Objective To investigate the effect of nonintubated intravenous anesthesia combined with local anesthesia on sympathetic nerve chain resection. Method One hundred and sixty palmar hyperhidrosis patients undergoing sympathetic nerve chain resection were divided into two groups, intubation general anesthesia (IGA) group and nonintubated intravenous anesthesia (NIA) group. The patients in IGA group were administrated with intubation general anesthesia. The patients in NIA group were administrated with nonintubated intravenous anesthesia. The physical signs, general anesthetics dosage, anesthesia time, hospital stays, hospitalization costs and postoperative complications were compared between two groups. Results In NIA group, the MAP after anesthesia , HR at 5 min and 10 min after anesthesia were lower than those in IGA group :MAP: (65.83 ± 12.53) , (68.19 ± 9.56), (69.72 ± 8.44), (68.58 ± 13.42) mmHg(1 mmHg = 0.133 kPa) vs. (98.47 ± 13.59), (93.53 ± 10.16), (86.13 ± 11.22), (81.52 ± 9.67) mmHg; HR:(76.36 ± 7.93), (78.42 ± 9.13) bpm vs. (102.67 ± 10.38), (97.66 ± 9.73) bpm, P<0.05. Similarly, the SpO2 and PaO2 after anesthesia in NIA group were also lower than those in IGA group:SpO2:0.93 ± 0.14, 0.94 ± 0.21, 0.93 ± 0.34, 0.94 ± 0.24 vs. 1.00 ± 0.13, 0.99 ± 0.16, 0.99 ± 0.20, 0.98 ± 0.13; PaO2: (83.73 ± 8.35), (68.57 ± 9.32), (63.93 ± 10.54), (65.51 ± 11.72) mmHg vs. (298.65 ± 25.19), (328.58 ± 30.61), (303.26 ± 29.34), (317.49 ± 28.15) mmHg , P<0.05. And the PaCO2 after anesthesia was higher than that in IGA group (52.93 ± 9.27), (61.47 ± 7.32), (71.58 ± 8.23), (68.13 ± 10.58) mmHg vs. (36.86 ± 5.52), ( 35.73 ± 6.14), (37.18 ± 7.39), (36.35 ± 5.87) mmHg, P<0.05. In NIA group, the dosages of propofol and remifentanil, anesthesia time were less than those in IGA group:(235.63 ± 19.42) mg, (446.58 ± 50.32)μg, (66.45 ± 13.35) min vs. (317.86 ± 28.36) mg, (623.47 ± 403.93)μg , (89.27 ± 16.38) min, P<0.05 or<0.01. In hospital stays, hospitalization costs, there were no significant differences between two groups (P>0.05). In NIA group, 8 patients needed artificial respiration, which were more than those in IGA group (8 vs. 0) (P<0.05). In NIA group, the incidences of throat discomfort, nausea and vomiting were lower than those in IGA group:0 vs. 32.5% (26/80) and 25.0% (20/80) vs. 11.2% (9/80), P<0.05. However, the incidence of lung infection was similar to that in IGA group (P>0.05). Conclusions Nonintubated intravenous anesthesia combined with local anesthesia is safe for palmar hyperhidrosis patients undergoing sympathetic nerve chain resection, with less complications and without increasing the workload.

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Objective To explore the effect of suledexide on renal injury and podocalyxin expression of podocytes in STZ diabetic desoxycorticosterone acetate (DOCA)-hypertensive rats. Methods Wistar rats were subjected to subcutaneous injection of streptozotocin(STZ), followed by uninephrectomy and subcutaneous administration of DOCA. Diabetic and hypertensive rats were randomly allocated to treatment with sulodexide or a combination of sulodexide and telmisartan for 8 weeks. Blood pressure (BP), 24-hour urinary albumin were measured every 2 weeks. Blood and urinary samples were collected to detect biochemical indexes of plasma and urinary β-acetyl-β-D-glucosaminidase (NAG) at the end of the study. Immunohistochemistry (IHC), RT-PCR and Western blot were performed to examine the expression and distribution of podocalyxin. Results STZ +DOCA-treated rats progressively developed hypertension, albuminuria and hyperglycemia. Hyperlipidemia and hypoinsulinemia were found in diabetic and hypertensive rats compared with controls. Albuminuia was significantly reduced in sulodexide group at week 8 and sulodexide plus telmisartan group at week 6 and week 8. Blood pressure decreased in sulodexide plus telmisartan group. No significant effects on lipid and glucose metabolism were observed in all treated groups. Histopathological index increased in STZ+DOCA-treated rats, but was significantly lower in sulodexide group as well as sulodexide plus telmisartan group. The number of podocytes on glomerular cross-section of the four groups were comparable. Segmental loss and down-regulation of podocalyxin were detected in STZ+DOCA-treated rats, which were greatly attenuated by sulodexinde, meanwhile, combination treatment preserved more podocalyxin expression in glomeruli than sulodexide monotherapy. Conclusion Sulodexide effectively reduces albuminuria, prevents loss of podocyte podocalyxin and alleviates renal damage in STZ diabetic DOCA-hypertensive rats.

Objective To determine the surfactant protein A (SP-A) subtype distribution and expression in human renal tissue and cultured human renal tubular epithelial cells(HK-2), and to explore the influence of Lipopolysaccharide (LPS) on the expression of SP-A subtypes mRNA and SP-A protein. Methods lmmunohistochemical staining was performed using SP-A polyclonal antibodies. RT-PCR was performed with mRNA from HK-2 cells and normal human kidney.Restriction fragment length polymorphism(RFLP) and sequencing were used to evaluate the subtypes of SP-A. The relative content of SP-A mRNA in human kidney and human lung was compared by real-time PCR. Western blotting analysis for SP-A was performed on protein from renal tissue and cultured HK-2 cells SP-A protein in human urine and culture supernatant of HK-2 cells was measured by enzyme-linked immunosorbent assay (ELISA) and Western blotting respectively. HK-2cells were treated with LPS at various concentrations (0,0.1,1,2,5,10 mg/L) for 8 h and at 5mg/L for various time points (0,2,4,8,16,24 h). Expression of SP-A mRNA and protein was analyzed by RT-PCR and Western blotting. Results SP-A was localized in renal tubular epithelial cells of both proximal and distal convoluted tubules. SP-A1, SP-A2 mRNA and protein could be detected in normal HK-2 cells and human kidney. The significant secretion of SP-A [urine: (106.614172.772) nmol/L, n=30; culture supernatant: (85.533±58.622) nmol/L, n=10] was shown. The levels of SP-A1, SP-A2 mRNA and Sp-A protein in HK-2 cells were significantly decreased after treatment with LPS. Conclusions Human renal tubular epithelial cells can express both SP-A1 and SP-A2 genes which may play an important role in inflammation modulation of kidney.

Objective To investigate the effect of surfactant protein D(SP-D)overexpression on lipopolysaccharide(LPS)-induced monocyte chemoattractant protein-1(MCP-1)expression in human renal proximal tubular epithelial cells(HK-2)and its mechanism. Methods HK-2 cells were treated with LPS at various concentrations (0, 0.1, 1, 2, 5, 10 mg/L)for 8 h and at 5 mg/L for various time points(0, 2, 4, 8, 16, 24 h). Expression of SP-D was detected by Western blotting and real-time PCR. Expression of MCP-1 was determined by ELISA and real-time PCR. Human SP-D cDNA eukaryotic expression vector pEE14-hSP-D was transfected to HK-2 cells. The changes in transfected cells of SP-D protein were observed by Western blotting. Expression of MCP-1 was detected by ELJSA and real-time PCR. Results SP-D was expressed in HK-2 cells. The levels of SP-D protein and mRNA in HK-2 cells were significantly decreased after treatment with LPS(P<0.05). Expression of MCP-1 protein and mRNA was increased remarkably after treatment with LPS(P<0.05). HK-2 cells transfected with pEE14-hSP-D showed up-regulated expression of SP-D. The overexpression of SP-D inhibited the LPS-inducedexpression of MCP-1(P<0.01). Conclusions SP-D inhibits LPS-induced expression of MCP-1 in HK-2 cells. SP-D may play an important role in the modulation of renal inflammation.

Objective To investigate the effect of angiotensin 1-7(Ang 1-7) on renal proximal tubular epithelial cell(HK-2) transdifferentiation induced by high glucose.Methods All the raised HK-2 cells were divided into 5 groups: normal control group,high glucose group,high glucose with Ang1-7 group,high glucose with Ang1-7 and A779 group,high glucose with pioglitazone group.Expression of peroxisome proliferator activated receptor-γ(PPAR-γ) and α-smooth muscle actin(α-SMA) was detected by Western blotting,real-time PCR and immunofluorescence.Results The levels of PPAR-γ protein and mRNA in HK-2 cells were significantly increased after treatment with high glucose and Ang 1-7.Expression of α-SMA protein and mRNA was inhibited remarkably after treatment with high glucose and Ang 1-7.These effects of Ang 1-7 on HK-2 cells could be reversed by Mas receptor antagonist A779.Conclusion Ang 1-7 inhibits high glucose-induced expression of o-SMA in HK-2 cells,which is in part through the Mas.

Objective To investigate the effects of angiotensin1-7 (Ang1-7) on renal tubulointerstitial fibrosis of diabetic rats.Methods Thirty-two male Wistar rats were randomly divided into four groups: normal control group,diabetic group,telmisartan group,Ang1-7-treated group.For 9 weeks after diabetes mellitus model established,24 h proteinuria,urine NAG/Cr,glucose,insulin,TG,TC,BUN,Scr,Na+ and K+ were assessed.Renal pathological changes were evaluated by PAS staining; Expression of TGF-β1,PPARγ and α-SMA mRNA was deteeted by real-time PCR; Protein levels of PPARγ,α-SMA and TGF-β1 were detected by Western blotting.Results (1)At the end of the ninth week,the blood pressure,proteinuria,renal weight/body weight in group DM were significantly higher than those in group NC (P＜0.05).(2)Renal interstitial fibrosis in group DM was obviously severe as compared to group NC (P＜0.05),but was improved in group TM and group T(P＜0.05).(3)TGF-β1 and α-SMA mRNA in group DM were significantly increased,and PPARγ mRNA was significantly decreased.Compared with group DM,TGF-β1 and α-SMA mRNA were significantly decreased,and PPARγ mRNA was significantly increased in group TM and group T,especially in group T.(4)TGF-β1 and α-SMA in group DM were significantly increased,and PPARγ decreased significantly.Compared with group DM,TGF-β1 and α-SMA decreased significantly,PPARγ increased significantly in group TM and group T,especially in group T.Conclusion Ang1-7 inhibits high glucose-induced α-SMA expression in vivo through up-regulating the PPAR expression and may inhibit renal tubulointerstitial fibrosis of diabetic rats.

ObjectiveTo investigate the effect of Simvastatin on LOX-1 and ROS in NRK52E induced by ox-LDL.MethodsNRK-52E cells were divided into three groups: Control group,ox-LDL group (50 μg/ml ox-LDL) and Simvastatin group (10 μmol/L Simvastatin +50 μg/ml ox-LDL).After incubation for 24 h,the expression of LOX-I was analyzed by Western blotting,and production of reactive oxygen species (ROS) was analyzed with confocal laser scanning microscopy.ResultsNRK-52E expressed LOX-1 at low level,50 μg/ml ox-LDL increased the expression of LOX-1 by 6.80 times.Pre - treatment with Simvastatin decreased LOX-1 expression by 65％.There was little ROS generation in NRK52E cells,50μg/ml ox-LDL promoted the expression of LOX-1 by 4.86.times.Pre - treatment with Simvastatin decreased ROS generation by 60％.ConclusionsSimvastatin upregulate LOX-1 expression and ROS generation induced by Ox-LDL in NRK52E cells.

Objective To evaluate the effect of aldosterone (Ald) on glomerular mesangial cells apoptosis and to explore the possible mechanisms.Methods Twenty-four Sprngue-Dawley rats were subcutaneously embedded with osmotic mini-pumps and randomly divided into 3 groups.Aldosterone (1.5 μg/h) was administrated subcutaneouly by osmotic mini-pumps in Ald group,eplerenone (Epl,100 mg·kg-1·d-1) and Ald (1.5 μg/h) was given to Epl group.And normal saline was used in control group (Con group).Systolic blood pressure and urinary albumin excretion rate (UAER) were detected on day 0,7,14,21,28.Blood and kidney samples were harvested on day 28.Plasma creatinine,potassium and aldosterone were measured.Renal paraffin sections were stained by PAS and the morphological changes were evaluated by light microscopy.Apoptosis index of mesangial cells were detected by TUNEL assay.The glomerular mesangial cells (MCs) were cultured in a DMEM-F12 media.MCs apoptosis was evaluated by staining cells with Annexin V and propidium iodide (PI) using flow cytometer.Expression of Bcl-2 and Bax mRNA was examined by RT-PCR.The protein level of Bad or phospho-Bad was measured by Western blotting.Results Ald-infused rats developed hyperaldosteronemia and hypokalemia.Rats in Ald group exhibited significant hypertension and marked albuminuria.Ald group rats showed increased number of TUNEL-positive mesangial cells when compared with control rats (P＜0.05).Aldosterone induced mesangial cells apoptosis in a time-dependent manner.Expression of Bcl-2 mRNA was decreased but Bax mRNA was increased in aldosterone treated MCs compared to that in Con group (P＜0.05).Aldosterone promoted dephosphorylation of cytosolic phospho-Bad compared with vehicle treated cells (P＜ 0.05).However,eplerenone attenuated these effects of aldosterone.Conclusion Aldosterone directly promotes mesangial cells apoptosis,and eplerenone can attenuate this effect of aldosterone.Dephosphorylation of cytosolic phospho-Bad may be the key role in the progression of mesangial cells apoptosis induced by aldosterone.