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Objective:To investigate the optimal dose of dexmedetomidine combined with propofol for anesthesia in patients undergoing modified electroconvulsive therapy (MECT).Methods:One hundred and sixty patients of both sexes, aged 20-60 yr, weighing 45-80 kg, of American Society of Anesthesiologists physical status Ⅰ or Ⅱ, scheduled for elective MECT, were allocated into 4 groups ( n=40 each) by a random number table method: different doses of dexmedetomidine combined with propofol group (D 1, D 2 and D 3 groups) and routine anesthesia group (group C). Dexmedetomidine 0.2, 0.4 and 0.6 μg/kg were intravenously injected in D 1, D 2 and D 3 groups, respectively, the equal volume of normal saline was given instead in group C, and propofol 1.0 mg/kg and succinylcholine 0.5 mg/kg were intravenously injected in turn 10 min later.Venous blood samples were collected before giving dexmedetomidine (T 0) and at 1 min after the end of MECT (T 1) for determination of the plasma epinephrine (E) and norepinephrine (NE) concentrations.Propofol consumption, occurrence of cardiovascular events, duration of epilespsy and energy suppression index were recorded. Results:Compared with group C, the plasma E and NE concentrations were significantly decreased at T 4, and the propofol consumption was reduced in D 1, D 2 and D 3 groups ( P<0.05). Compared with group D 2, the plasma E and NE concentrations were significantly increased at T 1 in group D 1 and decreased at T 1 in group D 3 ( P<0.05). The incidence of adverse cardiovascular events was significantly increased in group D 3 than in the other 3 groups ( P<0.05). There was no significant difference in duration of epilespsy or energy suppfession index among the 4 groups( P>0.05). Conclusion:The optimal dose of dexmedetomidine combined with propofol 1.0 mg/kg is 0.4 μg/kg when used for anesthesia in the patients undergoing MECT.
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Objective To evaluate the effects of sevoflurane preconditioning on caveolin-3 expression during myocardial ischemia-reperfusion (I/R) in rats.Methods Healthy male Wistar rats,aged 6-8 weeks,weighing 250-300 g,were anesthetized with intraperitoneal pentobarbital 30 mg/kg and heparin 1 000 IU/kg.Their hearts were excised and perfused with K-H solution in a Langendorff apparatus.Thirty isolated rat hearts were randomly assigned into 3 groups (n =10 each) using a random number table:control group (group C),I/R group and sevoflurane preconditioning group (group SP).After 30 min of equilibration,group C was continuously perfused with K-H solution for 90 min,group I/R underwent 30 min of ischemia followed by 60 min of reperfusion,and group SP was perfused with K-H solution saturated with 2％ sevoflurane for 10 min followed by 5 min washout with K-H solution,then underwent 30 min of ischemia followed by 60 min of reperfusion.HR,left ventricular enddiastolic pressure (LVEDP),+ dp/dtmax and-dp/dtmax were recorded at the end of equilibration,immediately before ischemia and at 30 and 60 min of reperfusion.Myocardial specimens were obtained from the cardiac apex for microscopic examination.Myocardial specimens were obtained from the left ventricle for determination of caveolin3 expression.Results Compared with group C,+ dp/dtmax and-dp/dtmax were significantly decreased immediately before ischemia,and HR,LVDEP,+ dp/dtmax and-dp/dtmax were decreased at 30 and 60 min of reperfusion in groups I/R and SP,and caveolin-3 expression was down-regulated in group I/R and up-regulated in group SP (P ＜ 0.05).Compared with group I/R,HR,LVDEP,+ dp/dtmax and-dp/dtmax were significantly decreased immediately before ischemia and increased at 30 and 60 min of reperfusion,and caveolin-3 expression was up-regulated in group SP (P ＜ 0.05).The pathological changes were significantly attenuated in group SP as compared with group I/R.Conclusion The mechanism by which sevoflurane preconditioning attenuates myocardial I/R injury in rats may be related to up-regulation of myocardial caveolin-3 expression.
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Objective To evaluate the role of Toll-like receptor 4 (TLR4) in mitigation of inflammatory responses following myocardial ischemia-reperfusion (I/R) injury by sufentanil postconditioning in rats.Methods Thirty Wistar rats were randomly divided into 3 groups (n =10 each):sham operation group (S group); I/R group; sufentanil postconditioning group (SP group).Myocardial I/R was produced by temporary ligation of left anterior descending branch of coronary artery for 30 min followed by 120 min reperfusion.In group SP,sufentanil 0.6 μg/kg was injected intravenously at 5 min before reperfusion.The myocardial specimens and blood samples were taken at the end of 120 min reperfusion for determination of the interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) concentrations and TLR4 content (by ELISA).Results Compared with S group,the levels of TLR4,IL-6 and TNF-α were significantly increased in the other two groups.Comparedwith I/R group,the levels of TLR4,IL-6 and TNF-α were significantly decreased in group SP.Conclusion The mechanism by which sufentanil postconditioning mitigates inflammatory responses following myocardial I/R injury may be related to downregulation of TLR4 expression in myocardial tissues of rats.
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Objective To investigate the role of Janus kinese 2-signal transducer and activator of transcription 3 (JAK2-STAT3) pathway in reduction of myocardial ischemia-reperfusion (I/R) injury by sufentanil postconditioning in dogs.Methods Twenty-four healthy dogs of either sex,weighing 10-15 kg,were randomly divided into 4 groups (n =6 each):sham operation group (group S); I/R group; sufentanil postconditioning group (group PO) and sufentanil postconditioning + specific JAK2 inhibitor AG490 group (group AG).In groups I/R,PO and AG,myocardial I/R was produced by occlusion of left anterior descending coronary artery for 30 min followed by 120 min reperfusion.In groups PO and AG,sufentanil 0.6 μg/kg was infused intravenously over 5 min before reperfusion and in addition in group AG,AG490 1 mg/kg was injected intravenously before sufentanil infusion.Myocardial specimens were taken at the end of 120 min reperfusion for microscopic examination and determination of the expression of caspase-3 and p-STAT3 by immuno-histochemistry and myocardial cell apoptosis index (AI) by TUNEL.Results AI and the expression of caspase-3 and p-STAT3 were significantly higher in groups I/R,PO and AG than in group S ( P ＜ 0.05).Compared with group I/R,AI and the expression of caspase-3 were significantly decreased in groups PO and AG,the expression of p-STAT3 was significantly increased in group PO,and the expression of p-STAT3 was significantly decreased in group AG ( P ＜ 0.05).AI and the expression of caspase-3 were significantly higher and the expression of p-STAT3 was significantly lower in group AG than in group PO (P ＜ 0.05).The pathologic changes were significantly attenuated in group PO compared with groups I/R and AG.Conclusion JAK2-STAT3 pathway is involved in reduction of myocardial I/R injury by sufentanil postconditioning in dogs.
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Objective To investigate the effect of sufentanil on norepinephrine (NE)-induced contraction of thoracic aorta isolated from rats with spontaneous hypertension (SH) .Methods Eight male rats with SH weighing 250-300 g were used in this study. The rats were decapitated and their thoracic aortas were isolated and cut into rings 2-3 mm in length. The aorta rings were suspended for isometric tension recording. The aortic rings obtained from SH rats were divided into 4 groups ( n = 8 each) : control group and 3 sufentanil groups. The contraction of aortic rings in response to NE in the absence (control) and presence of 3 concentrations of sufentanil 7 × 10-11 ,2 × 10-10 and 1 × 10-9 mol/L was recorded. Results The amplitude of NE-induced contraction of thoracic aorta was significantly greater in 3 sufentanil groups than in control group. Sufentanil significantly inhibited the NE-induced aortic contration in proportion to concentration. Conclusion Sufentanil can inhibit NE-induced contraction of thoracic aorta isolated from rats with SH in a concentration-dependent manner.
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Objective To investigate the effects of pretreatment with Shen-fu injection on mitochondrial permeability transition and mitochondrial transmembrane potential (△ψm) following myocardial ischemiareperfusion (IR) injury in rats. Methods Thirty SD rats of both sexes weighing 250-300 g were randomly divided into3 groups with 10 animals in each group:Ⅰ sham operation group (group S); Ⅱ IR group and Ⅲ Shen-fu injection group (group SFI). The animals were anesthetized with intraperitoneal 20% urethane 5 ml/kg. The chest was opened and the heart exposed. Myocardial IR was induced by temporary ligation of the anterior descending branch of left coronary artery maintained for 30 min, followed by 120 min reperfusion. Myocardial ischemia was confirmed by decoloration of apex and elevation of S-T segment (＞ 0.1 mV) or erection of T wave. In group SFI,SFI 10 ml/kg was infused at 15 min before ischemia, while in group S and IR equal volume of normal saline was infused instead of SFI. At 120 min of reperfusion, blood samples were collected from right internal carotid artery for determination of serum concentration of cTnI. The animals were then sacrificed and the hearts were immediately removed for measurement of myocardial mitochonerial permeability transition pore (MPTP) activity (by spectrophotometry at 540 nm) and myocardial △ψm (by fluorospectrophotometer using rhodamine 123 as fluorescent probe). Results Compared with group S, serum cTnI concentration and MPTP activity were significantly increased and △ψm was decreased in group IR. SFI pretreatment significantly attenuated the IRinduced increase in serum cTnI concentration and the MPTP activity and decrease in △ψm. Conclusion SFI pretreatment can protect myocardium from IR injury by attenuating the IR induced increase in MPTP opening and decrease in △ψm.
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Objective To investigate the effect of propofol on myocardial injury induced by hepatic ischemia/reperfusion (I/R) in rats and the role of PI3K/Akt signaling pathway. MethodsOne hundred and two male SD rats weighing 250-280 g were randomly divided into 5 groups:Ⅰ sham operation group (group S, n =6), ⅡI/R group ( n = 30), Ⅲ propofol group (group P, n = 30), Ⅳ propofol + LY294002 group (group P+ LY, n =18), and Ⅴ propofol + dimethylsulfoxide group (group P+ DMSO, n = 18). Hepatic I/R was produced by occlusion of hepatic pedicle for 30 min followed by reperfusion in group Ⅱ - Ⅴ. Propofol 12 mg/kg, propofol 12mg/kg + LY294002 (a specific PI3K inhibitor) 1.5 mg/kg, and propofol 12 mg/kg + DMSO 0.5 ml were injected I.v.via femoral vein at 10 min before ischemia in group Ⅲ -Ⅴ respectively, and then propofol was infused I.v. At a rate of 30 mg· kg- 1 · h - 1 and the administration was stopped before the rats were sacrificed in group Ⅲ - Ⅴ . At 0,30, 60, 120, and 240 min of reperfusion (T1-5) in group Ⅱ and Ⅲ , and at T3.5 in group Ⅳ and Ⅴ , six rata were sacrificed and myocardial tissues were taken for determination of the total Akt (t-Akt) and phosphorylated Akt (p-Akt) expression and Bcl-2 expression and apoptosis were detected at T3. The hepatic tissues were taken for microscopic examination. The rats were sacrificed at T1 and the parameters mentioned above were detected in group Ⅰ . ResultsCompared with group Ⅰ , p-Akt expression and apoptosis rate were significantly increased in the other4 groups, and Bcl-2 expression was up-regulated in group Ⅱ , Ⅲ and Ⅴ (P ＜ 0.05). Compared with group Ⅱ , p-Akt and Bcl-2 expression was up-regulated, and the apoptosis rate was significantly decreased in group Ⅲand Ⅴ ( P ＜ 0.05). Compared with group Ⅲ , p-Akt and Bcl-2 expression was down-regulated, and the apoptosis rate was significantly increased in group Ⅳ ( P ＜ 0.05). The microscopic examination showed that the injury to the hepatic tissues was less severer in group Ⅲ and Ⅴ than in group Ⅱ and Ⅳ. ConclusionPropofol can attenuate myocardial injury induced by hepatic I/R in rats by activation of PI3K/Akt signaling pathway.
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The present study was designed to confirm the use of GM-CSF, made by the Beijing United Biological Engineering Company, in leucocytopenia after chemotherapy in 12 patients with malignant tumor. In patients with malignant tumor the interval leucocytopenia needed shortened 5 days compared with that in control subjects. At the same time GM-CSF could be resistant to infection significantly, especially in patients with complicated infection, and the antibiotic applying time decreased. In addition, clinical experence had shown that there was no obvious side-effects in general dosage. Thus, these findings indicate that GM-CSF is a kind of essential drug in radical chemotherapy in patients with tumor.
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Electromagnetic blood flowmeter (EBF) and polygraph system were used for measuring the coronary blood flow (CBF), left ventricular systolic pressure (LVSP),mean aortic pressure (MAP ), heart rate respectively in anesthetized dogs. In group 1 (6 dogs ), after opening the chest,the left coronary artery was surrounded by a fitting flow prob of EBF and ploygraph system was connected with dogs. morphine (2mg. kg-1 ),morphine plus naloxone were intravenously injected into dogs respectively. It showed that CBF was increased 56. 8% with morphine, while the LVSP and MAP decreased, HR not changed. The effect mentioned above were partly antagonized by naloxone (0. 4mg/kg). In group 2(3 dogs) using same methods, HR.CBF. LVSP and MAP were decreased with high dose fentanyl (100ug/kg ). The results suggested that in clinic the use of high dose fentanyl should be careful during anesthesia for the patients with cardiopathy. However, the effect of morphine in increasing CBF may be beneficial for the patients with myocardial ischemia.