Objective To evaluate the efficacy of oxycodone hydrochloride for prevention of fentanylinduced cough during induction of anesthesia in patients.Methods One hundred patients,aged 18-64 yr,weighing 45-74 kg,of ASA physical status Ⅰ or Ⅱ,scheduled for elective surgery under general anesthesia,were randomly divided into 2 groups with 50 cases in each group:control group (group C) and oxycodone hydrochloride group (group O).In C and O groups,normal saline 5 ml and oxycodone hydrochloride injection 0.1 mg/kg (in 5 ml normal saline) were injected,respectively,5 min later fentanyl 3 μg/kg was injected intravenously over 5 s,and 2 min later other drugs for induction of anesthesia were given.The development and intensity of cough were observed within 2 min after fentanyl injection.Results Compared with group C,the incidence of cough was significantly decreased and the intensity of coughing was mitigated in group O.Conclusion Intravenous oxycodone hydrochloride 0.1 mg/kg can decrease the development and intensity of fentanyl-induced cough during induction of anesthesia in patients.

Objective To evaluate the role of c?Jun N?terminal kinase ( JNK) and p38 mitogen?ac?tivated protein kinase ( p38MAPK) signaling pathways in attenuation of myocardial ischemia?reperfusion ( I∕R) injury by morphine postconditioning. Methods Healthy adult male Sprague?Dawley rats, weighing 180-240 g, were used in the study. Their hearts were excised and retrogradely perfused in a Langendorff apparatus with Krebs?Ringer ( K?R) buffer saturated with 95% O2?5% O2 at 37℃. After 15 min of equili?bration, 52 isolated hearts were divided into 4 groups ( n=13 each) using a random number table: control group (group C), I∕R group, morphine postconditioning group (group MP), and morphine postcondition?ing plus anisomycin group ( group MP+A) . The hearts were continuously perfused with K?R buffer for 105 min in group C. In group I∕R, the hearts were subjected to 45 min of global ischemia by stopping perfusion with K?R buffer, followed by 60 min of reperfusion by restoration of perfusion with K?R buffer. In group MP, the hearts were subjected to 45 min of global ischemia, followed by 10 min of reperfusion with K?R buffer containing 3?0 μmol∕L morphine and then by 50 min of reperfusion with K?R buffer. In group MP+A, the hearts were subjected to 45 min of global ischemia, followed by 10 min of reperfusion with K?R buffer containing 3?0 μmol∕L morphine and 1?0 μmol∕L anisomycin ( an activator of JNK and p38MAPK) and then by 50 min of reperfusion with K?R buffer. At 60 min of reperfusion, 8 hearts in each group were selected for measurement of the myocardial infarction and amount of creatine kinase?MB ( CK?MB) released from the myocardium, and the myocardial infarct size was calculated. At 20 min of reperfusion, 5 hearts in each group were selected to detect the expression of phosphorylated JNK ( p?JNK ) , phosphorylated p38MAPK ( p?p38MAPK) and cytochrome c ( Cyt c) in myocardial tissues ( by Western blot) and content of nicotinamide adenine dinucleotide ( NAD+) in myocardial tissues ( by spectrophotometry ) . Results Compared to group C, the myocardial infarct size and amount of CK?MB released from the myocardium were significantly increased, the expression of p?JNK, p?p38MAPK and Cyt c was significantly up?regulated, and the content of NAD+ was significantly decreased in I∕R, MP and MP+A groups ( P<0?05) . Compared to group I∕R, the myocardial infarct size and amount of CK?MB released from the myocardium were signifi?cantly decreased in MP and MP+A groups, and the expression of p?JNK, p?p38MAPK and Cyt c was sig?nificantly down?regulated, and the content of NAD+ was significantly increased in group MP (P<0?05). Compared to group MP , the myocardial infarct size and amount of CK?MB released from the myocardium were significantly increased, the expression of p?JNK, p?p38MAPK and Cyt c was significantly up?regula?ted, and the content of NAD+ was significantly decreased in group MP+A (P<0?05). Conclusion The mechanism by which morphine postconditioning attenuates myocardial I∕R injury is related to inhibition of activation of JNK and p38MAPK signaling pathways in rats.

Objective To evaluate the effects of dexmedetomidine plus sufentanil during postoperative analgesia on sleep quality in patients undergoing abdominal hysterectomy.Methods Sixty patients (aged 30-55 years,ASA Ⅰ or Ⅱ) scheduled for hysterectomy were randomly divided into the following 2 groups: group C (n=30,sufentanil) and group D (n=30,sufentanil plus dexmedetomidine).Polysomnography measures were performed,the night before surgery (PSG1),the first night after surgery (PSG2),and the second night after surgery (PSG3).In addition,pain levels (visual analogue scale,VAS),sedation levels,sufentanil consumptions,and possible adverse effects on MAP,HR and SpO2 were investigated.Results Compared with PSG1,N1 stage sleep in group C and N2 stage sleep in group D were significantly increased (P<0.05),N1 stage sleep at PSG2 and PSG3 in group D was decreased (P<0.05);N3 and REM stage sleep,sleep efficiency index and subjective sleep quality were decreased,arousal index was increased in two groups (P<0.05).Compared with group C,N1 stage sleep was decreased,and N2 stage sleep was increased at PSG2 and PSG3 in group D (P<0.05);sleep efficiency index,subjective sleep quality were increased,arousal index in group D was decreased (P<0.05).Patients in group D had a lower VAS score and cumulative sufentanil consumption,MAP,HR at 6,24,48 h after surgery (P<0.05) and a higher sedation score at 6,24 h after surgery than those in group C (P<0.05).Conclusion Besides offering effective analgesia,postoperative dexmedetomidine infusion has positive effects on sleep disturbance in patients undergoing hysterectomy.