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 effects of hyperglycemia on ubiquitination and endoplasmic reticulum stress in renal intrinsic cells (podocytes and proximal tubular epithelial cells)and its role in pathogenesis of diabetic nephropathy.Methods Diabetic mice were induced by streptozotocin injection.After 16 weeks of hyperglycemia,immunofluorescence was used to detect the expressions of ubiquitination and glucose-regulating protein 94 (GRP94) in renal cortex and medulla area of kidney sections.Primary mouse podocyte and proximal tubular epithelial cells were isolated by flow cytometry,and exposed to 30 mmol/L glucose for indicated time (1 d,3 d and 7 d).Their ubiquitination and GRP94 expressions were evaluated by Western blotting.Results Diabetic mice presented microalbuminuria and slightly widened mesangium was found in glomerular area.Ubiquitinated proteins,mainly localized in podocytes and tubular epithelial cells,exhibited an apparently higher expression in diabetic mice than control mice (all P ＜ 0.05).Hyperglycemia promoted the ubiquitination in a time-dependent manner.Compared with their normal cells,primary mouse podocyte and primary tubular epithilial cells treated with high glucose for 3 d and 7 d showed increased ubiquitinated protein (all P ＜ 0.05).GRP94 was interspersed in podocytes and proximal tubular epithelial cells.Expression of GRP94 was significantly increased in glomerular area of diabetic mice and podocyte with 3 and 7 day-high glucose as compared with those in their control groups (all P ＜ 0.05).GRP94 expression had no significant change in tubular area and tubular epithilial cells treated with high glucose.Conclusions Hyperglycemia may lead to accumulation of ubiquitinated proteins in intrinsic kidney cells.The imbalance of protein homeostasis in podocyte may contribute to podocyte injury during the onset of diabetic nephropathy.

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.

Objective To investigate the effect of surfactant protein A (SP-A) on the production of MIP-2 and binding activity of NF-?B in rat tubular epithelial cells, and evaluate its possible role in renal inflammation. Methods Confluent cultures of NRK-52E cells (a renal tubular epithelial cell line of rat origin) were pretreated with various concentrations of SP-A(0 to 80 ?g/ml) and stimulated by lipopolysaccharide (LPS) (10 ?g/ml) with 2% serum. MIP-2 expression was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR). The effect of SP-A on NF-?B binding activity was assessed by electrophoretic mobility shift assay (EMSA). Results MIP-2 mRNA and protein was expressed and up-regulated in NRK-52E cells stimulated by LPS. The expression of MIP-2 was down-regulated by SP-A. NF-?B binding activity was inhibited by SP-A in a concentration-dependent manner. Conclusion SP-A binding activity and down-regulates the expression of MIP-2 in renal tubular epithelial cells, which may play an important role in the modulation of renal tissue inflammation.

Objective To evaluate the effect of ALD on podocyte apoptosis and the possible roles of Akt in ALD-induced apoptosis. Methods The cultured rat podocytes were incubated with increasing concentrations of ALD (10-9~10-5 mol/L) for variable time periods. Apoptosis was evaluated by cell nucleus staining and flow cytometry. RT-PCR was used to examine the expression of mineralocorticoid receptor (MR)and 11 Beta-hydroxysteroid dehydrogenase type 2 (11?-HSD2) mRNA in podocyte. Activation of Akt/PKB was evaluated by performing Akt kinase assay. Results ALD induced podocyte apoptosis in a dose- and time-dependent manner. The proapoptotic effect was attenuated by the presence of spironolactone (10-7mol/L). The expression of MR and 11P-HSD2 mRNA was demonstrated in the podocytes by RT-PCR. ALD also inhibited the activity of Akt in a dose-dependent manner, but the inhibitory effect was significantly ameliorated by the presence of spironolactone. The activity of Akt was negatively correlated with podocyte apoptosis. Conclusion ALD induces apoptosis in rat podocytes through the signaling mechanism by which Akt is inhibited.