The experiment of recirculating blood perfusion device showed that trimetazidine (TMZ ) 30 mol/L could significantly inhibit the arrhythmias induced by ischemia and reperfusion, decrease the content of malondialdehyde and improve superoxide dismutase activity of red blood cell in isolated rabbit hearts. In the experiment with coronary artery occlusion of rats, TMZ 4mg/kg administered intravenously could also inhibit arrhythmias induced by ischemia and reperfusion. The mechanism may be related to the depression of lipid peroxidation reaction.

Objective To investigate the expression and co-existence of fos-protein and enkephalin in CNS following enflurane anesthesia. Methods Twelve adult SD rats of both sexes weighing 195-223g were divided randomly into two equal groups: control group and enflurane group: The animals in enflurane group breathed 2% enflurane for 2h. The animals in control group underwent the same experimental steps except enflurane inhalation. Before experiment the animals were kept in a quiet place for 24h and strong light was avoided. After enflurane inhalation, chest was opened and 100 ml of normal saline was infused via left ventricle to wash Out blood from whole body, then followed by infusion of 4% polymerized formaldehyde 0.1mol/L PB 500 ml for fixation of tissue. 90 mm later the whole brain and spinal cord were harvested for determination of fos-protein and enkephalin expression and their location using double-labelled immunohistochemical technique. Results The control group showed more ELI(enkephalin like immunoactivity) neurons, less FLI(fos like immuneactivity) neurons and FLI/ELI(fos and enkephalin like immunoactivity) neurons were very rare. The enflurane group showed more FLI, ELI and FLI/ELI neurons. They were mainly distributed in frontal-cortex, lateral septal nucleus, basolateral amygdaloid nucleus, hippocampus CA1, paraventricular nucleus, ventral posterolateral nucleus, habenular nucleus, ventromedial hypothalamus nucleus, supraoptic nucleus, substantia nigra nucleus, interpeduncular nucleus, periaqueductal gray and dorsal horn. In enflurane group the number of FLI and ELI neurons in these nuclei was significantly higher(P

Objective:To observe the sedation effects of midazolam on maxillofacial postoperative patients with nasotracheal intubation. Methods:40 cases were equally and randomly divided into two groups: sufentanil group (group S) and sufentanil-midazolam group(group S-M).The continuous dose was 2 ml/h. If the patients feel uncomfortable, patient controlled intravenous analgesia (PCIA) was used. To observe the changes of circulation and respiration,the changes of visual analogue scale(VAS) and Ramsay score, the patients' bucking times within 24 h and the PCIA times, patients' total satisfactory degree and the complications during postoperative analgesia were recorded. Results:There were significant decreases in VAS of two groups after postoperative analgesia 1, 4, 12, 24, 48 hours(P

Aim To find new kinase inhibitors that o-vercome the imatinib resistance in the treatment of chronic myeloid leukemia ( CML ) by synthesizing C085, a novel derivative of curcumin , and testing its activities against wild-type( WT) and imatinib-resistant mutant Abl kinases , as well as in imatinib-resistant CML cells in vitro.Methods Cell proliferation and apoptosis were examined using MTT assay and flow cy-tometry, respectively;Kinase activity was measured u-sing Kinase-Glo Luminescent Kinase Assay Platform in recombinant WT and mutant ( Q252H, Y253F, and T315I) Abl kinases.The phosphorylation levels of Bcr-Abl initiated signaling proteins were analyzed using Western blotting .Colony forming units ( CFU ) growth was used to test the effects of C 085 on human leukemia progenitor/stem cells.Results C085 suppressed the growth of imatinib-resistant K562/G01 cells and po-tently inhibited both WT and mutant ( Q252H, Y253F, and T315I) Abl kinase activities in a non-ATP com-petitive manner with the values of IC 50 at low nanomole levels.C085 dose-dependently down-regulated Bcr-Abl kinase activity in K562/G01 cells as judged by auto-phosphorylation and Stat 5 , Crkl phosphorylation , and inhibited the phosphorylation of downstream targets Raf,Mek and Erk with protein content reducing .C085 could directly impact mitochondrial PT hole and make it open, which prevents the activation of caspase cas-cade reaction and induces the apoptosis .Furthermore, C085 significantly suppressed CFU growth , implicating that C085 could inhibit human leukemia progenitor/stem cells.Conclusion C085 may inhibit K562/G01 cells through inhibiting Bcr-Abl kinase activity and down-regulating the downstream signal proteins .Di-rectly acting on mitochondrial PT hole and then activa-ting apoptosis-associated proteins are also involved in the pro-apoptotic effect of C085.C085 is a promising compound for the treatment of CML patients with Bcr-Abl kinase domain mutations that confer imatinib re-sistance .

0.05) in VAS and ramsay scale, but side effects were significantly different in group B compared with those in group S. Conclusion: The analgesia efficacy of S is same as B in maxillofacial postoperation, but side effects are more significantly in group B, and group S is more safe and handy.

Objective To investigate the effects of inhaling isoflurane and enflurane on the spontaneous neural discharge of the neurones in rat hippocampus. Methods Whole cell patchclamp recording te chnique was used to observe the effects of isoflurane and enflurane on the spont aneous discharge rate of the neurons in the hippocampus on the brain slice of ne w-born SD rats. After decapitation, the whole brain of the rat was removed and put into artificial cerebrospinal fluid (ACSF) saturated with 1.36 g?L -1 O 2 and 0.098 g?L -1 CO 2 mixed gas at 4 ℃ . Brain was cut into 300～400 ? m thick slices containing the hippocampus. Whole cell patchc lamp recording technique was used to observe the effects of isoflurane with dif ferent concentrations on the spontaneous discharge rate of neurons in the hippoc ampus on the brain slices. Results Isoflurane and enfluran e could significantly inhibit the spontaneous neural discharge of neurons in the hippocampus in a dose-dependant manner. The effects of spontaneous neural disc harge of hippocampus inhibited by isoflurane (0.12 g?L -1 ～0.36 g?L -1 ) and enflurane (0.2 g?L -1 ～0.6 g?L -1 ) could be recove red following washing off with ACSF for 5 min. Conclusion T he spontaneous discharge rate of neurons in the hippocampus can be reversibly in hibited by isoflurane and enflurane. Hippocampus may be an important action site of anesthetics isoflurane and enflurane in the central nervous system.

Objective To study the protective effect of a hyperoxic solution on phosgene-induced lung injury by observing the changes in W/D ratio, lung water (LW), and L/B, and MDA contents, GSH-PX activity, and protein contents in broncho-alveolar lavage fluid (BALF). Methods The rabbits were divided into normal control group, hyperoxic solution (HO) and balance salt(BS) groups.Group HO and Group BS inhaled phosgene, and hyperoxic solution was given intravenously in group HO, but BS was given in group BS. W/D, LW, L/B, and MDA contents,GSH-PX activity,protein contents in broncho-alveolar lavage fluid (BALF) were determined. Results The MDA contents, W/D, LW and L/B were increased, and GSH-PX activity was decreased significantly in Group HO and Group BS compared with control group (P

Objective To investigate whether oral propofol has any inhibitory effects and dose-response relationship on the pain inducing tissue injury in mice. Methods The effect of propofol on pain was observed in formalin test and acetic acid writhing test in mice. Formalin was injected subcutaneously into the plantar surface of one hind paw. Spontaneous nocuous responses were immediately scored by counting the number of flinches of the injected hindpaw at every 5-minute interval during a 60-minute period. The number of writhing caused by intraperitoneal injection of 0.6% acetic acid was also observed in mice. Results Oral propofol in a dose of 100mg/kg did not significantly inhibit nocuous stimulation. With higher doses, propofol inhibited both the phases 1 and 2 of persistent spontaneous pain induced by subcutaneous formalin injection. Orally taken propofol also inhibited the number of writhing after intraperitoneal acetic acid injection in a dose dependent manner. Conclusion Oral propofol is effective in inhibiting pain induced by formalin and acetic acid.

Objective To investigate whether spinal cord is involved in the analgesic effect of propofol.Methods Fifteen adult SD rats of both sexes weighing 195～223g were randomly divided into three group of five animals each: control group received normal saline intraperitoneally(ip), fentanyl group received fentanyl 0 1mg/kg and propofol group propofol 100mg/kg ip 2 min later 4% formalin 150?l was injected subcutaneously into the planta region of right hindpaw 1h after formalin injection animals of all three groups were anesthetized with pentobarbital sodium ip After induction of anesthesia chest was open and 100 ml of normal saline was infused via left ventricle then followed by 4% formalin infusion for fixation of tissue, 90 min later spinal cord, L 3 5 sect, was removed for determination of c fos expression in spinal cord using fos immunohistochemistry technique Results In control group in less than 10 s after formalin intraplantar injection the animals were agitated, restless, lame and paw licking In fentanyl group and propofol group the righting reflex was suppressed for (19 4?7 8) min and (7 2?1 5)min and no pain response was seen during this period When righting reflex recovered the pain response was much lighter than that in the control group Formalin stimulation induced c fos expression was seen only in the ipsilateral spinal cord Both fentanyl and propofol significantly suppressed c fos expression evoked by formalin stimulation The number of fos like immunoreactivity neurons(FLIN) decreased by 57 8% and 36 3% respectively(P

Objective To determine the effects of enflurane and isoflurane on the spontaneous neural discharge of central amygdaloid nucleus in rats Methods SD rats (30 60 d) of either sex were decapitated Brain was immediately removed and kept in 4℃ artificial cerebral spinal fluid(ACSF) which was balanced with 95% O 2 and 5% CO 2 gas mixture Braine tissue containing central amyfdaloid nucleus was cut into slices of 300 400?m thick which were immersed in ACSF Enflurane and isoflurane were administered by balancing ACSF with enflurane (1 5%,3 0%,4 5%) or isoflurane (1 1%,2 2%,3 3%) The spontaneous neural discharge of central amygdaloid nucleus was measured before and after enflurane or isoflurane using whole cell patch clamp techniques Results Enflurane and isoflurane inhibited the frequencies of spontaneous neural discharge of central amygdaloid nucleus in a dose dependent manner The spontaneous neural discharge inhibited by enflurane (3 0%) and isoflurane (2 2%) could recover after the slices being washed with normal ACSF for 5 min Conclusions The results indicate that the spontaneous neural discharge of central amygdaloid nucleus can be inhibited reversibly by enflurane and isoflurane Central amygdaloid nucleus may by one of the sites of action of enflurane and isoflurane in central nervous system