NO generation in HUVECs were also much higher in CORM-2 treated group. Blocking of PI3K/Akt/eNOS signaling pathway markedly suppressed the enhanced migration and adhesion of HUVECs induced by CORM-2.

CONCLUSIONCORM-2 could promote endothelial repair, and inhibit neointima formation after carotid artery balloon injury, which might be associated with the function changes of HUVECs regulated by PI3K/Akt/eNOS pathway.

Animals ; Carbon Monoxide ; metabolism ; pharmacology ; Carotid Artery Injuries ; drug therapy ; immunology ; metabolism ; pathology ; Carotid Artery, Common ; drug effects ; immunology ; metabolism ; pathology ; Cell Adhesion ; drug effects ; Disease Models, Animal ; Endothelial Cells ; drug effects ; immunology ; metabolism ; pathology ; Endothelium, Vascular ; drug effects ; metabolism ; pathology ; Humans ; Male ; Rats ; Rats, Sprague-Dawley

Neointimal proliferation after vascular injury is a key mechanism of restenosis, a major cause of percutaneous transluminal angioplasty failure and artery bypass occlusion. Emodin, an anthraquinone with multiple physiological activities, has been reported to inhibit proliferation of vascular smooth muscle cells (VSMCs) that might cause intimal arterial thickening. Thus, in this study, we established a rat model of balloon-injured carotid artery and investigated the therapeutic effect of emodin and its underlying mechanism. Intimal thickness was analyzed by hematoxylin and eosin staining. Expression of Wnt4, dvl-1, beta-catenin and collagen was determined by immunohistochemistry and/or western blotting. The proliferation of VSMC was evaluated by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and electron microscopy. MicroRNA levels were quantified by real-time quantitative PCR. Emodin relieved injury-induced artery intimal thickness. Results of western blots and immunohistochemistry showed that emodin suppressed expression of signaling molecules Wnt4/Dvl-1/beta-catenin as well as collagen protein in the injured artery. In addition, emodin enhanced expression of an artery injury-related microRNA, miR-126. In vitro, MTT assay showed that emodin suppressed angiotensin II (AngII)-induced proliferation of VSMCs. Emodin reversed AngII-induced activation of Wnt4/Dvl-1/beta-catenin signaling by increasing expression of miR-126 that was strongly supported by transfection of mimic or inhibitor for miR-126. Emodin prevents intimal thickening via Wnt4/Dvl-1/beta-catenin signaling pathway mediated by miR-126 in balloon-injured carotid artery of rats.
Adaptor Proteins, Signal Transducing/*metabolism ; Animals ; Carotid Arteries/drug effects/metabolism/pathology ; Carotid Artery Injuries/*drug therapy/metabolism/pathology ; Cell Proliferation/drug effects ; Emodin/*therapeutic use ; Male ; MicroRNAs/*metabolism ; Phosphoproteins/*metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/drug effects ; Tunica Intima/*drug effects/metabolism/pathology ; Wnt4 Protein/*metabolism ; beta Catenin/*metabolism

OBJECTIVETo investigate the effect of atorvastatin on platelet aggregation and activation in the acute phase following balloon-induced carotid artery injury in rabbits fed cholesterol-enriched diet.

METHODSThirty rabbits were randomly divided into 5 equal groups, namely control group, high-cholesterol group, model group, low-dose (5 mg/kg daily) atorvastatin group, and high-dose (10 mg/kg daily) atorvastatin group. Platelet aggregation rate was measured in the rabbits by turbidimetric platelet aggregometry, and the changes of serum P-selectin and thromboxane B2 (TXB2) levels were detected with enzyme-linked immunosorbent assay (ELISA).

RESULTSCompared with those in the control group, serum P-selectin level increased significantly (P<0.01) but platelet aggregation rate and TXB2 level exhibited no obvious changes in high-cholesterol group. After carotid artery balloon injury, P-selectin and TXB2 levels and platelet aggregation significantly increased in cholesterol-fed rabbits, reaching the peak level at 24 h after the injury (P<0.01). Compared with the model group, low-dose atorvastatin treatment significantly decreased P-selectin and TXB2 levels and inhibited platelet aggregation in cholesterol-fed rabbits following carotid artery balloon injury (P<0.01), and such effects of atorvastatin were more prominent at a higher daily dose of 10 mg/kg (P<0.05).

CONCLUSIONSCarotid artery balloon injury in rabbits fed cholesterol-enriched diet can induce platelet activation and aggregation, which reaches the peak level at 24 h after balloon injury and can be dose-dependently inhibited by atorvastatin in the acute phase following the injury.

Animals ; Atorvastatin Calcium ; Blood Platelets ; Carotid Artery Injuries ; drug therapy ; Cholesterol ; Enzyme-Linked Immunosorbent Assay ; Heptanoic Acids ; pharmacology ; P-Selectin ; metabolism ; Platelet Activation ; Platelet Aggregation ; Pyrroles ; pharmacology ; Rabbits ; Thromboxane B2 ; metabolism

PURPOSE: This study was designed to investigate whether vascular smooth muscle cells (VSMC) from the neointima showed any different response to antiproliferative agents, such as rapamycin or imatinib mesylate, compared to VSMCs from normal artery. MATERIALS AND METHODS: Intimal hyperplasia was made by carotid balloon in jury in male rats. Neointimal cells at 4 weeks after injury and normal VSMCs were extracted by enzymatic isolation method and cultured. Cell viability and proliferation were tested in VSMCs from injured left carotid artery and uninjured right carotid artery. Tests were repeated with rapamycin, imatinib mesylate or both in various concentrations. RESULTS: Rapamycin decreased cell viability only at a high concentration of 10(-5) M in uninjured VSMCs. Combined drugs decreased cell viability at a lower concentration of 10(-7) M in uninjured VSMCs, and at a higher concentration of 10(-5) M in neointimal cells. Overall, rapamycin showed cytocidal effects at a high concentration of 10(-5) M, whereas imatinib did not. Cell proliferation of neointima was significantly decreased along with the drug concentration. Cell proliferation of uninjured VSMCs was significantly decreased at higher drug concentrations. Combined drug therapy showed synergistic effects. Overall, neointimal cells are more susceptible to the antiproliferative effects of the drugs. CONCLUSION: Neointimal cells from the injured carotid artery are more susceptible to the antiproliferative effect of imatinib and rapamycin. Both drugs can be a used for the prevention of intimal hyperplasia, which could be investigated through further in vivo studies.
Animals ; Arteries ; Carotid Arteries ; Carotid Artery Injuries ; Cell Proliferation ; Cell Survival ; Drug Therapy ; Humans ; Hyperplasia ; Male ; Mesylates* ; Muscle, Smooth, Vascular* ; Neointima ; Rats ; Sirolimus* ; Imatinib Mesylate

BACKGROUNDEverolimus, a derivative of sirolimus, is a potent immunosuppressant that has important anti-proliferative properties. In the present study, we demonstrated the inhibiting neointimal hyperplasia in injured carotid arteries in rats by using two different doses of everolimus administrated via the oral route for a long time.

METHODSA rat model of carotid artery injury was established by balloon inflation. Eighty rats were randomly divided into the sham-operated group (n = 20), injury group (n = 20), low dosage of everolimus group (n = 20), and high dosage of everolimus group (n = 20). The low dose of everolimus (1.5 mg/kg) was given one day before injuring the carotid artery by balloon, followed by 0.75 mg/kg per day for 28 days via intragastric gavage. High dose everolimus (2.5 mg/kg) was given one day before injuring the carotid artery by balloon, followed by 1 mg/kg per day for 28 days. Expression of eukaryotic translation initiation factor 4E (eIF-4E) and phosphorylation of ribosomal protein S6 kinase 1 (P70S6K) were determined by reverse transcription-polymerase chain reaction and Western blotting analysis.

RESULTSIn the injured carotid artery, neointimal hyperplasia was normally observed four weeks after injury. Everolimus inhibited neointimal hyperplasia after balloon injury in a dose dependent manner. At the same time, the study demonstrated that everolimus reduced the expression of P-P70S6K, eIF-4E, transforming growth factor (TGF)-β1 and of proliferating cell nuclear antigen (PCNA).

CONCLUSIONSEverolimus significantly inhibited neointimal hyperplasia of the injured carotid artery. The effect depended on dosage and was associated with the reduction of phosphorylation of P70S6K and the eIF-4E expression level.

Animals ; Carotid Arteries ; drug effects ; Carotid Artery Injuries ; drug therapy ; Carrier Proteins ; metabolism ; Everolimus ; Male ; Neointima ; drug therapy ; Phosphoproteins ; metabolism ; Phosphorylation ; drug effects ; Rats ; Rats, Sprague-Dawley ; Ribosomal Protein S6 Kinases, 70-kDa ; metabolism ; Sirolimus ; analogs & derivatives ; therapeutic use