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Objective To explore the influences of sufentanil and different dose midazolam coprocessing on myocardial injury in rats during myocardial ischemia-reperfusion (IR ). Methods Forty two healthy male SD rats were selected and randomly divided into 7 groups including,group A:rats were treated with sham operation;groups B0-B5:rat IR model was con-structed;group B0:rats were untreated with sufentanil or midazolam;group B1:rats were per-trea-ted with 3 μg/kg sufentanil;group B2:rats were post-treated with 0.1 mg/kg midazolam;group B3:rats were post-treated with 0.3 mg/kg midazolam;group B4:rats were per-treated with 1.5 μg/kg sufentanil and post-treated with 0.05 mg/kg midazolam;group B5:rats were per-treated with 1.5μg/kg sufentanil and post-treated with 0.15 mg/kg midazolam.Sufentanil was injected through cervi-cal vein before ischemia.Midazolam was injected through cervical vein after ischemia.After reperfu-sion,arterial blood was collected for detecting the activity of CK-MB,LDH or SOD,and the concen-tration of MDA,TNF-α,or IL-6.Rat hearts were picked off to measure the severity of myocardial in-farction (IS/AAR).The expressions of Bax,cleaved-caspase-3 and Bcl-2 in myocardial tissues were detected by Western blots.Results CK-MB activity,LDH activity,MDA concentration,TNF-αlev-el,IL-6 level,Bax and cleaved-caspase 3 expression levels in groups B0-B5 were obviously higher than those in group A (P <0.05),in groups B1-B5 were obviously lower than those in group B0 (P<0.05),in groups B3 and B4 were obviously lower than those in group B2 (P <0.05),in group B5 were obviously lower than those in groups B1-B4 (P < 0.05 );values of IS and IS/AAR (%)in groups B1-B5 were obviously lower than those in group B0 (P <0.05),in groups B3 and B4 were ob-viously lower than those in group B2 (P < 0.05 ),in group B5 were obviously lower than those in groups B1-B4 (P <0.05 );SOD activity and Bcl-2 expression level in groups B0-B5 were obviously lower than those in group A (P <0.05),in groups B1-B5 were obviously higher than those in group B0 (P <0.05),in groups B3 and B4 were obviously higher than those in group B2 (P <0.05 ),in group B5 were obviously higher than those in groups B1-B4 (P <0.05).CK-MB declined when com-pared with group B0;LDH declined;SOD rose;MDA declined;TNF-αdeclined;IL-6 declined;IS/AAR declined;Bcl-2 expression rose to 2.25 fold;Bax expression dropped to 54.89%;cleaved-caspase-3 expression dropped to 49.67%.Conclusion Sufentanil pretreatment combined with mid-azolam aftertreatment can significantly alleviate rat myocardial IR injury,which plays more effective cardioprotective effects than being used alone.
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Aim To investigate the effect of Salvianol-ic acid A (Sal A)on mice with isoproterenol (ISO)-induced myocardial infraction and its possible mecha-nisms.Methods The mice were subcutaneously in-jected with ISO (8 mg·kg-1 )to induce myocardial in-farction.The myocardial protective effect of Salvianolic acid A was evaluated from mortality rate,electrocardio-gram (ECG),heart function,myocardial infarction in-dex,serum myocardial enzymes and its action mecha-nisms were explored from inflammation,anti-oxidation and cells apoptosis.Results Salvianolic acid A dose-dependently enhanced the heart function of myocardial infarction mice,reduced the heart index,inhibited the myocardial enzyme leakage,showed obvious myocardi-al protection effects.ELISA results showed that Salvi- anolic acid A could reduce the expression of myocardial inflammatory cytokines such as IL-6(interleukin-6,IL-6),TNF-α(tumornecrosis factor-α,TNF-α).West-ern-blotting confirmed that Salvianolic acid A could in-crease the expression of anti-apoptotic proteins Bcl-2, reduce the expression of apoptosis protein Bax,and raise the phosphorylation level of PI3K and Akt.Con-clusion Salvianolic acid A displays a significant pro-tective effect against isoproterenol-induced myocardial infarction and its mechanism may be related to the in-crease of PI3K/Akt signal pathway and the inhibition of cell apoptosis and inflammatory reaction.
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ObjectiveTo study the effect of implantation of the bone marrow cells into infarction myo cardium on the secretion of basic fibroblast growth factor (bFGF), insulin-like growth factor 1 (IGF-1), transforming growth factor-?1 (TGF-?1 ), interleu kin-1 (IL-1), and interleukin-8 (IL-8).MethodsBone marrow cells were implanted into the region of acute myocardial infarct via topical injection. Specimens were harvested at first, 2nd, 4th, 8th week after implantation for the expression of cytokines and vascular density examination by immunohistochemical analysis and the levels of cytokines by radioimmunoassay. ResultsAt first, 2nd, 4th, 8th week after transplantation, the vascular density in the bone marrow cell implant group was significantly higher than that in the control group (P