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

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.

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

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 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.

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.

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.

Objective To evaluate the effect of remffentanil postconditioning on myocardial ischemiareperfusion (I/R) injury in patients undergoing open heart surgery under CPB.Methods Thirty patients (ASA grade Ⅱ or Ⅲ, NYHA class Ⅰ or Ⅱ ) of both sexes aged 18-45 yr undergoing repair: of ventricular septal defect and/or atrial septal defect under CPB were randomly divided into 2 groups ( n = 15 each): control group (group C)and remifentanil postconditioning group (group R). Anesthesia was induced with midazolam, sufcntanil, propofol and rocuronium. The patients received 5 min infusion of remifentanil at 4 μg · kg- 1 · min - 1 8 min before aortic unclamping in group R, while the patients received equal volume of normal saline in group C. Blood samples were obtained from the right internal jugular vein for determination of plasma concentrations of cardiac troponin-I (cTnI)and MDA and activities of CK-MB and SOD before induction of anesthesia (baseline) and at4, 8, 24 and48 h after aortic unclamping. Results The plasma concentrations of cTnI and MDA and activity of CK-MB were significantly lower, while the plasma SOD activity was significantly higher at 4 and 8 h after aortic unclmping, and the plasma concentration of MDA was significantly lower at 24 h after aortic unclamping in group R than in group C ( P ＜ 0.05 ). Conclusion Remifentanil postconditioning can attenuate myocardial I/R injury in patients undergoing open heart surgery under CPB through inhibiting lipid peroxidation.

Objective To evaluate the effect of emulsified isoflurane preconditioning on myocardial iachemia-reperfusion (I/R) injury in rabbits.Methods Thixty-two male New Zealand white rabbits weighing 2.5-3.0 kg were randomly divided into 4 groups(n=8 each):group Ⅰ I/R;group Ⅱ isoflurane preconditioning (group Ⅰ);group Ⅲ emulsified isoflurane preconditioning (group EI) and group Ⅳ intralipid (group INT).Myocardial I/R was induced by 30 min occlusion of left anterior descending branch of coronary artery followed by 180 min of reperfusion.After 30 min of post-preparation equilibration.the animal inhaled 3%isoflurane for 30 min followed by 15 min washout in group Ⅰ(group Ⅱ);8% emulsified isoflurane 8-10 ml was injected iv at 1 ml/s followed by continuous infusion at 6-8 ml·kg-1·h-1,maintaining end-tidal isoflurane concentration at 1.28% for 30 min in group EI (groupⅢ);30% intralipid 9 ml was injected iv at 1 ml/s fullowed by continuous infusion at 7 ml·kg-1·h-1 for 30 min in group INT (group IV).HR and BP were monitored and recorded at 30 min of post-preparatory equilibration(T0),before ischemia(T1),at the beginning of ischemia(T2),at 30 min ofischemia(T3),60,120 and 180 min of reperfnsion(T4,5,6).HR-SP product (RPP) was calculated.Infarct size (IS) was determined by TIC staining.Blood samples were taken from carotid artery at T6 for determination of serum CK and LDH activities and IL-6 and IL-10 concentrations.Results HR,MAP and RPP were decreasing during T2-6, but there was no significant difference in HR, MAP and RPP among the 4 groups.The infarct size was signigicantly smaller, serum CK and LDH activities and IL-6 concentration were significantly lower while serum IL-10 concentration was significantly higher in group I and EI than in group I/R and INT.Conclusion Emulsified isoflurane preconditioning can attenuate myocardial I/R injury by inhibiting inflammatory response.

Objective To investigate effect of diabetes mellitus factor on attenuation of myocardial ischemia-reperfusion injury by sufentanil postconditioning in rats.Methods Diabetes mellitus was established by intraperitoneal streptozotocin 50 mg/kg and was confirmed by blood glucose ≥ 16.7 mmol/L.Thirty healthy adult male SD rats,weighing 250-300 g which diabetes mellitus model was successfully established were randomly divided into 3 groups ( n =10 each):diabetic mellitus sham operation group (group DM-S),diabetic mellitus ischemia-reperfusion group (group DM-IR) and diabetic meltitus sufentanil postconditioning group (group DM-SP).Another 30nondiabetic mellitus rats were also randomly divided into 3 group ( n =10 each):nondiabetic mellitus sham operation group (group NDM-S),nondiabetic mellitus ischemia-reperfusion group (group NDM-IR) and nondiabetic mellitus sufentanil postconditioning group (group NDM-SP).Myocardial ischemia-reperfusion was induced by 30 min occlusion of left anterior descending branch of coronary artery followed by reperfusion.Sufentanil postconditioning was induced by iv injection of sufentanil 1.0 μg/kg at 5 min before reperfusion.MAP,SBP,HR and RPP (HR × SBP) were recorded before ischemia,30 min of ischemia and 120 min of reperfusion.Arterial blood samples were collected at 120 min of reperfusion for measurement of plasma cardiac troponin 1 (cTnI) concentration.The animals were then sacrificed for determination of total areas of right and left ventricles ( LV + RV),infarct area (IS),area at risk (AAR) and IS/AAR.Results MAP and RPP were significantly lower,while plasma cTnI concentration was higher during myocardial ischemia reperfusion in diabetic and nondiabetic rats.Sufentanil postconditioning significantly decreased IS,IS/AAR and plasma cTnI concentration in nondiabetic rats during myocardial ischemia reperfusion but had no effect on IS,IS/AAR and plasma cTnI concentration in diabetic rats.The IS,IS/AAR and plasma cTnI concentration were significantly higher in DM-SP group than in NDM-SP gnoup ( P ＜ 0.05).Conclusion Diabetes mellitus factor can negate sufentanil postconditioning induced protection against myocardial ischemia-reperfusion injury in rats.