Objective To investigate the effects of nicorandil (Nic) pretreatment on myocardial apoptosis in a rabbit model of myocardial ischemia/reperfusion (I/R) .Methods Forty healthy male New Zealand white rabbits aged 4 months weighing 2.0-2.5 kg were randomly allocated to one of 5 groups ( n = 8 each); group 1 sham operation; group 2 I/R; group 3 Nic; group 4 Nic + 5-hydroxydecanoic acid (5-HD) and group 5 Nic + glibenclamide (Gli) . The animals were anesthetized with IV pentobarbital 30 mg?kg-1 and tracheotomized and breathing spontaneously. A piece of thread was placed around the circumflex branch of left coronary artery, which was reversibly occluded for 30 min and released for 120 min reperfusion. In group 3, 4 and 5 a loading dose of 100 ?g?kg-1 Nic was given IV 10 min before myocardial ischemia followed by Nic infusion at 10 ?g?kg-1 ?min-1 until myocardial ischemia was started. In group 4 and S 5-HD 5 mg? kg-1 or Gli 5 mg? kg-1 was given IV 20 min before ischemia. At the end of 120 min reperfusion the animals were killed and the hearts removed. The area of myocardial infarct (AI), and the ischemic risk zone (AR) were determined by computer morphometry. The early apoptotic myocytes were detected by flow cytometry (Beckman, Coulter Co). The expression of caspase-3 protein was determined by immuno-histochemistry. The myocardial ultrastructure was examined with transmission electron microscope.Results Compared to group 2 (I/R) , in nicorandil group (group 3) the size of myocardial infarct and the number of early apoptotic cells were significantly reduced, the ultrastructure of myocardium was well-preserved and the expression of activated caspase-3 protein decreased. The protective effect of Nic preconditioning was greatly inhibited by 5-HD and Gli pretreatment. Conclusion Nicorandil pretreatment exerts protective effect against myocardial I/R injury through activation of mito-KATP C and inhibition of activation of caspase-3.

0. 5mV or change in color of myocardium in the ischemic area. Blood samples were taken from right atrium for determination of plasma levels of TXB2 and 6-keto-PGFla before epidural block (T0), 40 min after occlusion of coronary artery(T1 ) and 1, 3 and 5 h after reperfusion was started(T2-4 ) . Results There was no significant changes in MAP, HR and CVP in group Ⅱ while in group Ⅰ MAP decreased by 22%, HR 25% and CVP 28% after epidural block as compared with the baseline at T0 . TXB2 levels and TXB2/6-keto-PGF1a ratio increased gradually and significantly from T2-4 as compared with the baseline (T0) and those at T1 in both groups. TXB2 levels and TXB2/6-keto-PGF1a ratio were higher in group Ⅱ those in group 1111111 at T1-4 (P

0.5 mV and change in color of myocardium. Blood samples were taken from right atrium for determination of plasma SOD activity and plasma MDA level and from coronary sinus and artery for determination of blood lactate level before occlusion of LAD ( T0 ) , before reperfusion (T1),1,2,3,4,5,6 h after reperfusion (T2-7 ) . Myocardial lactate production was calculated from the difference between coronary sinus and arterial blood lactate concentrations. Results ( 1) In HTEA group HR, MAP and CVP decreased by 22% , 25% and 28% after epidural blockade, while in control group there was no significant change after epidural saline. (2) In HTEA group plasma SOD activity started increasing at T6 and blood MDA level decreased at T4 and T5, whereas in control group blood SOD activity started decreasing and blood MDA level started increasing at T3 . (3) Myocardium released no lactate before ischemia. Myocardial lactate release greatly increased during ischemia and started decreasing after reperfusion in both groups. But myocardial lactate production was significantly less in HTEA group than that in control group. (4) One animal died from ventricular fibrillation at the beginning of reperfusion in HTEA group while in control group four animals died. Conclusion HTEA can alleviate the myocardial ischemia-reperfusion injyry by blocking sympathetic nervous activity.

Objective To evaluate the effect of desflurane on blood flow velocity in the middle cerebral artery (VmMCA) and cerebrospinal fluid pressure (CSFP).Methods Sixty patients were randomly assigned to two groups. In group A,the anesthesia was maintained with desflurane, and in group B, with isoflurane. In either group, patients were allocated to three subgroups according to different doses(05,08,1.1MAC). CSFP was measured through a lumbar subarachnoid catheter before surgical procedures,from induction to administration of the inhalational agent for 45min.VmMCA was measured by transcranial Doppler at baseline , postintubation and administration of agent for 45min. Results As compared with baseline,CSFP increased gradually and reached to 16.90?4.01mmHg in subgroup 1.1MAC of group A (P0.05). Compared with baseline, VmMCA increased significantly at 45th min following administration of agent in subgroup 11MAC of group A(P005). In group A , a significant parallel correlation existed between the MAC levels and the values of VmMCA or CSFP (r=0.52,P

Objective To investigate the influences of hypothermia on hemodynamics and hemorrheology .Methods The body temperature of 10 mongrel dogs decreased at 35℃ ,and was kept for 30 min, and then warmed to normal degree with physical methods. The parameters of hemodynamics and hemorrheology were measured with the polygraph system (RM 6000, Nihon Kohden).Results Compared with the baselines, 30 min following hypothermia heart rate, mean arterial pressure, cardiac output, maximum rate of rise and decline of pressure(?dp/dtmax),cardiac index, left ventricular stroke work index were significantly reduced, while systemic peripheral resistance , blood viscosity were higher than those under normal body temperature (P

Objective In addition to myocardial ischemia,massive inflammatory mediators and different enzymes are released and free radicals increase during cardiopulmonary bypass(CPB) due to the contact of blood with foregin material Leukocytes play an important role The purpose of this study was to evaluate the myocardial protective effect of leukocyte depleted blood perfusion during open heart surgery Methods Thirty adult ASA II IV patients scheduled for elective orthotopic valve replacement received fentanyl enflurane anesthesia A bolus of 3 mg/kg intravenous heparin was given before CPB Cardiac arrest was induced with 4 ℃ hyperkalemic crystalliod cardioplegic solution Patients were randomly allocated to one of 3 groups based on the types of cardioplegic solution used during CPB: crystalloid solution(group CS, n=10),whole blood (group WB,n=10), and leukocyte depleted blood (group LD,n=10) Blood samples were taken from peripheral artery before heparinization, 5 min after initiation of CPB ,5 min before and 30 min, 1 h, 2 h and 24 h after declamping of aorta respectively for determinations of creatine kinase MB(CK MB), interleukin 8(IL 8) and tumor necrosis factor alpha(TNF?) Myocardial tissuses were obtained from right atrium before cross clamping of aorta, before and 15 min after declamping of aorta for determinations of water content,Ca 2+ content and ultrastructure examination of myocardium Results After declamping plasma concentrations of CK MB and IL 8 significantly increased in all groups as compared to the values before declamping (P

Objective To investigate the effect of sevoflurane preconditioning-postconditioning on thromboxane A2 and prostaglandin I2 during myocardial ischemia-reperfusion (I/R) in rats. Methods Fifty healthy male Wistar rats weighing 250-280 g were randomly divided into 5 groups (n = 10 each) : sham operation group (group S) , I/R group, sevoflurane preconditioning group (group Spr), sevoflurane postconditioning group (group Spo)and combination of sevoflurane preconditioning and postconditioning group (group Spr + po). Myocardial I/R was produced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 2 h reperfusion in anesthetized rats. In group S the anterior descending branch was only exposed but not ligated. Group Spr received 15 min inhalation of 2.5 % sevoflurane and 15 min wash-out 30 min before ischemia. Group Spo received 5 min inhalation of 2.5% sevoflurane 1 min before reperfusion. Arterial blood samples were taken at 2 h of reperfusion for determination of the levels of MB isoenzyme of creatine kinase (CK-MB) , lactate dehydrogenase (LDH) , cardiac troponin I (cTnI), thromboxane B2(TXB2), and 6-keto-prostaglandin (6-keto-PGF1α) and platelet maximum aggregation rate. TXB2/6-keto-PGF1α ratio was calculated. The myocardial tissues were taken for microscopic examination. Mitochondria] injury was assessed by using Flameng score and stereology (Specific surface, δ and Numerical density on area, NA) .Results Compared with group S, the levels of CK-MB, LDH, cTnI, TXE2 and 6-ketoPGF1α, TXB2/6-keto-PGF1α ratio, platelet maximum aggregation rate and Flameng score were significantly increased, while δ and NA were significantly decreased in group I/R (P < 0.05 or 0.01) . The levels of CK-MB,LDH and cTnI, TXB2/6-keto-PGF1α ratio and Flameng score were significantly lower, and 6-keto-PGF1α level, δand NA were significantly higher in Spr and Spo groups than in group I/R ( P < 0.05 or 0.01) . The levels of CKMB, LDH, cTnI and TXB2 , TXB2/6-keto-PGF1α ratio, platelet maximum aggregation rate and Flameng score were significantly lower and 6-keto-PGF1α level,δ and NA were significantly higher in group Spr + po than in Spr and Spo groups(P < 0.05). Conclusion Sevoflurane preconditioning-postconditioning can reduce myocardial I/R injury through inhibiting the release of thromboxane A2 and promoting the release of prostaglandin I2 in rats.

Objective To investigate the role of acid-sensing ion channels (ASICs) in global cerebral ischemia-reperfusion (I/R) injury in rats. Methods Forty-eight adult male Sprague-Dawley rats weighing 250-310 g were randomly divided into 4 groups ( n = 12 each): sham operation group (group S); global cerebral I/R group (group I/R); normal saline group (group NS) and specific ASIC blocker amiloride group (group A). Global cerebral I/R was produced by occlusion of 3 vessels ( 10 min occlusion of the bilateral common carotid arteries and basilar artery) followed by reperfusion. In group NS and A, NS 6 ml/kg and amiloride 0.6 mg/kg were injected through femoral vein immediately before reperfusion respectively. Six rats in each group were selected, the dialysate in CA1 area was collected before ischemia (baseline), immediately after ischemia and during 20 min reperfusion (once every 10 min) for determination of lactate concentrations. The left 6 rats in each group were elected at 8 h of reperfusion and the open field test and inclined plane test were peeformed to assess neurological behavior.The rats were then sacrificed and brain tissues taken for microscopic examination and brain water content was calculated. Results Compared with group S, the concentration of lactate in the dialysate and brain water content were significantly increased and neurological deficits developed in group I/R and NS (P ＜ 0.05). Compared with group I/R, the concentration of lactate in the dialysate and brain water content were significantly decreased and neurological deficits were improved in group A ( P ＜ 0.05 ), but no significant change in the parameters mentioned above was found in group NS ( P ＞ 0.05). Microscopic examination showed that the damage to the brain tissues was attenuated in group A compared with group I/R. Conclusion ASICs are involved in the development of global cerebral I/R injury in rats.

Objective To study the effect of dexmedetomidine and midazolam on hemodynamics and sedation in patients with nasal intubation.Methods Forty patients whose ASA grade Ⅰ-Ⅱ and anticipated difficult airway were randomly divided into dexmedetomidine group(group D,20 cases)and midazolam group(group M,20 cases)according to the admission number.In group D,dexmedetomidine 1 μ g/kg were constant speed pumped in 10 minutes.In group M,midazolam 0.03 mg/kg were intravenous injected.Then nasal intubation were carried.Systolic blood pressure(SBP),diastolic blood pressure(DBP),mean arterial blood pressure(MAP),heart rate(HR),pulse oxygen saturation(SpO2),Ramsay sedation score,rate-pressure product(RPP),tip perfusion index(TPI)were recorded and compared before anesthesia (T0),fiberoptic bronchoscope pass by later nostril(T1),to spy on epiglottis(T2),intubation succeed(T3),after intubation 1 minute(T4)and after intubation 3 minutes(T5).Airway score and postoperative visit were evaluated.Results SBP,DBP,MAP,HR,RPP in group M were significantly higher at T1-T3 than those at T0 (P＜0.05),and were significantly higher than those in group D at the same time(P＜ 0.05).There was no significant difference in group D(P ＞ 0.05).Ramsay sedation score and TPI at T1-T3 in group M were significantly lower than those at To(P ＜0.05).Ramsay sedation score and TPI at T1-T5 in group D were significantly higher than those at T0(P ＜ 0.05),and were significantly higher than those in group M at the same time(P ＜ 0.05).The rate of airway score 1 score and intubation satisfaction in group D were significantly higher than those in group M[100％(20/20)vs.30％(6/20),90％(18/20)vs.50％(10/20)](P＜ 0.05).The rate of throat ache in group D was significantly lower than that in group M[5％(1/20)vs.35％(7/20)](P ＜0.05).Conclusions For difficult airway patients with nasal intubation during dexmedetomidine infusion,hemodynamics is stable and sedation is satisfied.

Objective To evaluate the effect of Ganoderma lucidum on drug resistance of the cisplantin-resistant ovarian cancer cell line(A2780CP).Methods The A2780CP cells were randomly divided into control group and test group.The cells in control group and test group were incubated in culture media alone and in culture media containing Ganoderma lucidum 0.5 mg/ml for 48 h respectively.The resistance index(RI) of A2780CP was determined by WST-1 assay.The expression of Akt,Bcl-2 and p53 protein was measured by Western blot.Results The RI was significantly deeressed,the expression of Akt and Bcl-2 protein was down-regulated,while p53 protein expression was up-regulated in test group as compared with control group(P<0.05).Conclusion Ganoderma lueidum can reduce the resistance of A2780 CP cells to cisplantin by down-regulating the expression of Akt and Bcl-2 and up-regulating p53 expression in A2780CP cells.