Objective To investigate the role of KATP channel in cardioprotective effects of remifentanil preconditioning (RFC) against ischemia-reperfusion (I/R) injury.Methods Forty-eight male SD rats weighing 200-250 g were killed and the hearts were immediately removed and perfused retrogradely at 100 cm H2 O with Krebs- Ringer's solution aerated with 95 % O2 and 5 % CO2 in an Langendorff apparatus. Myocardial ischemia was achieved by tightening the snare which was placed around anterior descending branch of left coronary artery and confirmed by the appearance of a regional cyanosis, decrease in coronary flow (CF) and S-T segment changes on ECG. After 15 min stabilization all hearts were subjected to 30 min ischemia followed by 120 min reperfusion. The 48 isolated hearts were randomly divided into 6 group ( n = 8 each): ( I ) I/R group; ( II ) RPC group received 3 episodes of 5 min remifentanil (100 ?g ? L-1 ) perfusion at 5 min interval before ischemia; ( III ) HMR group; (IV ) 5-HD group; ( V ) HMR + RPC group and ( VI) 5-HD + RPC group. Group III and IV received HMR-1098, a selective sarcolemmal KATP channel blocker (1? 10-4 mol?L-1 ) or 5-HD, a selective mitochondrial KATP channel blocker (1 ? 10 3 mol?L-1 ) perfusion for 45 min before ischemia. In group V and \1 HMR-1098 or 5-HD perfusion was started 10 min before RPC. Infarct size (IS) was determined by 2, 3, 5-triphenyl-tetrazolium staining. Coronary outflow was collected and recorded and lactate dehydrogenase (LDH) activity in coronary outflow was measured. Results The infarct size was significantly smaller and significantly less LDH was released in group II (RPC) than in I/R group. The protective effects of RPC was abolished by pretreatrnent with 5-HD but not HMR-1098. RPC and HMR-1098 caused a slight but significant increase in CF, however there was no significant difference in CF among ail groups during ischemia and reperfusion. Conclusion Mitochondrisl KATP channel activation is involved in the protective effect of RPC on myocardium against I/R injury.

0.05). Conclusion:Administering propofol or midazolam is helpful in avoiding cerebral oxygenation imbalance during CPB.

Objective To elucidate the direct effect of remifentanil on intracellular Ca2+ ( [Ca2+ ]) transients using electrically stimulated individual rat ventricular cardiomyocytes. Methods Male SD rats weighing 190-210 g were used. The animals were decapitated and their hearts were immediately removed. Fresh ventricular cardiomyocytes were enzymatically isolated with collagenase. For measurement of the electrically induced [ Ca2 + ] transients, cells were first loaded with fura-2/AM as a Ca2+ indicator and [Ca2+ ] transient was determined by spectrofluorometric method. The fluorescence ratio of 340/380 run was used as an index of [ Ca2+]. Myocytes were placed in a chamber and perfused with a bicarbonate Kreb's solution at room temperature. Myocytes were randomly divided into 10 groups according to the different concentrations of remifentanil contained in Kreb's solution: control group (no remifentanil n = 8) and 9 remifentanil groups (0.1, 0.3, 1.0, 3.0, 10, 30, 100, 300 and 1 000 ng ?ml-1) ( n = 8 each) .Results Remifentanil caused decrease in [Ca2+ ] transients in a dose-dependent manner. Except for group remifentanil 0.1 and remifentanil 0.3, [ Ca2+] transients were significantly lower in remifentanil groups than in control group (P

The teaching team of undergraduates of anesthesiology in Anhui Medical University applied the primary trauma care system of encourage, heuristic teaching and practical teaching to further deepen the educational reform and improve teaching quality for undergraduate education.They designed the diversified section such as drills, discussion, teaching, questions, feedback and so on, implemented the simulation training of anesthesia crisis management skills and completed the feedback evaluation of comprehensive ability before and after the teaching, and then achieved the effect of improving the actual operation ability and clinical thinking capacity of students.So it is a good method and worth extending.

Objective To evaluate the effect of dexmedetomidine on the intestinal mucosal injury in the patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Forty patients of both sexes with rheumatic heart disease,aged 32-64 yr,weighing 40-75 kg,of ASA physical status Ⅱ or Ⅲ (NYHA class Ⅱ or Ⅲ),scheduled for elective cardiac valve replacement with CPB,were randomly divided into 2 groups (n =20 each) using a random number table:control group (group C) and dexmedetomidine group (group D).After induction of anesthesia,the patients were endotracheally intubated and mechanically ventilated.Anesthesia was maintained with 0.8％-2.0％ sevoflurane inhalation and intermittent iv boluses of sufentanil 0.5-1.0 μg/kg and vecuronium 0.04-0.06 mg/kg.Before routine induction of anesthesia,a loading dose of dexmedetomidine 1 μg/kg was injected intravenously over 10 min,followed by continuous infusion at 0.3 μg · kg-1 · h-1 until the end of surgery in group D,while the equal volume of normal saline was given in group C.Before CPB,at 30 min after aortic clamping,at the termination of CPB,at the end of surgery and at 6 and 24 h after surgery,central venous blood samples were taken for determination of concentrations of tumor necrosis factor-alpha,interleukin-6 (IL-6) and IL-10 and intestinal fatty acid binding protein in plasma (by ELISA),and the plasma concentration of endotoxin (using turbidimetry).The time of postoperative mechanical ventilation and duration of ICU stay were recorded.Results Compared with group C,the concentrations of tumor necrosis factor-alpha,IL-6,IL-10 and endotoxin and intestinal fatty acid binding protein in plasma were significantly decreased,and the time of postoperative mechanical ventilation and duration of ICU stay were shortened in group D.Conclusion Dexmedetomidine infused continuously at 0.3 μg · kg-1 · h-1 (until the end of surgery) after a loading dose of 1 μg/kg before routine induction of anesthesia can reduce intestinal mucosal injury in the patients undergoing cardiac valve replacement with CPB.

Aim To determine whether remifentanil preconditioning has cardioprotection against ischemia and reperfusion induced injury via opioid receptor(OR) in rats.Method Male Sprague-Dawley rats of 300～350 g were anaesthetized and the chests were opened and hearts exposed via a left thoracotomy.They were randomly assigned to 12 groups:Control(CON,saline vehicle),naltrindole(NTD,5 mg?kg~(-1) iv.10 min before 30 min ischemia);CTOP(CTOP,1 mg?kg~(-1) iv.10 min before ischemia),nor-binaltorphimine(nor-BNI,5 mg?kg~(-1),iv.15 min before 30 min ischemia);remifentanil preconditioning(RPC,6 ?g?kg~(-1)?min~(-1)),ischemic preconditioning(IPC),NTD+RPC or NTD+IPC(naltrindole 5 mg?kg~(-1) iv.10 min before RPC or IPC),nor-BNI+RPC or nor-BNI+IPC(nor-binaltorphimine 5 mg?kg~(-1),iv.15 min before RPC or IPC),CTOP+RPC or CTOP+IPC(CTOP 1 mg?kg~(-1) iv.before RPC or IPC).Infarct size(IS),a percentage of the area at risk(AAR),was determined by triphenyltetrazolium(TTC) staining.Results IPC and RPC markedly reduced IS/AAR from(52.7?1.8)% to(12.9?2.7)% and(16.2?2.4)%,respectively. CTOP,a selective ?-OR antagonist,or NTD,a selective ?-OR antagonist,administered 10 min before remifentanil PC completely abolished,while nor-BNI,a selective ?-OR antagonist,administered 15 min before RPC attenuated the cardioprotective effect of RPC.In the group preconditioned with ischemia,blockade of ?-OR with NTD abolished,while blockade of ?-OR with nor-BNI attenuated the protection.Blockade of ?-OR with CTOP did not alter the cardioprotective effect of IPC.Conclusion The cardioprotective effect of RPC was abolished by all the three OR antagonist,CTOP,naltrindole and nor-binaltorphimine,suggesting that this effect is mediated via ?-,?-and ?-ORs.Part of the effect of RPC may be produced by ?-OR agonist activity outside the heart.

ObjectiveTo investigate the effects of intravenous (iv) remifentanil infusion on myocardial oxidative stress in rats.MethodsOne hundred and eighty male SD rats weighing 250-300 g were randomly divided into 15 groups (n =12 each):group control (group C); group ischemic preconditioning (group IPC); group remifentanil preconditioning ( group RPC ) ; while ia iv remifentanil infusion groups,iv remifentanil was infused at 4 different rates ( 1,5,10,20μg· kg- 1 · min- 1 ) and each rate was maintained for 15,60 and 120 min respectively.Myocardial ischemia was induced by occlusion of left coronary artery anterior descending branch for 30 min followed by 120 min reperfusion in 6 rats in each group.In group IPC myocardial ischemia was preceded by 3 cycles of 5min ischemia-5min reperfusion;whilein group RPC3cycles of 5min remifentanil infusion at 5 μg· kg-1 · min-1 were applied at 5 min interval before ischemia.Six rats in which I/R was produced were sacrificed in each group,myocardial infarct size (IS) and the area at risk (AAR) were measured and IS/AAR was calculated.The left 6 rats in each group were sacrificed at the corresponding time point (the end of each treatment)and superoxide radical expression and MDA and nitrotyrosine contents in myocardium were determined.Results IS/AAR was significantly decreased in groups IPC,RPC,1 μg·kg-1 ·min-1 × 120 min,5 μg·kg-1 ·min-1 × 60or 120 min and 10 μg· kg- 1 · min- 1 × 60 min as compared with group C.Compared with group C,the myocardial superoxide radical expression was significantly up-regulated in groups 1 μg· kg-1· min-1 × 120 min, 5 μg·kg-1 ·min-1 ×60 or 120 min,10μg·kg-1 ·min-1 ×60 or 120 min and 20 μg·kg-1 ·min-1 × 15,60 or 120min,and myocardial MDA and nitrotyrosine contents were significantly increased in group 20 μg· kg-1 · min-1 ×15,60 or 120 min.ConclusionLonger duration of high rate remifentanil infusion can induce myocardial oxidative stress in rats.

Objective To investigate the effect of sufentanil postconditioning on myocardial ischemiareperfusion (I/R) injury in patients undergoing cardiac valve replacement under cardiopulmonary bypass (CPB).Methods Sixty ASA Ⅱ or Ⅲ patients ( NYHA Ⅱ or Ⅲ ) of both sexes,aged 19-64 yr,scheduled for cardiac valve rreplacement under CPB,were randomly divided into 4 groups ( n =15 each):control group ( group C),sufentanil 0.5 μg/kg group (group S1 ),sufentanil 1.0 μg/kg group (group S2 ) and sufentanil 2.0 μg/kg group ( group S3 ).In groups S1,S2 and S3,sufentanil 0.5,1.0 and 2.0 μg/kg were infused over 2 min via aortic root 5 min before aortic unclamping respectively.In group C,the equal volume of normal saline (2 ml/kg) was infused instead of sufentanil.Blood samples were taken from the radial artery immediately before induction of anesthesia ( T2 ) and at 2,4,8,24 and 48 h after aortic unclamping ( T1-5 ) for determination of plasma concentrations of cardiac troponin-I (cTnI) and malondialdehyde (MDA) and activities of creatine kinase isoenzyme-MB (CK-MB) and superoxide dismutase (SOD).The duration of CPB,time of aortic clamping,extubation time,duration of stay in ICU,and myocardial contractility score and volume of drainage at 24 h after the operation were recorded.The restoration of spontaneous heart beat and adverse cardiovascular events were observed.Results The plasma cTnI,and MDA concentrations and CK-MB activity were significantly lower,while the SOD activity was significantly higher at T1-3 in group S1 than in group C ( P ＜ 0.05).The plasma cTnl concentration and CK-MB activity were significantly lower at T1-5,the plasma MDA concentration was significantly lower at T1-4,and SOD activity was significantly higher at T1-4,the extubation time and duration of stay in ICU were significantly shorter,and the myocardial contractility score at 24 h after the operation and incidence of adverse cardiovascular events were significantly lower in groups S2,3 than in group C ( P ＜ 0.05),The plasma cTnl concentration and CK-MB activity were significantly lower at T4,5,The plasma MDA concentration was significantly lower at T4,the SOD activity was significantly higher at T3,4,and the myocardial contractility score at 24 h after the operation was significantly lower in groups S2,3 than in group S1 ( P ＜ 0.05).Conclusion Sufentanil postconditioning can relieve myocardial I/R injury in patients undergoing cardiac valve replacement under CPB,and the mechanism is related to inhibition of lipid peroxidation.

Objective To investigate the effect of type 2 diabetes mellitus (DM) on the attenuation of myocardial ischemia-reperfusion (I/R) injury by sufentanil postconditioning in rats.Methods Male pathogen-free Sprague-Dawley rats,weighing 160-180 g,were used in the study.A model for type 2 DM was established by the feeding of high-fat diet-induced insulin resistance and intraperitoneal streptozocin 35 mg/kg.DM was confirmed by blood glucose level ≥ 16.7 mmol/L one week after injection.Eighteen type 2 diabetic rats were randomly divided into 3 groups (n =6 each):DM sham operation group (DM-S group) ; DM-I/R group; DM sufentanil postconditioning group (DM-SP group).Another 18 healthy nondiabetic rats were chosen and randomly divided into 3 groups (n =6 each):nondiabetes mellitus sham operation group (NDM-S group) ; nondiabetes mellitus I/R group (NDM-I/R group) ; nondiabetes mellitus sufentanil postconditioning group (NDM-SP group).Myocardial I/R was induced by 30 min occlusion of the left anterior descending branch of coronary artery (after 30 min of equilibration) followed by 120 min of reperfusion.Sufentanil 1.0 μg/kg was injected via the right jugular vein 5 min before reperfusion in NDM-SP and DM-SP groups.MAP,SP and HR were recorded immediately before ischemia,at 30 min of ischemia and at 120 min of reperfusion and rate-pressure product (RPP) was calculated.Arterial blood samples were collected at 120 min of reperfusion for measurement of plasma cardiac troponin Ⅰ (cTnⅠ) concentration.The rats were then sacrificed for determination of the myocardial infract size.Results MAP and RPP were decreased,while the plasma cTnl concentration was increased during reperfusion in diabetic and nondiabetic rats.Sufentanil postconditioning decreased the myocardial infract size and plasma concentrations of cTnⅠ,and increased MAP and RPP during reperfusion in nondiabetic rats,but had no effect on the parameters in diabetic rats.Conclusion Type 2 DM interferes with sufentanil postconditioning-induced myocardial protection in rats.

Objective To evaluate the role of different opioid receptors in sufentanil postconditioning-induced attenuation of myocardial ischemia-reperfusion (I/R) injury in rats.Methods Fifty adult male Sprague-Dawley rats,aged 4-6 months,weighing 200-330 g,were randomly divided into 9 groups:I/R group (n =7),ischemic postconditioning (IPC) group (n =7),sufentanil postconditiong (SP) group (n =6),κ-opioid receptor antagonist nor-binaltorphimine (nor-BNI) + SP group (group BNI + SP,n =5),δ-opioid receptor antagonist naltrindole + SP group (group NTD + SP,n =5) and μ-opioid receptor antagonist CTOP + SP group (group CTOP +SP,n =5).Myocardial I/R was produced by 30 min occlusion of left anterior descending branch of coronary artery followed by 120 min reperfusion.IPC was induced by 3 episodes of 10 s reperfusion followed by 10 s ischemia at the end of 30 min myocardial ischemia.Sufentanil 1 μg/kg was injected intravenously at 5 min before reperfusion in SP group.In groups BNI + SP,NTD + SP and CTOP + SP,nor-BNI 5 mg/kg,naltrindole 5 mg/kg and CTOP 1 mg/kg were injected intravenously,respectively,before SP and the corresponding doses of nor-BNI,naltrindole and CTOP were injected intravenously,respectively,at 5 min before reperfusion.Arterial blood samples were collected at 120 min of reperfusion for measurement of the plasma cardiac tropnin I (cTnI) concentration.The rats were then sacrificed and hearts removed for determination of myocardial infarct size (IS) and area at risk (AAR).IS/AAR was calculated.Results Compared with I/R group,the plasma cTnI concentration and IS/AAR were significantly decreased in groups IPC,SP,BNI + SP and NTD + SP (P ＜ 0.05),and no significant change was found in the plasma cTnI concentration and IS/AAR in groups CTOP + SP,NTD,BNI and CTOP (P ＞ 0.05).Compared with SP group,IS/AAR was increased in NTD + SP and BNI + SP groups and the plasma cTnI concentration and IS/AAR were significantly increased in CTOP + SP group (P ＜ 0.05).Conclusion The μ-,κ-and δ-opioid receptors mediate sufentanil postconditioning-induced attenuation of myocardial I/R injury in rats.