Using 70 SD white rats, diveded in two groups at random, after the common carotid artery wa(?) exposed, anastomosis of the artery was done by whole-layer suture and suture without including the endothelial layer, respectively. The rate of patency of both groups immediately after operation was 100 percent, where as in late stage, 94 percent and 97 percent, respectively. From the histologic exam ination, it was found that in the group of whole-layer suture, the time required to cover the sutureline with endothelium was delayed and there was rupture of the clastic fibers.
Objective To investigate the possible mechanism of the fibroblasts inducing the vascularization of dermal substitute. Methods Fibroblasts were seeded on the surface of acellular dermal matrix and cultivated in vitro to construct the living dermal substitute. The release of interleukin 8 (IL 8) and transfonming growth factor β 1(TGF β 1) in culture supernatants were assayed by enzyme linked immunosorbent assay, the mRNA expression of acid fibroblast growth factor (aFGF) and basic fibroblast growth factor (bFGF) were detected by RT-PCR. Then, the living substtute was sutured to fullth ickness excised wound on BALBouml;C m ice, and the fate of fibroblast w as observed by using in situ hybridizat ion. Results Fibroblasts cultured on acellular dermalmat rix p ro liferated and reached a single2layer confluence. Fibroblasts could secret IL 28 (192. 3±15. 9) pgouml;m l and TGF-B1 (1. 105±0. 051) pgouml;m l. There w as the mRNA exparession of aFGF and bFGF. Fibroblasts still survived and proliferated 3 weeks after graft ing. Conclusion Pept ides secreted by fibroblasts and its survival after graft ing may be relat ive to the vascularizat ion of the dermal subst itute.
Abstract The narrow pedicled intercostal cutaneous perforater (np-ICP) thin flaps were successfully used for reconstruction of hand deformity from scar contraction. This flap was designed with a narrow pedicle (3～5cm in width) which included ICPs of 4th～9th intercostal spaces, and with awide distal part (the maximum is 15cm×15cm) which covered the lower chest and upper abdomen. The thickness of flap was cut until the subdermal vascular networkwas observed. The pedicle was divided between the 7th～14th days after operation. Sixteen flaps in 15 cases were transferred for covering of the skin defects at the dorsum of the hand. The perforators which were included in the narrow pediclewere mostly from the 7th intercostal spaces in 9 flaps. Fifteen of the 16 flapswere survived almost completely, except in one case there was necrosis of the distal portion of the flap. It seemed that this flap was more useful than the conventional methods, not only functionally but also aesthetically. Moreover, the operative techinque was more simple and safer than the island or free intercostalflap due to without the necessity to dissect the main trunk of the intercostalneurovascular bundle. Gentle pressure on the thinning portion of the flap for a short time after operation was important.
Objective To evaluate repair and reconstructionof the femoral pseudoaneurysm caused by drug injection. Methods From May 2000 to May 2005, 15 cases of femoral pseudoaneurysm caused by drug injection underwent operation treatment. All patients were male, aging 20-36 years. The disease course was 18-52 days(mean 35 days) and the course of druginjection was 3-17 months. The locations were the left side in 5 cases and theright side in 10 cases. After having been bandaged with pressure and supportedwith nutrition, they had been all operated. One case received fistula repair, and 14 cases received vascular grafting with ePTFE man-made blood vessel. Results The wounds healed by the first intention in 14 cases. All limbs survived. The complexion, temperature and response of involved leg were in gear. The postoperative color ultrasound Doppler detection showed that all the vascular grafts were of patency. The function of the involved limbs restored to normal. Conclusion Complete debridement, vascular reconstruction and better microsurgery skill were the key factors of treating successfullythe femoral pseudoaneurysm caused by drug injection.
OBJECTIVE: To measure the length and extent of the injured blood vessels in an avulsion amputation model. METHODS: Twenty rabbits were randomly divided into 2 groups. Group A was a sharp amputation group, and group B was an avulsion amputation group. The length and extent of the injured blood vessel was observed with naked eye, operation microscope and electron microscope, and the limbs were replanted. Group A and B were explored at three days and ten days after the replantation respectively. The patency rate and healing process were compared. RESULTS: All the severed ends of vessels in group A were neat with almost the same injured range in the three layers of the vessel wall about 1 mm away from the severed end. The vessels of group B were damaged seriously, the endothelial cells were deleted. The "jumping-like" damage could be observed in the elastic fibers. The injury of 2 to 3 mm away from the normal vessel wall could be observed by operation microscope. CONCLUSION: The damage of avulsion amputation vessels was irregular, 2 to 3 mm or more tissues should be excised under the microscope in the process of operation in order to ensure the healthy intact blood vessel walls.
摘要:目的: 探讨激活转录因子(ATF1)在血管紧张素Ⅱ(AngⅡ)诱导血管平滑肌细胞(VSMCs)中NOX1基因表达增加的作用。 方法 :体外培养大鼠主动脉VSMCs,用荧光实时定量逆转录PCR(Realtime RTPCR)检测NOX1基因表达的量,Western Blot检测ATF1蛋白在AngⅡ的刺激是否引起NOX1基因的高表达并用RNA干扰(RNAi)技术转染VSMCs使ATF1基因沉默来观察NOX1的表达。 结果 :AngⅡ能够诱导 NOX1基因的表达增加以及增强ATF1的磷酸化及活性,ATF1基因沉默反过来可抑制AngⅡ诱导的NOX1基因表达的增加。 结论 :在大鼠的VSMCs中,ATF1是介导NOX1基因表达的一个必须的转录因子。Abstract: Objective: To detect the role of activating transcription factor (ATF1) involved in angiotensinⅡ(AngⅡ) stimulated NOX1 gene expression.Methods :Rat aortic vascellum smooth muscle cells(VSMCs) were cultured in vitro.Use Realtime RTPCR to measure the expression of NOX1 gene.Western Blot Analysis was carried out to test the activity of ATF1 protein. RNA interference was used and transfected into VSMCs to knockdown ATF1 gene expression, and then measured NOX1 gene expression.Results : AngⅡ stimulated NOX1 gene expression and phosphorylation of ATF1 Gene silencing of ATF1 attenuated the upregulation of NOX1 mRNA by AngⅡ. Conclusion :ATF1 is an essential transcription factor that mediates expression of NOX1 gene in VSMCs by AngⅡ.
Objective To evaluate the inhibited effects of small interfering RNA targeting Rac1 (Rac1-siRNA) on rat retinal neovascularization in retinae. Methods Retinal vein occlusion was induced by retinal photodynamic medthod in 25 Sprague-Dawley rats. Rac1-siRNA vector DNA was injected into the vitrous of one eye of those rats (gene intervention group), and empty vector DNA was injected into the fellow eye (blank control group). Rac1-siRNA vector was injected in other 25 SD rats without retinal vein occlusion (blank intervention group). Two weeks after injection, fluorescein isothiocyanate (FITC)-dextran was perfused into the hearts of all the rats, and the retinal wholemount was made to observe the neovascularization. The numbers of endothelial cells which break through the internal limiting membrane were counted after hematoxylin-eosin staining. Results A massive of neovascularization and FITC leakage were found in blank control group. Small part of neovascularization and a little FITC leakage were observed in the gene intervention group. Retinal vessels were normal in blank intervention group. Compared with blank contrast group and blank intervention group, the difference of the mean numbers of endothelial cells which broke through the internal limiting membrane in the gene intervention group was significant（t=? P=0.000??lt;0.05）. Conclusion Rac1-siRNA can inhibit retinal neovascularization induced by retinal vein occlusion in rats.
rough the ultramicroscopic observation on muscle and microcirculation, Group A,where a largeamount of DXM combined with heporin was given svstematically and locally into the femoral artery of the severed limb before replantation, and in Group B only heporin was given, and Group C and D ascontrol.The results showed that if the hormone and heparin were administred in large dosage, it wasadvantageous to reduce the tissues from reperfusion injury during delayed replantation.
OBJECTIVE To investigate the mechanism of electrothrombosis by copper needle, in order to supply the referential data for clinical treatment of vessel deformity. METHODS The mechanism and condition of thrombus formation by copper needle were studied in vivo and in vitro using electrophysics, atom absorption spectrophtometry, histological, and histochemical methods. RESULTS Great deal of copper ion was dissociated, and agglutination of red blood cells(RBC) in blood could be observed in vitro after the current applied by copper needles. Formation of stable thrombus was related to voltage and time of application of electric current. CONCLUSION Dissociation of copper ion and agglutination of RBC are the basic principle of electrothrombosis with copper needle. A 4V direct current and 17.5 minutes are the safe and effective conditions for thrombus formation in the blood vessels.
The femoral veins were excised from 28 dogs and distended with pressure of 40, 80 and 120 kPa, respectively before grafted to femoral arteries. The veins were harvested at different times and Pollak sections were prepared which revealed different stains of elastin, collagen and smooth muscle in each section. The sections were led to image analysis system to computerize the relative contents of theabove components. The results were as follows: Elastin decreased significantly at 4 weeks (P lt;0.01), and was constant between 4 and 16 weeks. No statistical difference was found in 40, 80 kPa and the control group (P gt;0.05), but the elastin of 120 kPa group by the 16th week was still decreasing. Collagen of each group had no difference, but C/E increased significantly with time. Smooth muscle contents were correlated positively with time, and negatively with the pressure at 1 week, then positively with the pressure at 16th week. The changes of the above trends were the same as development of intimal hyperplasia. The contentions were the value of C/E was determined by the arterial pressure but that of 120 kPa pressure was more higher. The preimplant pressure distension was a possible significantfactor leading to excessive intimal hyperplasia of early and middle stage of autogenous vein grafts.