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To verify the efficacy of transcutaneous electrical acupoint stimulation (TEAS) on catheter related bladder discomfort after ureteroscopic lithotripsy.Sixty male patients with selective ureteroscopic lithotripsy under general anesthesia were randomly divided into a TEAS group (30 cases, one case dropped off) and a sham TEAS group (30 cases, 2 cases dropped off). Before anesthesia induction, the patients in the TEAS group were treated with TEAS at Guanyuan (CV 4), Zhongji (CV 3), Zusanli (ST 36) and Sanyinjiao (SP 6) for 30 min, with disperse-dense wave, frequency of 2 Hz/ 15 Hz and current intensity of 6 to 10 mA. The patients in the sham TEAS group were treated with the same TEAS device at the same acupoints, but no electrical stimulation was given. After 30 min, anesthesia induction started. The total dosages of propofol and remifentanil in the two groups were recorded, and the time of operation and anesthesia, the time of wake-up and the time of stay in postanesthesia care unit (PACU) were recorded. The postoperative recovery was evaluated 5 min (TThe dosage of remifentanil in the TEAS group was significantly lower than that in the sham TEAS group (The 30-min TEAS at Guanyuan (CV 4), Zhongji (CV 3), Zusanli (ST 36) and Sanyinjiao (SP 6) before anesthesia induction could significantly control the severity of postoperative urinary tract irritation in patients with ureteroscopic lithotripsy, reduce the dosage of anesthetic drugs and relieve postoperative pain.

Transcatheter aortic-valve implantation is an alternative to open surgery in high-risk patients with severe aortic stenosis during which the role of the anesthesiologists. is pivotal to the success of the operation. In this review, we summarize recent advances in monitoring and management during anesthesia for transcatheter aortic-valve implantation, and present current information on anesthesia for clinical anesthesiologists. We introduce the latest developments in preoperative assessment techniques and methods of anesthesia, intraoperative monitoring, and intra- and postoperative management, and review innovations in anesthesia for transcatheter aortic-valve implantation. Studies on anesthesia for transcatheter aortic-valve implantation are scarce, but concur that safety and effective monitoring by anesthesiologists are key to a successful operation.

Objective To observe the effects of sevoflurane post-conditioning on the expression of Aquaporin 8 (AQP8) and intestinal fatty acid binding protein (I-FABP), in order to investigate the protective role of sevoflurane post-conditioning on intestinal injury and its underlying mechanism. Methods Eighteen bama miniature pigs were randomly divided into three groups (6 each) using a random number table: control group (S group), hemorrhagic shock group (HS group), and sevoflurane post-coditioning group (Post/ Sev group). Experimental animals were fasted for 8 hours before surgery, and propofol 3mg/kg was given viathe ear vein. Endotracheal intubation was done when the animal fell asleep. Bloodletting from the femoral artery after anesthesia was done to reproduce hemorrhagic shock. In Post/Sev group, 2% sevoflurane was given by inhalation for 30min (post-conditioning) after successful reproduction of the model. Blood samples were collected prior to anesthesia (T0) and 30min (T1), 1h (T2), 1.5h (T3), 2h (T4), 3h (T5), 4h (T6) after hemorrhagic shock. The quantity of blood I-FABP and intestinal AQP8 levels were determined with ELISA. Water content in the intestinal tissue was determined by wet and dry weight method. Histopathological changes in the intestinal tissue were observed with HE staining. Results Compared with the control group, the serum I-FABP content, the expressions of intestinal AQP8, and water content in the intestinal tissue were significantly increased in HS group and Post/Sev (P

The aim of the present study was to explore the roles and possible molecular mechanism of the alleviating effect of sevoflurane pre‑treatment on the extracorporeal circulation and to investigate the possible involvement of the Toll‑like receptor (TLR3) signaling pathway. A total of 64 male Sprague Dawley rats were randomly divided into three groups: The sham operation group (H group; n=8), cardiopulmonary bypass (CPB) group (C group; n=24) and sevoflurane pre‑conditioning group (S group; n=32). The C group was subjected to tracheal intubation and mechanical ventilation, vessel puncture and catheter placement in the right femoral artery and right internal jugular vein, while no CPB was performed in the H group. The S group was pre‑treated with 2.4% sevoflurane for 1 h prior to establishing the CPB model. The CPB in the C and S groups was performed for 1 h. Blood of the rats was analyzed and clinical parameters were detected prior to, during and at various time‑points after CPB. In addition, eight rats from the C and S groups each were sacrificed at these time‑points and brain tissue samples were analyzed. The levels of the brain damage‑specific protein S100‑β as well as IL‑6 and IFN‑β in the serum were detected by ELISA; furthermore, the expression levels of TLR3 and TIR‑domain‑containing adapter‑inducing interferon‑β (TRIF) in the left hippocampus were assessed by ELISA and/or western blot analysis. The right hippocampus was assessed for neuronal apoptosis by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The mean arterial pressure, heart rate and hematocrit were significantly decreased following CPB (P

This study was to investigate the protective effect of recombinant human bone morphogenetic protein-7 (rhBMP-7) on focal cerebral ischemia-reperfusion (IR) injuries and their underlying mechanisms. An intraluminal suture method was used to generate a middle cerebral artery occlusion model in rats, which was followed by reperfusion. A sham operation (SO) group underwent the procedure without occlusion, whereas an IR group and rhBMP-7 treated group (RT) underwent occlusion in the absence and presence of rhBMP-7 (250 μg/kg) administered via a femoral vein injection 30 minutes prior to reperfusion. Twenty-four hours after reperfusion, neurological function, brain water content and morphological alterations were examined. Apoptosis was detected using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assays, and immunohistochemical staining and Western blot assays were used to detect nuclear nuclear factor-kappa B (NF-κB) p65 expression. Compared with the SO group, IR rats showed a decrease in neurological function, an increase in brain water content, and pathological and morphological damage (p < 0.05). Higher levels of apoptosis were also detected in the infarct region area. In contrast, RT rats had reduced injury after IR. In addition, while immunohistochemical staining and western blot assays consistently detected increased expression of nuclear NF-κB after IR, these levels were reduced in the RT group. Administration of rhBMP-7 prior to reperfusion effectively inhibited the extent of IR injury by attenuating cerebral edema and ameliorating ultrastructural damage. The underlying mechanisms responsible for these observations potentially involve the inhibition of apoptosis induced by IR by rhBMP-7 via an NF-κB-related signaling cascade.

Aim To evaluate the acting mechanism of bone morphogenetic protein-7 in anti-ischemic protective effect, we investigate the effects of BMP-7 transfection on cell apoptosis, NF-kappaB activity, and downstream genes in neonatal rat cardiomyocytes during simulated ischemia-reperfusion. Method In vitro cultured neonatal rat cardiomyocytes were divided into four groups: normal control group (Group C), simulated ischemia-reperfusion group (Group IR: cultured cardiomyocytes were subjected to 2 hours hypoxia followed by 4 hours reoxygenation), transfected group (Group BT: after transfection with pcDNA3.1-BMP-7 plasmid, cardiomyocytes were subjected to 2 hours hypoxia/4 hours reoxygenation), and empty vector control group (Group ET: same as group BT except that cells were transfected with empty pcDNA3.1 vector). Malondialdehyde content, superoxide dismutase activity, and Ca(2+) concentration were measured. Terminal deoxynucleotide transferase-mediated dUTP nick-end labeling staining and fluorescence activated cell sorting assay were applied to determine the apoptotic rate of cardiomyocytes and immunocytochemistry and Western blot were used to detect nuclear expression of NF-kappaB in cardiomyocytes. Reverse transcription-polymerase chain reaction was used to detect mRNA expression of monocyte chemoattractant protein-1 and intercellular cell adhesion molecule-1. Results Compared with Group IR, malondialdehyde content of Group BT significantly decreased, whereas superoxide dismutase activity significantly elevated. In addition, intracellular Ca(2+) concentration of Group BT significantly reduced and apoptotic cells were significantly less. Decreased optical density ratio of NF-kappaB in the nucleus and reduced monocyte chemoattractant protein-1 and intercellular cell adhesion molecule-1 mRNA expression were also detected. Conclusion These results suggest that rat recombinant BMP-7 transfection provides sustained support for the repair of myocardium from ischemia injury through reducing cell apoptosis, inhibiting lipid peroxidation, antagonizing intracellular Ca(2+) overload, and preventing the activation of downstream signaling factors in signal transduction pathway mediated by NF-kappaB.

1. In the present study, we investigated the impact of 1.0% ropivacaine on the ultrastructure and proteome of the rat spinal cord. 2. Rats received three injections (90-min intervals, 0.2 mL/kg) of 0.9% NaCl, 0.5% ropivacaine or 1.0% ropivacaine via an implanted intrathecal catheter. Transmission electron microscopy was performed to exam the ultrastructure of the spinal cord. Two-dimensional electrophoresis followed by mass spectrometry identification were carried out to investigate the proteome. 3. In the rats administered 1.0% ropivacaine, deformed organelles, detached myelinated nerve fiber layer, and incomplete inner and outer shaft membranes were observed in the spinal cord and posterior root shrunken nuclei. Furthermore, in the rat spinal cord 1.0% ropivacaine induced the down-regulation of voltage-dependent anion channel 2 (VDAC2) and mitochondrial pyruvate dehydrogenase subunit alpha (ODPA), the upregulation of myelin basic protein (MBP), the disappearance of myelin transcription factor 1 (MYT1) and the appearance of heat shock protein 25 (HSP25). Little change was observed in the 0.5% ropivacaine or control groups. 4. Our results suggest that 1.0% ropivacaine treatment led to neurotoxicity, as shown by ultrastructural and proteomic changes in the rat spinal cord. Specific proteins were identified that are implicated in 1.0% ropivacaine-induced neurotoxicity.

Postoperative cognitive dysfunction (POCD) is associated with cardiopulmonary bypass (CPB). We investigated the effect of different doses of inhaled sevoflurane administered prior to CPB on cerebral oxygen supply and demand, and the incidence of associated early POCD. One hundred and twenty patients were randomly allocated into four treatment groups (n = 30, each) and administered a high- [1.5 minimum alveolar concentration (MAC)], moderate- (1.0 MAC), low- (0.5 MAC), or no- sevoflurane dose prior to CPB. Standard blood gas parameters, serum S-100 protein, and neuron-specific enolase (NSE) were measured at different time points. The mini-mental state examination (MMSE) was administered 1 day before and 24 and 72 h after surgery. The jugular bulb venous oxygen saturation (SjvO2) in the moderate- and high-dose groups at a nasopharyngeal temperature of 25–28 °C was significantly higher compared with the control group, while the arteriovenous oxygen content difference (AVDO2) and cerebral extraction of oxygen (CEO2) were significantly reduced. The serum S-100 protein and NSE concentrations of the moderate- and high-dose groups at 1 and 6 h after the cessation of CPB were significantly lower than that of the control group. The 24 h postoperative MMSE scores of the moderate- and high-dose groups were significantly higher than those of the low-dose and control groups. An inhaled optimal concentration of sevoflurane may be beneficial for cerebral oxygen balance during CPB, and may ameliorate cognitive damage. However, the effect is dose-dependent.

To investigate the preventive effect of endothelial nitric oxide synthase (eNOS) gene transfer on chronic hypoxic pulmonary hypertension (CHPH) in rats.Twenty-four male Wistar rats were randomly divided into four groups with 6 rats in each group: normoxia group (group N), hypoxia group (group H), hypoxia with LacZ group (group H-LacZ) and hypoxia with eNOS group (group H-eNOS). AdCMVceNOS, AdCMVLacZ or normal saline (NS) was injected intratracheally 3 days before the beginning of exposure to normoxia or hypoxia. Rats in group H-eNOS received 50 microl of AdCMVceNOS (5 x 10(12)pfu/L), rats in group H-LacZ received equal dose of AdCMVLacZ, rats in group N and group H received equal dose of NS. Hemodynamic parameters [including mean systemic arterial pressure (MSAP), heart rate (HR) and mean pulmonary arterial pressure (MPAP)], pulmonary vascular remodeling (percentage of muscularized arteries in small pulmonary vessels) and right ventricular hypertrophy (ratio of right ventricle to left ventricle + septum weight) were measured after 2 weeks of exposure to normoxia or hypoxia. The expression of eNOS, cyclic guanosine monophosphate (cGMP) and nitric oxide (NO) level were also measured in lungs.The MPAP, right ventricular hypertrophy index and pulmonary vascular remodeling in rats in group H-eNOS were obviously lower than those in group H and H-LacZ, but higher than that in group N (all P0.01). There was no significant difference with regard to HR and MSAP in rats in all groups (all P0.05). The eNOS protein in group H and H-LacZ was obviously higher than that in group N, but obviously lower than that in group H-eNOS (all P0.01). The NO level in rat lungs in group H and H-LacZ was obviously lower than that in group N, and value in group H-eNOS was higher than that in the other groups (P0.05 or P0.01). With regard to cGMP in rat lungs, there was no significant difference among group N, H and H-LacZ (all P0.05), but they were all obviously lower than that in group H-eNOS (all P0.01).Intratracheal eNOS gene transfer upregulates the activity of eNOS protein, elevates the level of NO/cGMP in lungs, and alleviates CHPH in rats.

To determine the effects of Varglaucocalyx on c-fos gene expression during global myocardial ischemia-reperfusion.Forty Wistar rats were divided into 5 groups: group N as control; group CN as ischemia-reperfusion control and group XH, XM and XL treated with Varglaucocalyx 5%, 1%, 0.5% respectively prior to ischemia-reperfusion. The isolated rat hearts were perfused in condition of constant temperature and pressure, and then the left ventricular myocardiums were extracted for use. The expression of c-fos protein was detected by immunochemical method. The expression of c-fos protein were quantified by using computer image analysis system.Compared with the values of group N, protein expressions relative area of c-fos gene (PERA) were increased significantly in group CN, XH, XM, XL(P0.01), but decreased significantly in group XH, XM, XL, compared with those of group CN (P0.05). The PERA of c-fos gene in group XM, XL were significantly lower than in group XH (P0.01), and the PERA of c-fos gene in group XM were lower than in group XL(P0.05).Varglaucocalyx can effectively depress the expression of c-fos gene in myocardium which may account for its protection against myocardial ischemia-reperfusion injury, and the middle and the low concentrations of Varglaucocalyx are more effective than the high concentrations.