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Objective To investigate the analgesic effect of ultrasound-guided vertical spinal block (ESPB) in elderly patients after thoracoscopic surgery.Methods 40 elderly patients,aged 60-75 years,were selected for selective thoracoscopic surgery.Patients were randomly divided into two groups,ESPB group (E group) and paravertebral block (PVB) group (P group).In the E group,0.33％ ropivacaine 30 ml was injected between the T5 vertebral body transverse and the erector spines before surgery,and 0.33％ ropivacaine 30 ml was injected into the thoracic paravertebral space of T5-T6 in the P group.Patients in both groups were treated with sufentanil for postoperative patient controlled analgesia (PCA).The dosage of remifentanil intraoperative and sufentanil postoperative,remedial cases recorded in post anesthesia care unit (PACU),numeric rating scale (NRS) score at postoperative 1 h,6 h,12 h and 24 h were recorded,and intraoperative hypotension,postoperative nausea and vomiting cases,and operation time were documented.Results There was no significant difference in remifentanil dosage between the two groups (P ＞ 0.05).The total consumption of sufentanil in group E 24 hours after operation was higher than that in group P (P ＜ 0.05).The operation time of ultrasound-guided nerve block in group E was shorter than that in group P (P ＜ 0.05).The number of PACU remedial cases in group E was higher than that in group P (P ＞ 0.05).The NRS score recorded at postoperative 1 h,6 h,12 h and 24 h show no difference.There was no significant difference in the incidence of nausea and vomiting and intraoperative hypotension in the two groups.Conclusions Ultrasound-guided single ESPB block provides postoperative analgesia,which is similar but weaker compared with PVB and easy to operate.
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Objective To evaluate the effect of Critical Incident Reporting System on the quality of clinical anesthesia.Methods Anesthesia-related critical incidents happened in the perioperative period were reported in voluntary,anonymous,no punishment and confidential manners.The data was collected,classified and documented by assigned professionals on a regular basis from September 2012 to August 2016.The critical incidents were retrospectively analyzed after the risk was assessed.The 4-year reporting rate was collected.The risk of critical incidents was assessed using severity and probability analysis,and the critical incidents-inducing risk factors were analyzed.Results The 4-year reporting rate of critical incidents was 0.551％.From 1st to 4th year,the reporting rates were 0.729％,0.598％,0.819％ and 0.368％,respectively,and the incidence of injury incidents was 0.112％,0.106％,0.133％ and 0.031％,respectively.The reporting rate of critical incidents and incidence and reporting rate of the injury incidents showed a decreasing trend for 1st and 2nd year,significantly increased for 3rd year and decreased for 4th year (P＜0.05).The first three critical incident categories were equipment use and respiratory system-and workflowrelated incidents.Patient injury during surgery was considered an extremely high risk incident;the factor of the medical staff in the department of anesthesiology is the first critical incidents-inducing risk factor.Conclusion Critical Incident Reporting System can discover and correct the system-related risk and the inducing factors in the department of anesthesiology and is an effective method of improving the service quality of clinical anesthesia.
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Objective To investigate the effects of autophagy on lipopolysaccharide (LPS)-induced vascular hyper-permeability. Methods ① In vitro: Human umbilical vein endothelial cells (HUVECs) were randomly divided into blank group, LPS group (5 mg/L LPS stimulation), autophagy inhibitor 6-amino-3-methyl purine (3-MA) + LPS group (5 mmol/L 3-MA pretreatment for 30 minutes + 5 mg/L LPS stimulation) and autophagy revulsive Rapamycin (RAP) + LPS group (10 nmol/L RAP pretreatment for 30 minutes + 5 mg/L LPS stimulation). After LPS simulation for 60 minutes in four groups, endothelial permeability was detected by trans-endothelial electrical resistance (TER) determination. The protein expressions of autophagy marker protein microtubule-associated protein 1 light chain 3 (LC3 Ⅱ/Ⅰ) and autophagy related gene Beclin-1 were detected by Western Blot. Cell apoptosis was evaluated by using flow cytometry. Caspase-3 activity was detected by fluorometric assay kit. ② In vivo: 24 Sprague-Dawley (SD) rats were randomly assigned to four groups according to random number table, with 6 rats in each group. The rats in control group received no treatment; rats in model group were tail intravenous injected 10 mg/kg of LPS. The rats in 3-MA pretreatment and RAP pretreatment groups were tail intravenous injected 10 mg/kg of 3-MA or 2 mg/kg of RAP pretreatment for 30 minutes before 10 mg/kg LPS injection. The extravasation of FITC-albumin in mesenteric post-capillary venules was observed by fluorescence microscope. Then the change in fluorescence intensity of FITC-albumin between the intravascular and extravascular space (ΔI) were measured to reflect vascular permeability. Results ① In vitro, compared with blank group, the LC3 Ⅱ/Ⅰ protein, Beclin-1 protein, caspase-3 activity and rate of cell apoptosis in LPS group were increased, and the TER was decreased. Compared with LPS group, the LC3 Ⅱ/Ⅰ, Beclin-1, caspase-3 activity and rate of cell apoptosis in 3-MA+LPS group were decreased, and the TER was increased [LC3 Ⅱ/Ⅰ protein: (288.2±33.3)% vs. (420.5±39.4)%, Beclin-1 protein: (185.3±26.4)% vs. (293.3±36.1)%, caspase-3 activity: (196.6±28.5)% vs. (339.5±25.4)%, rate of cell apoptosis: (9.50±0.99)% vs. (15.40±1.55)%, TER: 0.88±0.09 vs. 0.63±0.05, all P < 0.05]. Compared with LPS group, the LC3 Ⅱ/Ⅰ, Beclin-1, caspase-3 activity and rate of cell apoptosis in RAP+LPS group were further increased, and the TER was further decreased [LC3 Ⅱ/Ⅰ protein: (519.6±45.2)% vs. (420.5±39.4)%, Beclin-1 protein: (359.0±38.3)% vs. (293.3±36.1)%, caspase-3 activity: (449.1±31.0)% vs. (339.5±25.4)%, rate of cell apoptosis: (19.30±1.72)% vs. (15.40±1.55)%, TER: 0.54±0.05 vs. 0.63±0.05, all P < 0.05]. ② In vivo, the albumin extravasation and vascular permeability were increased in model group as compared with those of control group (ΔI: 0.54±0.07 vs. 0.13±0.03, P < 0.05). The albumin extravasation and vascular permeability were obviously decreased in 3-MA pretreatment group as compared with those of model group (ΔI: 0.25±0.05 vs. 0.54±0.07, P < 0.05). The albumin extravasation and vascular permeability were obviously increased in RAP pretreatment group as compared with those of model group (ΔI: 0.67±0.07 vs. 0.54±0.07, P < 0.05). Conclusions Inhibition of autophagy can reduce the LPS-induced vascular hyper-permeability, and enhanced autophagy can further increase vascular permeability. The mechanism of autophagy mediate vascular permeability may be related to the endothelial cells apoptosis.
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Objective To investigate the protective effect and potential mechanisms of hypertonic sodium chloride hydroxyethyl starch solution (HSH) against the cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH).Methods Twenty-four male Sprague-Dawley (SD) rats were randomly assigned to four groups according to the random number table,with 6 rats in each group.The SAH-CVS model was reproduced by injection of the blood twice through the cisterna magna.Rats in both model and HSH treatment groups received 8 mL/kg normal saline (NS) or HSH treatment everyday via caudal vein.Rats in sham group were injected with 1.5 mL/kg NS into cisterna magna followed by 8 mL/kg NS treatment.Rats in normal group received no treatment.Rats were sacrificed to harvest basilar artery after 7 days.The thickness of vessel wall and lumen area were measured using hematoxylin-eosin (HE) staining.The rate of apoptosis of vascular smooth muscle cell (VSMC) was assessed using flow cytometry.Caspase-3 activity was measured by a fluorometric assay.The expressions of Bax and Bcl-2 were determined by Western Blot.Intracellular reactive oxygen species (ROS) was detected by H2DCFDA.Results Compared with normal group,increased thickness of vessel wall (μm:27.72 ± 1.94 vs.18.30 ± 1.10,P＜0.05),decreased lumen area (μm2:26 115 ± 1 991 vs.55 080 ± 2 091,P＜0.05),and elevation of rate of apoptosis of VSMCs [(35.05 ± 5.54) ％ vs.(5.93 ± 1.53) ％,P＜ 0.05] were found in model group.Compared with model group,decreased thickness of vessel wall (μm:22.55 ± 1.50 vs.27.72 ± 1.94,P＜0.05),increase of lumen area (μm2:48 115 ±2 460 vs.26 115 ± 1 991,P＜0.05),and depressed rate of apoptosis of VSMCs [(16.54 ± 5.94) ％ vs.(35.05 ± 5.54) ％,P＜ 0.05] were found in HSH treatment group.Caspase-3 activity,intracellular ROS level,Bax and Bcl-2 expressions in model group were (188.40 ± 19.35)％,(163.50 ± 17.02)％,(208.71 ± 26.04)％ and (44.52 ± 9.61) ％ of those of normal group,and the differences of these parameters between model and normal groups were statistically significant (all P＜0.05).Caspase-3 activity,intracellular ROS level,Bax and Bcl-2 expressions in HSH treatment group were (135.05 ± 19.52)％,(119.44 ± 11.50)％,(139.20 ± 18.04)％ and (85.35 ± 13.12)％ of those of normal group,respectively,and the differences of these parameters between HSH treatment and model groups were statistically significant (all P＜0.05).The differences of all measurements between sham and normal groups were not statistically significant.Conclusion The current results demonstrate that HSH attenuates the SAH-induced CVS,alleviates thickness of vessel wall,and increases lumen area via inhibition of VSMCs apoptosis.