OBJECTIVETo explore the expression and changes of protooncogene c-myc in early restenosis after carotid endarterectomy (CEA).

METHODSUsing New Zealand Rabbits, carotid atherosclerotic stenosis (CASS) model were created. The expression of c-myc in early restenosis after CEA were detected by quantitative real-time polymerase chain reaction (qRT-PCR).

RESULTSIn this experiment protooncogene c-myc was analysed at pre-operation, 4 hours and 1 d after CEA by qRT-PCR, and the level of mRNA of c-myc was reached maximum at 4 hours, and decreased following significantly, but still higher than pre-operation.

CONCLUSIONSThe activation of protooncogene c-myc may be generator factor of vascular smooth muscle cell proliferation.

Animals ; Carotid Arteries ; metabolism ; pathology ; surgery ; Carotid Artery Diseases ; surgery ; Carotid Stenosis ; etiology ; genetics ; physiopathology ; Disease Models, Animal ; Endarterectomy, Carotid ; adverse effects ; methods ; Gene Expression ; Male ; Postoperative Complications ; etiology ; metabolism ; physiopathology ; Proto-Oncogene Proteins c-myc ; genetics ; RNA, Messenger ; genetics ; metabolism ; Rabbits ; Random Allocation ; Reverse Transcriptase Polymerase Chain Reaction

PURPOSE: During carotid angioplasty and stenting (CAS), hemodynamic instability (HDI) can occur, possibly causing post-procedural ischemic complications. The goal of this study was to investigate the risk factors of HDI focusing on characteristics of plaque. MATERIALS AND METHODS: Thirty nine CAS patients were retrospectively evaluated for HDI. Prolonged HDI that lasted over 30 minutes was analyzed in relation to characteristics of calcified plaque. RESULTS: Nineteen (48.7%) patients had HDI. Ten of the 19 had both bradycardia and hypotension, and nine had only bradycardia. All bradycardia was treated well with a transcutaneous temporary cardiac pacemaker. But eight patients presented with prolonged hypotension in spite of recovery of bradycardia. Calcified plaque was a related factor associated with HDI (odds ratio, 8.571; 95% confidence interval, 1.321-55.62; p=0.024). Extensive and eccentric type calcified plaques were associated with prolonged hypotension (p=0.04, and p=0.028, respectively). CONCLUSION: The calcification of plaque is a predictable factor of HDI during CAS, and its extensive and eccentric calcified plaques may be related to prolonged HDI.
Aged ; Angioplasty/*adverse effects ; Bradycardia/complications ; Carotid Arteries/*surgery ; Carotid Stenosis/*physiopathology ; Female ; *Hemodynamics ; Humans ; Hypotension/complications ; Intraoperative Complications/*etiology/radiography ; Intraoperative Period ; Logistic Models ; Male ; Middle Aged ; Retrospective Studies ; Risk Factors ; Stents ; Tomography, X-Ray Computed

Endovascular repair of inflammatory aortic aneurysms has been reported as an alternative to open surgical treatment. In selective cases, adjunctive bypass surgery may be required to provide an adequate landing zone. We report a case of endovascular repair of an inflammatory aortic aneurysm in a patient with Behcet's disease using a carotid-carotid bypass graft to provide an adequate landing zone. A 45-yr-old man with a voice change was referred to our hospital with the diagnosis of saccular aneurysm of the distal aortic arch resulting from vasculitis. Computed tomography showed a thoracic aortic aneurysm with thrombosis. Right to left carotid-carotid bypass grafting was performed. After 8 days, the patient underwent an endovascular stent graft placement distal to the origin of the innominate artery. The patient was discharged with medication and without postoperative complications after 5 days. Hybrid endovascular treatment may be suitable a complementary modality for repairing inflammatory aortic aneurysms.
Aortic Aneurysm, Thoracic/complications/radiography/*surgery ; Behcet Syndrome/*complications/surgery ; Blood Vessel Prosthesis Implantation/*methods ; Carotid Arteries/physiopathology/*surgery ; Coronary Artery Bypass ; Endovascular Procedures ; Humans ; Male ; Middle Aged ; Stents ; Thrombosis/complications ; Tomography Scanners, X-Ray Computed ; Vasculitis/complications

Brief episodes of cerebral hypoxia-ischemia cause transient ischemic tolerance to subsequent ischemic events that are otherwise lethal. This study was conducted to evaluate the protective effect of hypoxic preconditioning on hypoxic-ischemic injury in the neonatal rat and the persistence of a protective window after hypoxic preconditioning. The rats were preconditioned with hypoxia (8% oxygen, 92% nitrogen) for three hours, subjected to ischemia using ligation of the right common carotid artery, and then exposed to another three hours of hypoxia. Using proton magnetic resonance spectroscopy, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining, and morphologic scores, this study shows that hypoxic preconditioning 6-hr to 1-day before hypoxic-ischemic injury increases survival rates and has neuroprotective effects against subsequent hypoxic-ischemic injury. The mechanism of the protective effects of hypoxic preconditioning in the newborn rat brain may involve downregulation of apoptotic cell death.
Animals ; Animals, Newborn ; Apoptosis ; Aspartic Acid/analogs & derivatives/analysis ; Brain/metabolism/pathology ; Carotid Arteries/surgery ; Creatine/analysis ; Hypoxia-Ischemia, Brain/metabolism/pathology/*physiopathology ; In Situ Nick-End Labeling ; Ischemic Preconditioning/*methods ; Magnetic Resonance Spectroscopy ; Rats ; Rats, Sprague-Dawley ; Survival Rate