The formation of an arteriovenous fistual for dialysis by routine interrupted sutures anastomosing the vein and artery is difficult to perform and time-consuming. A new method, telescopic adhesive anastomosis was studied and applied in 10 hemodialysis patients, who were in need of an arteriovenous fistula. The external diameter of the vessels anastomosed was 2.40 +/- 0.20 mm (radial artery) or 2.40 +/- 0.35 mm (cephalic vein). After thorough debridement of the vascular ends, the arterial end was put in the venous lumen. In order to fix the telescopic vessels, two stitches were applied 180 degrees apart from each other and tied. Each stitch was inserted from vein (penetrating the whole wall) to artery (just through the adventitia and partial thickness of the media vasorum). The distance from the stitch to the edge of the vein was 0.5 mm, and that of the artery was approximated to the external diameter of the vessle. The medical adhesive was then applied for sealing the anastomotic adventitia. Ten seconds were given for the solidification of the adhesive. The patients were followed up for 8 months. The patency rate was 100%, and the rate of blood flow was more than 300 ml/min (measured by ultrasonography). It was shown that this method could be managed easily and quickly, and the so-formed fistula would fulfill the need of hemodialysis.
Cerebral small vessel disease (CSVD) encompasses a group of progressive disorders involving the small vessels of the brain with complex etiologies. Inflammation plays a pivotal role in both the onset and progression of CSVD. In age-related CSVD, chronic inflammation can exacerbate brain tissue damage by impairing endothelial function and disrupting the blood-brain barrier. In contrast, in inflammatory CSVD subtypes driven primarily by immune dysregulation, inflammation itself constitutes the core pathogenic mechanism. These subtypes present with diverse clinical manifestations, posing significant challenges for diagnosis and treatment. A deeper understanding of the inflammatory mechanisms involved in CSVD and the unresolved issues in this field may provide new avenues for personalized interventions and improved prognosis.
Cerebral small vessel disease refers to a series of clinical, imaging, and pathological syndromes caused by various factors affecting small blood vessels in the brain. Cognitive impairment is one of the most common complications of cerebral small vessel disease. Current researches have found that cognitive impairment is related to various factors such as hypoxia. Hyperbaric oxygen therapy can achieve certain therapeutic effects by improving hypoxia. This article reviews the pathogenesis of cerebral small vessel disease, biomarkers of cerebral small vessel disease, research progress on hyperbaric oxygen therapy for cognitive impairment, and focuses on the research progress of hyperbaric oxygen therapy for mild cognitive impairment and dementia, providing more references for clinical treatment.
OBJECTIVE: To explore an ideal way of small vessel anastomosis for microsurgery. METHODS: Anastomosis of both carotid arteries were performed in 20 rabbits. One side of the arteries were anastomosed with anastomotic clips, the other side of the arteries, as comparison, were anastomosed with suture. The vessels were harvested at first and 14th day after operation and were evaluated using operating microscope, light microscope and electronic microscope. RESULTS: The average anastomotic time for suture was about 15 minutes, while for the clips was 2 to 5 minutes. There were no difference in patency between the two techniques. Endothelialization at the anastomotic sites were both completed 14 days postoperatively. However, for the anastomotic clips, there were no endothelia damage and foreign bodies formation inside the vessels. CONCLUSION: This experiment has confirmed that the anastomotic clip’s procedure provides a very safe and easy way to perform anastomosis and reduce the incidence of thromboses.
OBJECTIVE To investigate the clinical result in repair of soft tissue defect with combined skin flap vascularized by pedicle on the one end and vascular anastomosis on the other end. METHODS From October 1990 to August 1995, 5 cases with soft tissue defect at the extremities and 1 cases with sacral bed sore were repaired by the combined skin flaps transfer, ranged from 15 cm x 30 cm to 16 cm x 70 cm in defect, among them, 5 cases with myocutaneous flap and 1 case with skin flap, and the size of the combined skin flaps was 15 cm x 40 cm to 12 cm x 80 cm. RESULTS All the flaps were survived with satisfactory effect. Followed up 3 to 6 years, there was no obvious complication. CONCLUSION Transfer of combined skin flaps vascularized by pedicle and vascular anastomosis is suitable to repair the soft tissue defect, especially in large area defect.
Objective To study the effect of silencing the NOD-like receptor family, pyrin domain containing protein 3 (NLRP3) gene on the production of inflammatory factors induced by lipopolysaccharide (LPS) and adenosine triphosphate (ATP) in rat brain microvascular endothelial cells (BMECs), and whether NLRP3 inflammasome signaling pathway plays a role in the BMEC model of cerebral small vessel disease induced by proinflammatory agents. Methods BMECs from male Wistar rats were extracted in vitro and the morphology and purity of endothelial cells were identified. BMECs in normal culture were divided into blank control group and LPS+ATP group. The expression levels of NLRP3 inflammasome and downstream inflammatory factor Caspase-1 were detected by Western blot and real-time polymerase chain reaction, and compared by student’s t test between the two groups. Small interfering RNA (siRNA) was used to silence the specific gene NLRP3 in BMECs. After transfection of siRNA NLRP3 and siRNA plasmid negative control into BMECs, the transfected cells were divided into four groups, namely, siNC group (non silenced target gene), siNLRP3 group (silenced target gene), siNC+LPS+ATP group (non silenced target gene and added proinflammatory agents) and siNLRP3+LPS+ATP group (silenced target gene and added proinflammatory agents). The expression levels of NLRP3 and Caspase-1 were detected by Western blot and real-time polymerase chain reaction, and analyzed by analysis of variance for 2-factor factorial design. Results The microvascular segments of rat BMECs were “beaded” after 24 h of isolation and culture; after 48 h, “island” cell clusters were formed; after 72 h, “paving stone” like monolayer cells adhered to the wall and grew. After that, the cells gradually became dense and reached the convergence degree of 80%. The positive rate of BMECs detected by immunofluorescence staining was 96%. In the normally cultured cells, the protein and mRNA expression levels of NLRP3 and Caspase-1 in the LPS+ATP group were higher than those in the blank control group (P<0.05). In the RNA interference cultured cells, the protein and mRNA expression levels of NLRP3 and Caspase-1 in the siNLRP3 group were lower than those in the siNC group, and those expression levels in the siNLRP3+LPS+ATP group were lower than those in the siNC+LPS+ATP group (P<0.05); the protein and mRNA expression levels of NLRP3 and Caspase-1 in the siNC+LPS+ATP group were higher than those in the siNC group, and those expression levels in the siNLRP3+LPS+ATP group were higher than those in the siNLRP3 group (P<0.05). Plasmid transfection and proinflammatory agents intervention had statistically significant interaction effect on the mRNA expression of NLRP3 and Caspase-1 (P<0.05). Conclusions LPS and ATP can promote the release of NLRP3 and Caspase-1 in BMECs. Silencing NLRP3 gene expression can reduce the induction of proinflammatory agents. NLRP3 inflammasome signaling pathway may play a role in the cerebral small vessel disease cell model of rat BMECs induced by proinflammatory agents.
Cerebral small vessel disease refers to a group of pathological processes, neuroimaging features, and clinical symptoms, with various etiologies that affect the small arteries, arterioles, venules, and capillaries of the brain. The onset of cerebral small vessel disease can be insidious. It has various symptoms, some of which can attack acutely. Acute cerebral small vessel disease is characterized by lacunar stroke and brain parenchymal hemorrhage. The latter mainly includes hypertensive hemorrhage and cerebral amyloid angiopathy. This article summarizes the research advances of acute cerebral small vessel disease from the aspects of pathogenesis, clinical manifestations, neuroimaging features, and treatment methods, discussing characteristics and clinical challenges.
ObjectiveTo investigate the relationship between the level of homocysteine (HCY) and the overall burden of cerebral small vessel disease (CSVD) in patients with ischemic stroke.MethodsA total of 322 patients with first-ever ischemic stroke admitted to the People’s Hospital of Deyang City between January 2016 and December 2017 were enrolled. The patients’ demographic information, clinical information, and serum HCY concentration were collected after admission. The presence or absence of a CSVD was assessed by MRI and the overall burden score for the CSVD was determined. Multivariate logistic regression analysis was used to assess whether serum HCY level was associated with the overall burden of CSVD.ResultsThe median level of HCY was 13.2 μmol/L (inter-quartile range: 4.3 to 22.6 μmol/L). Univariate analysis showed that the difference of HCY levels among patients with different total CSVD scores was statistically significant (F=6.874, P=0.001); Spearman correlation analyses showed that the HCY level grouped by quartiles was correlated to the number of lacunar infarctions (rs=0.267, P=0.001), Fazekas score of white matter lesions (rs=0.122, P=0.042), and enlarged perivascular space (EPV) score (rs=0.319, P=0.001), but was not correlated to cerebral microhemorrhage (rs=−0.010, P=0.869). After multivariate regression analysis to adjust the effects of other factors, compared with the patients with HCY levels in the lowest quartile group, the patients with HCY levels in the highest quartile group were more likely to develop lacunar infarction [odds ratio (OR)=1.892, 95% confidence interval (CI) (1.012, 2.987)], white matter lesions [OR=1.548, 95%CI (1.018, 1.654)], severe EPV [OR=6.347, 95%CI (3.592, 13.978)], and the increase in the CSVD score [OR=2.981, 95%CI (1.974, 5.398)].ConclusionIn patients with ischemic stroke, elevated HCY levels may be associated with the overall burden of the CSVD.