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Objective:To study the personality development of obsessive-compulsive disorder (OCD) from the perspective of memory-tracing.Methods:From January 2016 to May 2017, totally 103 patients with OCD (patient group) and 88 normal subjects (control group) matched with age, gender, and educational level in the national urban population norm database of Wang Weidong memory-tracing personality developmental inventory (WMPI) were included.WMPI was used to evaluate and compare all subjects.SPSS 22.0 software and nonparametric test were used for statistically analysis, and independent sample t-test and nonparametric test were used for data camparison. Results:1.In terms of external influencing factors of personality development: on the part of life events, the score of family affair in the patient group was higher than that in the control group( P<0.05) in childhood.In terms of upbringing, the scores of strictness (5.637±3.463) and punishment (6.275±4.565) in the patient group were higher than those ((4.341±3.092), (5.000±3.698)) in the control group in childhood( t=-2.703, -2.093, both P<0.05). 2.In the aspect of personality elements: (1) Among courage subscales, the scores of natural fear (7.686±3.441) and adaptability (15.000±5.321) in the patient group were higher than those((6.023±3.991), (12.841±6.070)) in the control group in childhood ( t=-3.085, -2.613, both P<0.05) .For all three stages, interpersonal fear scores in the patient group ((20.284±8.255), (22.804±7.458), (22.725±7.145))were all higher than those ((16.205±7.937), (19.841±6.319), (18.364±6.277))in the control group( t=-3.458, -2.929, -4.437, P<0.01). (2) Among interpersonal relationship, the dependence dimension scores were higher in the patient group (10.804±3.621) than those (8.830±4.850) in the control group during childhood( t=-3.205, P<0.01). (3) Among sex development, the scores of heterosexual communications (11.941±4.878), love concept (15.098±4.180) and sexual concept (8.892±2.988) were higher in the patient group than those ((9.125±5.040), (11.761±5.202), (6.943±3.288)) in the control group in adolescence(all P<0.01). (4) Among ego, the score of self-care dimension in the patient group (6.465±2.890) was higher than that in the control group(4.239±2.861) in childhood ( P<0.01). In the dimension of autonomy, the scores of the patient group ((10.772±2.694), (11.347±2.621)) were higher than those in the control group ((8.011±4.039), (9.818±2.693)) in childhood and adolescence (both P<0.01). (5) Among the way of thinking, the score of absolute thinking dimension in the patient group was higher than that in control group in childhood ( P<0.01). In the dimension of cautious, the scores of patient group were higher than those in the control group in childhood and adolescence (both P<0.01). (6)Among volition, the scores of decisive dimension in the patient group were higher than those in the control group in adolescence and youth (both P<0.01). In the dimension of consciousness, the score of patient group was higher than that in the control group in youth( P<0.01). In the dimension of insistence, the score of the patient group were higher than those in the control group in childhood and youth (both P<0.01). (7) Among worldviews, the scores of motivations, perspective of career and perspective of friendship in the patient group were higher than those in the control group in adolescence (all P<0.01). The score of value dimension in patient group was lower than that in the control group in the youth ( P<0.01). Conclusion:Patients with OCD have more strictness and punishment during their childhood in terms of upbringing.This leads to a lack of courage, poor interpersonal relationships, low self-care or autonomy, high attachment, absolutization of thinking and suppressing themself more in their childhood.In their adolescence and youth, their lack of courage, poor self-care or autonomy and the way of thinking cautious and stubborn will further aggravate and gradually show a more conservative sexual development and traditional world outlook.
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Objective To evaluate the role of Ras homolog family member A (RhoA)/Rho-associated coiled-coil containing protein kinase 2 (ROCK2) signaling pathway in propofol-induced neuroapoptosis in the hippocampus of newborn rats.Methods Experiment Ⅰ Primarily cultured hippocampal neurons were seeded in 6-well culture plates at a density of 1×106 cells/ml and divided into 2 groups (n=6 each) using a random number table:solvent control group (C group) and propofol group (P group).Propofol was added with the final concentration of 60 μg/ml in group P.Dimethyl sulfoxide was added with the final concentration of 0.04％ in group C.The expression of RhoA and ROCK2 in hippocampal neurons was measured by Western blot at 24 h of incubation.Experiment Ⅱ Primarily cultured hippocampal neurons were seeded in 6-well culture plates at a density of 1 × 106 cells/ml and divided into 3 groups (n =6 each) using a random number table:solvent control group (C group),propofol group (P group) and propofol plus specific RhoA/ROCK2 signaling pathway blocker Y27632 group (P+Y group).Propofol was added with the final concentration of 60 μg/ml in group P.Propofol at the final concentration of 60 μg/ml and Y27632 at the final concentration of 10 μmol/L were added in group P+Y.Dimethyl sulfoxide was added with the final concentrauon of 0.04％ in group C.At 24 h of incubation,the neuroapoptosis in hippocampi was detected by flow cytometry,and the expression of activated caspase-3 in hippocampal neurons was measured by Western blot.The apoptotic rate was calculated.Results Experiment Ⅰ Compared with group C,the expression of RhoA and ROCK2 in hippocampal neurons was significantly up-regulated in group P (P＜0.05).Experiment Ⅱ Compared with group C,the apoptotic rate of hippocampal neurons was significantly increased,and the expression of activated caspase-3 was up-regulated in P and P+Y groups (P＜0.05 or 0.01).Compared with group P,the apoptotic rate of hippocampal neurons was significantly decreased,and the expression of activated caspase-3 was down-rcgulatcd in group P + Y (P＜ 0.05).Conclusion Activation of RhoA/ROCK2 signaling pathway is involved in propofol-induced neuroapoptosis in hippocampi of newborn rats.
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Objective To evaluate the role of conventional protein kinase Cγ (cPKCγ)/growthassociated protein-43 (GAP-43) signaling pathway in ketamine-induced apoptosis in hippocampal neurons of developing rats in an in vitro experiment.Methods Primarily cultured hippocampal neurons were seeded in culture plates at a density of 1×10.6 cells/ml and divided into 2 groups (n=10 each) using a random number table:control group (C group) and ketamine group (K group).Group C received no treatment.Ketamine was added with the final concentration of 300 μmol/L in group K.At 12 h of culture or incubation,the apoptosis in hippocampal neurons was detected by flow cytometry.The apoptotic rate was calculated.The expression of cPKCγ,GAP-43 and phosphorylated GAP-43 in hippocampal neurons was measured by Western blot.Results Compared with group C,the apoptotic rates of hippocampal neurons were significantly increased,and the expression of cPKCγ,GAP-43 and phosphorylated GAP-43 was down-regulated in group K (P<0.01).Conclusion The mechanism by which ketamine induces apoptosis in hippocampal neurons of developing rats may be related to inhibition of cPKCγ/GAP-43 signaling pathway activation in an in vitro experiment.
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Objective To evaluate the effect of chronic low potassium on K+uptake rate in the my?ocardium and skeletal muscle of rabbits. Methods Thirty?two adult male rabbits, aged 12-14 weeks, weighing 2?0-2?7 kg, were randomly divided into 4 groups ( n=8 each) using a random number table:normal feeding group ( group N) , low potassium feeding group ( group L) , potassium supplementation con?trol group ( group SC ) and potassium supplementation experimental group ( group SE ) . N and SC groups were given a normal diet only, and L and SE groups were fed with a low potassium diet for 15 days. Potassi?um chloride ( KCl) 0?5 mol∕L was then infused intravenously at the initial rate of 60 μmol·kg-1 ·min-1 in SE and SC groups. Blood samples were obtained from the central artery of the left ear every 5 min for meas?urement of plasma K+ concentrations. The infusion rat of KCl was then adjusted until the plasma K+concen?tration reached 5?5 mmol∕L and maintained at this level for 1 h, and then infusion was stopped. The total volume of KCl infused was recorded. The hearts and soleus muscle of animals were excised for determination of K+content. K+uptake and uptake rate were calculated. Results Compared with N group, the plasma K+concentration, and K+content in the myocardium and soleus muscle were significantly decreased in group L ( P<0?05) . Compared with SC group, the total volume of KCl infused, and K+uptake and uptake rate in the myocardium and soleus muscle were significantly increased in group SE ( P<0?05) . Conclusion Chro?nic hypokalaemia can increase K+ uptake rate in the myocardium and skeletal muscle of rabbits.
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Objective To investigate the effects of sevoflurane postconditioning on cardiomyocyte apoptosis during myocardial ischemia-repeffusion (I/R) in rats.Methods Forty-five healthy male Wistar rats weighing 250-280 g were randomly divided into 3 groups ( n =15 each):group sham operation ( group S) ; group I/R and group sevoflurane postconditioning (group Spo).The animals were anesthetized with intraperitoneal 3％ pentobarbital 45 mg/kg,tracheally intubated and mechanically ventilated.Myocardial I/R was produced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 120 min reperfusion in groups I/R and Spo.In group Spo the animals inhaled 2.5％ sevoflurane for 5 min starting from 1 min before reperfusion was started.The animals were sacrificed at the end of 120 min reperfusion.Their hearts were removed for measurement of infarct size and the area at risk and determination of apoptotic index (the number of apoptotic cells/the total number of cells) and Bcl-2 and Bax protein and mRNA expression.Results Sevoflurane postconditioning significantly reduced infarct size in group Spo as compared with group I/R.There was no significant difference in area at risk between groups I/R and Spo.Myocardial I/R significantly increased the apoptotic index,Bcl-2 and Bax protein and mRNA expression in group I/R as compared with group S.Sevoflurane postconditioning significantly decreased apoptotic index and Bax protein and mRNA expression but increased Bcl-2 protein and mRNA expression in group Spo as compared with group I/R.Conclusion Sevoflurane postconditioning attenuates myocardial I/R injury by redncing myocardial apoptosis,up-regulating Bcl-2 expression and down-regulating Bax expression.
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Objective To investigate the role of PI3-kinase-Akt-endothelial nitric oxide synthase (PI3KAkt-eNOS) signaling pathway in the attenuation of myocardial ischemia-reperfusion (I/R) injury by sevoflurane postconditioning in rats.Methods Fifty healthy male Wistar rats weighing 250-280 g aged 2-3 months were randomly divided into 5 groups ( n =10 each):sham operation group (group S),I/R group,sevoflurane postconditioning group (group Spo),sevoflurane postconditioning + dimethyl sulfoxide (DMSO) group (group Spo + D),and sevoflurane postconditioning + LY294002 (a specific PI3K inhibitor) group (group Spo+ L).I/R was produced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 120 min reperfusion in anesthetized rats.In group Spo,sevoflurane was inhaled for 5 min after the end-tidal concentration reached 2.5％-3.0％ at 1 min before reperfusion.In group Spo + L,LY294002 0.3 mg/kg in 0.02％ DMSO was injected intravenously at 5 min before reperfusion,and then sevoflurane postconditioning was performed.In group Spo + D,0.02％ DMSO equal to the volume of LY294002 was injected intravenously at 5 min before reperfusion,and then sevoflurane postconditioning was performed.Arterial blood samples were taken at 120 min of reperfusion for determination of the levels of creatine kinase isoenzyme MB (CK-MB),lactate dehydrogenase (LDH) and cardiac Troponin Ⅰ (cTnI).The myocardial infarct size (IS) and area at risk (AAR) were measured and IS/AAR ratio was calculated.The rats were sacrificed at 120 min of reperfusion and the myocardial tissues in the area at risk were taken for determination of the expression of Akt,phosphorylated Akt (p-Akt),eNOS and phosphorylated eNOS (peNOS) by Western blot.The ratios of p-Akt/Akt and p-eNOS/eNOS were calculated.Results Compared with group S,the levels of CK-MB,LDH and cTnI,IS/AAR ratio,p-Akt/Akt ratio and p-eNOS/eNOS ratio were significantly increased in the other groups ( P ＜ 0.05 or 0.01 ).Compared with group I/R,no significant change was found in the parameters mentioned above in group Spo+ L (P ＞ 0.05),and the levels of CK-MB,LDH and cTnI and IS/AAR ratio were significantly decreased,and the ratios of p-Akt/Akt and p-eNOS/eNOS were significantly increased in groups Spo and Spo + D ( P ＜ 0.05 or 0.01 ).There was no significant difference in the parameters mentioned above between group Spo and group Spo + D (P ＞ 0.05).Conclusion PI3K-Akt-eNOS signaling pathway mediates the attenuation of myocardial I/R injury by sevoflurane postconditioning in rats.
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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.
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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.
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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.
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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.
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Objective To investigate the effect of sevoflurane postconditioning on the activities of Na+ -K+ -ATPase and Ca2+ -Mg2+ -ATPase during myocardial ischemia-reperfusion (I/R) in rats and the possible mechanism. Methods Forty-five healthy male Wistar rats weighing 250-280 g were randomly divided into 3 groups ( n = 15 each): sham operation group (group S), I/R group and sevoflurane postconditioning group (group Spo). Myocardial I/R was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 120 min of reperfusion. In group S the anterior descending branch was only exposed but not ligated. Group Spo received 5 min inhlation of 2.5% sevoflurane 1 min before reperfusion. The myocardial tissues were taken at 2 h of reperfusion for determination of infarct size and activities of Na+ -K+ -ATPase and Ca2 * -Mg2 * -ATPase. Results The infarct size was significantly larger and the activities of Na+ -K+ -ATPase and Ca2+ -Mg2+ -ATPase were signifi cantly lower in group I/R than in group S ( P ＜ 0.05). The infarct size was significantly smaller and the activities of Na+ -K+ -ATPase and Ca2+ -Mg2+ -ATPase were significantly higher in group Spo than in group I/R (P ＜ 0.05 ). Conclusion Sevoflurane postconditioning can reduce myocardial I/R injury through increasing the activities of Na+ -K+ -ATPase and Ca2+ -Mg2+ -ATPase.
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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
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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
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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.
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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
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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
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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.