Objective:To evaluate the effects of biorhythm factors on the occurrence of acute kidney injury (AKI) after cardiac surgery using cardiopulmonary bypass.Methods:This was a retrospective cohort study. Data from patients undergoing heart surgery involving cardiopulmonary bypass from June 2018 to December 2019 were collected and divided into 2 groups ( n=125 each) based on the time of anesthesia operation: morning rhythm group (group Ⅰ) and afternoon rhythm group (group Ⅱ). Anesthesia operation was performed from 8: 00 to 12: 00 in group Ⅰ. Anesthesia was performed from 14: 00 to 18: 00 in group Ⅱ. The occurrence of postoperative AKI and other postoperative complications (pulmonary infection, sepsis, cerebral infarction) was recorded. Results:Compared with group Ⅱ, the incidence of postoperative AKI was significantly increased, the relative risk was 3.2 (95% confidence interval 1.31-7.70), and no significant change was found in the incidence of pulmonary infection, sepsis and cerebral infarction in group Ⅰ ( P>0.05). Conclusions:Biorhythm factors affect the development of AKI after cardiac surgery using cardiopulmonary bypass, and performing surgeries in the afternoon rather than the morning helps reduce the risk of postoperative AKI.

Objective:To investigate the relationship between lateral hypothalamus and melatonin-induced reduction of wakefulness in rats and the receptor mechanism.Methods:Forty clean-grade adult male Sprague-Dawley rats, weighing 250-300 g, were divided into 4 groups ( n=10 each) using a random number table method: control group (group C), melatonin group (group M), melatonin type-1/2 receptor (MT 1R) antagonist luzindole plus melatonin group (group L+ M), and melatonin type-2 receptor (MT 2R) antagonist 4P-PDOT plus melatonin group (P+ M group). In group C, 0.5 μl of 0.9% NaCl solution was microinjected into the lateral hypothalamus.In group M, 1 μmol/L melatonin 0.5 μl was microinjected into the lateral hypothalamus.In group L+ M, 1 μmol/L MT 1/2R and 1 μmol/L melatonin (0.5 μl in total) was microinjected into the lateral hypothalamus.The microinjection time was from 19: 30 to 20: 00.The changes in sleep-wake duration and the oscillating energy in different frequency bands of electroencephalogram were detected by using electroencephalogram and electromyogram recording technology. Results:Compared with group C, the percentage of wakefulness time was significantly decreased, the percentage of non-rapid eye movement sleep and rapid eye movement sleep time was increased, the energy for delta oscillation was increased, the energy for theta oscillation was decreased, and no significant change was found in the energy for alpha oscillation in M and P+ M groups ( P<0.01), and no significant change was found in the parameters mentioned above in group L+ M ( P>0.05). Compared with group M, the percentage of wakefulness time was significantly increased, the percentage of non-rapid eye movement sleep and rapid eye movement sleep time was decreased, the energy for delta oscillation was decreased, and the energy for theta oscillation was increased in group L+ M ( P<0.01), and no significant change was found in the parameters mentioned above in group P+ M ( P>0.05). Conclusion:The lateral hypothalamus may be involved in melatonin-induced reduction of wakefulness in rats, and the mechanism may be related to activating MT 1R in the lateral hypothalamus.

Objective:To evaluate the relationship between degrees of biliary obstruction and levels of lipid peroxidation in patients.Methods:A total of 140 patients of both sexes, with biliary obstruction, without biliary puncture and drainage, aged 40-64 yr, with body mass index of 18.5-23.9 kg/m 2, of American Society of Anesthesiologists physical status Ⅱ or Ⅲ, were selected.The patients with different degrees of biliary obstruction were divided into 4 groups ( n=35 each) according to Child-Pugh grade total bilirubin (TBIL) concentrations: group A (TBIL<17 μmol/L), group B (17 μmol/L≤TBIL<34 μmol/L), group C (34 μmol/L≤TBIL<51 μmol/L) and group D (TBIL≥51 μmol/L). The serum TBIL, direct bilirubin (DBIL), indirect bilirubin (IBIL), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bile acid (TBA) and malondialdehyde (MDA) concentrations were measured.The correlation between serum MDA concentration and degree of biliary obstruction was tested by Spearman correlation analysis. Results:Compared with group A and group B, the serum DBIL, IBIL, ALT, AST, TBA and MDA concentrations were significantly increased in group C and group D ( P<0.05), and there was no significant difference in the parameters mentioned above between group A and group B ( P>0.05). Compared with group C, the serum DBIL, IBIL, ALT, AST, TBA and MDA concentrations were significantly increased in group D ( P<0.05). Serum MDA concentration was positively correlated with degree of biliary obstruction ( r=0.54, P<0.05). Conclusion:The degree of biliary obstruction can reflect the level of lipid peroxidation in patients.

Objective:To evaluate the effect of melatonin on prefrontal cortex ischemia-induced cognitive impairment in rats and to investigate the receptor mechanism.Methods:Clean-grade adult male Sprague-Dawley rats, weighing 300 g, were selected, and a catheter was implanted into the prefrontal cortex.The experiment was performed in two parts.Experiment Ⅰ Twenty-four rats, in which catheters were successfully inserted into the prefrontal cortex, were assigned into 3 groups ( n=8 each) using a random number table method: control group (group C), model group (group M) and melatonin group (group ME). Normal saline 0.5 μl was injected into the prefrontal cortex in group C, 1 μmol/L endothelin 0.5 μl was microinjected into the prefrontal cortex in group M, and 1 μmol/L endothelin and 1 μmol/L melatonin 0.5 μl were injected into the prefrontal cortex in group ME.Experiment Ⅱ Forty-four rats, in which catheters were successfully inserted into the prefrontal cortex, were assigned into 4 groups ( n=11 each) using a random number table method: model group (group M), melatonin group (group ME), MT 1/2R antagonist luzindole + melatonin group (group L + ME) and MT 2R antagonist 4p-pdot + melatonin group (group P + ME). In group M, 1 μmol/l endothelin 0.5 μl was microinjected into the prefrontal cortex.In group ME, 1 μmol/L endothelin + 1 μmol/L melatonin 0.5 μl was injected into the prefrontal cortex.In group L + ME, 1 μmol/L endothelin + 1 μmol/L MT 1/2R antagonist + 1 μmol/L melatonin 0.5 μl was injected into the prefrontal cortex.In group P + ME, 1 μmol/L endothelin + 1 μmol/L MT 2R antagonist + 1 μmol/L melatonin 0.5 μl was injected into the prefrontal cortex.T-maze and the open field tests were performed at 1 week after administration. Results:Experiment Ⅰ There was no significant difference in the locomotor speed in open field test among C, M and ME groups ( P>0.05). The rate of correct selection in T-maze test was significantly lower in M and ME groups than in group C and higher in group ME than in group M( P<0.05). Experiment Ⅱ There was no significant difference in the locomotor speed in open field test among the four groups( P>0.05). Compared with group M, the rate of correct selection in open field test was significantly increased in ME and P+ ME groups ( P<0.05), and no significant change was found in group L+ ME ( P>0.05). Compared with group ME, the rate of correct selection in open field test was significantly decreased in group L+ ME ( P<0.05), and no significant change was found in group P+ ME( P>0.05). Conclusion:Melatonin can attenuate prefrontal cortex ischemia-induced cognitive impairment in the rats, and the mechanism is related to activation of MT 1R.

Objective:To evaluate the effect of propofol on excitability of pyramidal neurons in orbitofrontal cortex of mice and the underlying ion channel mechanism.Methods:Brain slices of 400 μm thickness from healthy male C57 mice (aged 8-12 weeks)were prepared.This experiment was performed in two parts.Part Ⅰ The brain slices were divided into 2 groups ( n=7 each) based on the random number table method: control group (C group) and propofol group (P group). Cells were perfused with vehicle in group C and with 10 μmol/L propofol in group P. Part Ⅱ The brain slices were divided into 5 groups ( n=8 each) using the random number table method: propofol group (P group), hyperpolarization-activated non-selective cation channel antagonist ZD7288 plus propofol group (Z + P group), inward rectifier potassium channel antagonist topiramate plus propofol group(T + P group), transient activation of voltage-gated potassium channel antagonist 4-aminopyridine (4AP) plus propofol group (A + P group), and delayed activation of voltage-gated potassium channel antagonist tetraethylammonium (TEA) plus propofol group (TEA + P group). Cells were perfused with 10 μmol/L propofol for 2 min in P group, with 5 μmol/L ZD7288 and 10 μmol/L melatonin for 2 min in Z+ P group, with 5 μmol/L topiramate and 10 μmol/L propofol for 2 min in T + P group, with 10 μ mol/L 4-aminopyridine and 10 μmol/L propofol for 2 min in A+ P group, and with 10 μmol/L TEA and 10 μmol/L propofol for 2 min in TEA+ P group.The whole-cell currents, membrane potential and discharge frequency of pyramidal neurons in the orbitofrontal cortex were recorded by whole-cell patch-clamp. Results:Part Ⅰ Compared with C group, whole-cell currents were significantly increased, and the membrane potential and discharge frequency were decreased in P group ( P<0.01). Part Ⅱ Compared with P group, no significant change was found in the whole-cell currents, membrane potentials and discharge frequency in Z+ P group, T+ P group and A+ P group ( P>0.05), and the whole-cell currents were significantly decreased, and the membrane potentials and discharge frequency were increased in TEA+ P group ( P<0.05). Conclusion:Propofol can inhibit the excitability of pyramidal neurons in the orbitofrontal cortex, and the mechanism is related to activating delayed activation of voltage-gated potassium channels in mice.

Clinical teaching round is one of main teaching methods during standardized training for residents. However, the particularity of standardized resident training in clinical anesthesia determines that it is difficult to apply the teaching round model of other disciplines. In this study, seven core contents of Mini-Clinical Evaluation Exercise (Mini-CEX) were modified after considering the characteristics of anesthesia specialty and applied to the teaching rounds of standardized training for residents of anesthesia , thus promoting the standardization and improving the quality of anesthesia teaching rounds.

Objective To evaluate the effects of melatonin on the excitability of pyramidal neurons in the prefrontal cortex and the role of melatonin receptor 1 (MT1 R)-cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling pathway.Methods Brains were obtained from male SpragueDawley rats between 14 and 21 days after birth.The brain slices of 350-μm thick were prepared and placed in artificial cerebrospinal fluid.The brain slices were divided into 5 groups (n =6 each) using a random number table method:control group (C group),melatonin group (M group),MT1/2R antagonist luzindole plus melatonin group (L+M group),MT2R antagonist 4P-PDOT plus melatonin group (P+M group) and PKA inhibitor Rp-cAMPS plus melatonin group (R+M group).Cells were perfused for 2 min with artificial cerebrospinal fluid in group C.Cells were perfused for 2 min with 1 μmol/L melatonin in group M.Cells were perfused for 2 min with the mixture of 1 μmol/L MT1/2R antagonist luzindole and 1 μmol/L melatonin in group L+M.Cells were perfused for 2 min with the mixture of 1 μmol/L MT2R antagonist 4P-PDOT and 1 μmol/L melatonin in group P+M.In group R+M,1 mmol/L PKA inhibitor Rp-cAMPS was continuously added to the pipette solution,and cells were perfused for 2 min with 1 μmol/L melatonin.The whole-cell patch-clamp technique was used to record the membrane potential and clamp current of pyramidal neurons in the prefrontal cortex.Results Compared with group C,the clamp current was significantly increased,and the membrane potential was decreased in group M (P＜0.05).Compared with group M,the clamp current was significantly decreased,and the membrane potential was increased in L + M and R + M groups (P＜0.05),and no significant change was found in the clamp current or membrane potential in group P+M (P＞0.05).Conclusion Melatonin inhibits the excitability of pyramidal neutrons in the prefrontal cortex,and the mechanism is related to activating MT1 R-cAMP-PKA signaling pathway.

Objective To evaluate the changes in the expression of Talin1 and F-actin during ser-um-induced proliferation of pulmonary artery smooth muscle cells ( PASMCs) of rats with hepatopulmonary syndrome ( HPS) . Methods Twenty healthy male Sprague-Dawley rats, weighing 220-250 g, were used for producing HPS by chronic ligation of the common bile duct. Blood samples from the abdominal aorta were collected to prepare serum. Primarily cultured PASMCs obtained from rats were seed in 6- or 96-well plates and divided into 2 groups using a random number table method: control group ( group C) and HPS group ( group HPS) , with 24 wells in each group ( for 6-well plates) or with 30 wells in each group ( for 96-well plates) . In C and HPS groups, normal rat serum or HPS rat serum were added, respectively, with the final concentration of 5％. At 24, 48 and 72 h of incubation, the expression of Talin1, F-actin and G-actin was determined by Western blot, the F-actin∕G-actin ratio was calculated, and the proliferation of PASMCs was measured by 3H-TdR incorporation and CCK-8 assays. Results Compared with group C, the proliferation of PASMCs was significantly enhanced, the expression of Talin1 was up-regulated, and the F-actin∕G-actin ratio was increased in group HPS ( P<0. 05) . The proliferation of PASMCs was gradually en-hanced, the expression of Talin1 was gradually up-regulated, and the F-actin∕G-actin ratio was gradually increased with the prolonged incubation time in group HPS (P<0. 05). Conclusion The mechanism by which the HPS rat serum induces proliferation of PASMCs may be related to up-regulating the expression of Talin1 and F-actin.

Objective To evaluate the relationship between prefrontal cortex and propofol-induced cognitive dysfunction in rats. Methods SPF healthy male Sprague-Dawley rats, weighing 300-350 g, aged 16 weeks, were used in this study. Thirty rats in which catheters were successfully implanted into the prefrontal lobe were divided into 2 groups ( n=15 each ) using a random number table method: control group (group C) and propofol group (group P). In group P, 50μmol/L propofol 0. 5μl was microinjected into the prefrontal cortex at day 7 after operation, and the equal volume of normal saline was given instead in group C. T-maze test and open field test were performed at 15 min after administration. Results Com-pared with group C, the correct rate of selection in T-maze was significantly decreased ( P＜0. 05) , and no significant change was found in the total locomotor or number of rearing in open field test in group P ( P＞0. 05) . Conclusion Prefrontal cortex may be involved in propofol-induced cognitive dysfunction in rats.

Objective To evaluate the efficacy of acetate Ringer's solution for fluid therapy in the patients with dangerous placenta previa undergoing cesarean section. Methods One hundred fifty-two pa-tients, aged 22-41 yr, with body mass index of 20-30 kg/m2 , of American Society of Anesthesiologists physical status Ⅱ or Ⅲ, scheduled for elective cesarean section under general anesthesia, were allocated to 2 groups ( n=76 each) using a random number table method: acetate Ringer's solution group ( group AR) and lactated Ringer's solution group ( group LR) . Acetate Ringer's solution and lactated Ringer's so-lution 500 ml were intravenously infused at an initial rate of 15 ml·kg-1 ·h-1 followed by an infusion of 10 ml·kg-1·h-1 until patients leaved the operating room in two groups. Blood samples were collected from the left radial artery immediately before fluid replacement, at the end of fluid replacement and at 6 h after sur-gery for blood gas analysis. The development of arrhythmia was recorded during fluid replacement. The postpartum hemorrhage at 2 h after surgery was calculated. Results Compared with group LR, the Mg2+level was significantly increased and blood glucose was decreased at the end of fluid replacement, the inci-dence of arrhythmia was decreased ( P ＜ 0. 05) , and no significant change was found in each parameter of blood gas analysis at 6 h after surgery, postpartum hemorrhage at 2 h after surgery or consumption of ephed-rine in group AR ( P＞0. 05) . Conclusion Acetate Ringer's solution can be effectively used for fluid ther-apy, maintain the internal environment stable and prevent the occurrence of arrhythmia effectively during cesarean section in the patients with dangerous placenta previa.