Objective To investigate the effect of hypercapnia on cerebral oxygen metabolism under propofol anesthesia during one-lung ventilation (OLV) in patients.Methods Forty ASA physical status [or Ⅱ patients,aged 53-63 yr,scheduled for elective lobectomy performed via video-assisted thoracoscope,were enrolled in the study.Anesthesia was induced with iv injection of midazolam,fentanyl and vecuronium and target-controlled infusion of propofol and maintained with target-controlled infusion of propofol and intermittent iv boluses of fentanyl and vecuronium.BIS value was maintained at 40-60 during surgery.At 15 min of OLV,hypercapnia was performed and PaCO2 was maintained at 50-55 mm Hg lasting for 15 min,and then respiratory rate was adjusted to maintain PaCO2 at 40-45 mm Hg.Immediately before OLV (T0),at 15 min of OLV and hypercapnia (T1,2),and at 15 min after the end of hypercapnia (T3),arterial and jugular bulb venous blood samples were obtained for determination of arterial partial pressure of oxygen (PaO2),arterial oxygen saturation (SaO2),jugular bulb venous oxygen partial pressure (PjO2) and hemoglobin saturation (SjO2).The arterial to venous oxygen content difference (Da-jO2) and cerebral extraction rate of oxygen (CERO2) were calculated.Results SaO2 and PaO2 at T1-3,SjO2 and PjO2 at T1 and T3 and Da-jO2 at T2 were significantly lower and CERO2 at T1 and T3 was higher than those at T0 (P ＜ 0.05).SjO2 and PjO2 were significantly increased and Da-jO2 and CERO2 were significantly decreased at T2(P ＜0.05) and no significant changes were found in the parameters of cerebral oxygen metabolism at T3 as compared with those at T1 (P ＞ 0.05).Conclusion Hypercapnia can improve cerebral oxygen metabolism under propofol anesthesia during OLV in patients.

Objective To determine the optimum dose of oxycodone inhibiting responses to tracheal intubation with a double-lumen endobronchial tube in patients undergoing one-lung ventilation (OLV).Methods Sixty adult patients aged 55-64 yr, weighing 60-80 kg, with American Society of Anesthesiologists physical status Ⅰ or Ⅱ, scheduled for elective thoracic surgery requiring OLV, were randomly divided into 3 different doses of oxycodone groups (O1-3 groups, n =20 each).Anesthesia was induced with iv midazolam 0.05 mg/kg, oxycodone 0.30, 0.35 and 0.40 mg/kg (O1.3 groups, respectively) , propofol 1.5 mg/kg and rocuronium 0.9 mg/kg.The patients were tracheally intubated using a double-lumen endobronchial tube and mechanically ventilated.Before anesthesia induction (T0) , immediately before and after intubation (T1,2) , and 1 and 5 min after intubation (T3.4) , arterial blood samples were taken to determine the concentrations of serum norepinephrine (NE) and epinephrine (E) using high-performance liquid chromatography.The occurrence of bucking, body movement, hypertension, and tachycardia were observed.Results The concentrations of serum NE and E were significantly increased at T2,3 than at T1 in group O1 (P＜0.05).Compared with group O1 , the concentrations of serum NE and E were significantly decreased at T2,3 , and the incidence of bucking, body movement, hypertension, and tachycardia was decreased in O2 and O3 groups (P＜0.05).There was no significant difference in the parameters mentioned above between O2 and O3 groups (P ＞ 0.05).Conclusion The optimum dose of oxycodone inhibiting responses to tracheal intubation with a double-lumen endobronchial tube is 0.35 mg/kg in patients undergoing OLV.

Objective To evaluate the efficacy of gabapentin for prevention of post-thoracotomy pain syndrome (PTPS).Methods Sixty-nine ASA physical status Ⅰ or Ⅱ patients of both sexes,aged 46-69 yr,weighing 47-78 kg,scheduled for elective resection for lung cancer under general anesthesia combined with epidural block,were randomly divided into 2 groups using a random number table:group A (n =36) and group B (n =33).In group A,gabapentin 300 mg was given orally at 2 h before operation and gabapentin 100 mg was given orally three times a day from 1st day after operation until 10th day after operation.Group B received placebo instead of gabapentin.Epidural blockade with ropivacaine and sufentanil was performed before induction of anesthesia and the level of block was controlled at T4-10.Patient-controlled epidural analgesia (PCEA) was performed within 3 days after operation and VAS scores were maintained ≤ 3.The development of pain (numeric rating scale score ＞ 4) within 6 months after operation and the duration were recorded.The consumption of propofol and remifentanil during operation and the number of attempts for PCEA after operation were recorded.The adverse reactions such as postoperative drowsiness,dizziness,fatigue were also recorded.Results Compared with B group,the incidence of pain within 6 months after operation was significantly decreased,the duration of pain was shortened (P ＜ 0.05),and no significant changes were found in the consumption of propofol and remifentanil during operation and the number of attempts for PCEA after operation in A group (P ＞ 0.05).No adverse reactions developed in group B.Mild dizziness and fatigue occurred in 2 patients in group A.Conclusion Gabapentin (continuous application at 2 h before operation and 10 days after operation) can reduce the development of PTPS in patients with no obvious adverse reactions.

Objeoctive To compare the effects of etomidate and propofol on cerebral oxygen metabolism in patients undergoing abdominal surgery.Methods Thirty-six ASA Ⅰ or Ⅱ patients aged 30-64 yr weighing 42-73 kg undergoing abdominal surgery under general anesthesia were randomly divided into 2 groups (n=18 each):group E etomidate and group P propofol.Left radial artery was cannulated for continuous direct BP monitoring.A catheter was inserted into right internal jugular vein(LJV) and advanced cephalad until jngatar bulb for blood sampling.Both groups received midazolam 0.08 ms/ks,fentanyl 3μg/kg and vecurunium 0.1 mg/kg and in addition group P received propofol 1.5 mg/ks and group E etomidate 0.3 mg/kg respectively for induction of anesthesia.Anesthesia was maintained with propofol infusion at 4-6 mg·kg-1·h-1 in group P and etomidate infusion at 0.4-0.7 mg·kg-1·h-1 in group E and intermittent iv boluses of fentanyl and vecuronium.ECG,MAP,HR,SpO2 and PET CO2 were continuously monitored.Blood samples were taken from radial artery and IJV for blood gas analysis and lactic acid measurement before induction of anesthesia(T1),immediately after intubation (T2),30 min after skin incision (T3) and at the end of operation(T4).The rate of cerebral O2 extraction (CERO2) was calculated.Results The hemodynamic variables were within the normal range throughout the anesthesia and operation.The oxygen saturation and oxygen partial pressure of both arterial and venous blood(SaO2,SjvO2,PaO2,PjvO2) rose significantly after induction of anesthesia in both groups.There was no significant difference in arterial and venous blood lactic acid level and SaO2,SjvO2,CaO2,CjvO2,Da-jvO2 or CERO2 at all time points between the two groups.Conclusion Both etomidate and propofol combined with midazolam and fentanyl can decrease cerebral O2 metabolic rate and there is no significant difference between the two groups.

To investigate the cellular target selectivity of small molecules targeting thioredoxin reductase 1, we reported the construction and functional research of a stable TrxR1 gene (encode thioredoxin reductase 1) knockout HCT-116 cell line. We designed and selected TrxR1 knockout sites according to the TrxR1 gene sequence and CRISPR/Cas9 target designing principles. SgRNA oligos based on the selected TrxR1 knockout sites were obtained. Next, we constructed knockout plasmid by cloning the sgRNA into the pCasCMV-Puro-U6 vector. After transfection of the plasmid into HCT-116 cells, TrxR1 knockout HCT-116 cells were selected using puromycin resistance. The TrxR1 knockout efficiency was identified and verified by DNA sequencing, immunoblotting, TRFS-green fluorescent probe, and cellular TrxR1 enzyme activity detection. Finally, the correlation between TrxR1 expression and cellular effects of drugs specifically targeting TrxR1 was investigated by CCK-8 assay. The results demonstrated that the knockout plasmid expressing the sgRNA effectively knocked-out TrxR1 gene within HCT-116 cells, and no expression of TrxR1 protein could be observed in stable TrxR1 knockout HCT-116 (HCT116-TrxR1-KO) cells. The TrxR1-targeting inhibitor auranofin did not show any inhibitory activity against either cellular TrxR1 enzyme activity or cell proliferation. Based on these results, we conclude that a stable TrxR1 gene knockout HCT-116 cell line was obtained through CRISPR/Cas9 techniques, which may facilitate investigating the role of TrxR1 in various diseases.
CRISPR-Cas Systems/genetics* ; Gene Editing ; Gene Knockout Techniques ; HCT116 Cells ; Humans ; RNA, Guide/metabolism*