Negative-pressure wound therapy (NPWT) for the treatment of pacemaker pocket infection in patients unable or unwilling to undergo CIED extraction.

PURPOSE: The occurrence of cardiac pacemaker pocket infection has markedly increased and has become a new problem facing cardiovascular internists. The aim of our study was to investigate the effectiveness and safety of treating cardiac pacemaker pocket infection using negative-pressure wound therapy (NPWT) in patients who are unwilling or unable to have their cardiac implantable electronic devices (CIEDs) removed. METHODS: From March 2013 to April 2019, NPWT was applied to 26 patients with cardiac pacemaker pocket infection who were unwilling or unable to have their CIEDs removed. In the first stage, a negative-pressure drainage system was placed in the pacemaker pocket after debridement. Then, NPWT was used to seal the wound, and the negative pressure (300-400 mmHg) was sustained for 5-7 days. In the second stage, the pacemaker was relocated to the subpectoral layer, and the wound was closed. RESULTS: In all but three of our 26 patients, the wound healed completely without complications and without evidence of residual infection. The average follow-up period was 26.92 ± 9.46 months. Only 3 diabetic patients whose tissue bacterial cultures revealed that methicillin-resistant Staphylococcus epidermidis developed uncontrolled infections. Eventually, the entire original pacemaker systems were removed, and new pacemakers were implanted in the contralateral chest wall. CONCLUSIONS: When warranted by strictly selected indications, the method of NPWT without CIED extraction can be considered as a new and effective treatment for patients with pacemaker pocket infection who are unwilling or unable to have the device removed.

[Experimental study on the effect of desferrioxamine on targeted homing and angiogenesis of bone marrow mesenchymal stem cells].

Objective: To investigate whether desferrioxamine (DFO) can enhance the homing of bone marrow mesenchymal stem cells (BMSCs) and improve neovascularization in random flaps of rats. Methods: BMSCs and fibroblasts (FB) of luciferase transgenic Lewis rats were isolated and cultured. Forty 4-week-old Lewis male rats were used to form a 10 cm×3 cm rectangular flap on their back. The experimental animals were randomly divided into 4 groups with 10 rats in each group: in group A, 200 µL PBS were injected through retrobulbar venous plexus; in group B, 200 µL FB with a concentration of 1×10 6 cells/mL were injected; in group C, 200 µL BMSCs with a concentration of 1×10 6 cells/mL were injected; in group D, cells transplantation was the same as that in group C, after cells transplantation, DFO [100 mg/(kg·d)] were injected intraperitoneally for 7 days. On the 7th day after operation, the survival rate of flaps in each group was observed and calculated; the blood perfusion was observed by laser speckle imaging. Bioluminescence imaging was used to detect the distribution of transplanted cells in rats at 30 minutes and 1, 4, 7, and 14 days after operation. Immunofluorescence staining was performed at 7 days after operation to observe CD31 staining and count capillary density under 200-fold visual field and to detect the expressions of stromal cell derived factor 1 (SDF-1), epidermal growth factor (EGF), fibroblast growth factor (FGF), and Ki67. Transplanted BMSCs were labeled with luciferase antibody and observed by immunofluorescence staining whether they participated in the repair of injured tissues. Results: The necrosis boundary of ischemic flaps in each group was clear at 7 days after operation. The survival rate of flaps in groups C and D was significantly higher than that in groups A and B, and in group D than in group C ( P<0.05). Laser speckle imaging showed that the blood perfusion units of flaps in groups C and D was significantly higher than that in groups A and B, and in group D than in group C ( P<0.05). Bioluminescence imaging showed that BMSCs gradually migrated to the ischemia and hypoxia area and eventually distributed to the ischemic tissues. The photon signal of group D was significantly stronger than that of other groups at 14 days after operation ( P<0.05). CD31 immunofluorescence staining showed that capillary density in groups C and D was significantly higher than that in groups A and B, and in group D than in group C ( P<0.05). The expressions of SDF-1, EGF, FGF, and Ki67 in groups C and D were significantly stronger than those in groups A and B, and in group D than in group C. Luciferase-labeled BMSCs were expressed in the elastic layer of arteries, capillaries, and hair follicles at 7 days after transplantation. Conclusion: DFO can enhance the migration and homing of BMSCs to the hypoxic area of random flap, accelerate the differentiation of BMSCs in ischemic tissue, and improve the neovascularization of ischemic tissue.

Dexmedetomidine Protects Against Chemical Hypoxia-Induced Neurotoxicity in Differentiated PC12 Cells Via Inhibition of NADPH Oxidase 2-Mediated Oxidative Stress.

Dexmedetomidine (Dex) is a widely used sedative in anesthesia and critical care units, and it exhibits neuroprotective activity. However, the precise mechanism of Dex-exerted neuroprotection is not clear. Increased neuronal NADPH oxidase 2 (NOX2) contributes to oxidative stress and neuronal damage in various hypoxia-related neurodegenerative disorders. The present study investigated whether Dex regulated neuronal NOX2 to exert its protective effects under hypoxic conditions. Well-differentiated PC12 cells were exposed to cobalt chloride (CoCl2) to mimic a neuronal model of chemical hypoxia-mediated neurotoxicity. The data showed that Dex pretreatment of PC12 cells significantly suppressed CoCl2-induced neurotoxicity, as evidenced by the enhanced cell viability, restoration of cellular morphology, and reduction in apoptotic cells. Dex improved mitochondrial function and inhibited CoCl2-induced mitochondrial apoptotic pathways. We further demonstrated that Dex attenuated oxidative stress, downregulated NOX2 protein expression and activity, and inhibited intracellular calcium ([Ca2+]i) overload in CoCl2-treated PC12 cells. Moreover, knockdown of the NOX2 gene markedly improved mitochondrial function and attenuated apoptosis under hypoxic conditions. These results demonstrated that the protective effects of Dex against hypoxia-induced neurotoxicity in neural cells were mediated, at least partially, via inhibition of NOX2-mediated oxidative stress.