RÉSUMÉ
Objective To investigate the clinical significance of BNP, cTnI, T3 combined detection in elderly heart failure. Methods A total of 138 cases of elderly patients with heart failure (HF group) selected from October 2012 to December 2013 in our hospital were retrospectⅣe analyzed, according to the New York Heart Association (NYHA) classification standards will HF cardiac function of patients 60 cases of class Ⅱ, Ⅲ-Ⅳ grade 78 cases. The control group was 70 cases, were selected to our hospital for physical examination of healthy subjects on the same period with HF patients. BNP, cTnI, T3 were alone tested and joint detected. Results BNP, cTnI levels of NYHA Ⅱ level, NY-HAⅢ-Ⅳ-class before treatment were higher than the control group , T3 levels were lower than the control group;BNP, cTnI levels of NYHAⅢ-Ⅳ-class before treatment were higher than NYHA Ⅱ level, T3 levels were lower than NYHA Ⅱ level; BNP NYHAⅢ-Ⅳ level after treatment, cTnI levels before treatment appeared reduce, T3 levels ap-pear higher, the difference was significant (P<0.05). BNP+cTnI+T3 detect sensitⅣe were higher than BNP, cTnI, T3 alone testing, the difference was significant(P<0.05). Conclusion BNP, cTnI, T3 joint detection has high sensitⅣity for early diagnosis of HF has important significance.
RÉSUMÉ
Objective To investigate the effect of nicorandil pretreatment on myocardial mitochondria in a rabbit model of myocardial ischemia-reperfusion (I/R). Methods Tirty-two healthy male New Zealand white rabbits weighing 2.0-2.5 kg aged 4 months were randomly allocated into 4 groups ( n = 8 each): Ⅰ group sham operation (group S); Ⅱ group I/R; Ⅲ group nicorandil pretreatment (group N) and Ⅳ group nicorandil + 5 hydroxydecanoic acid (group N + 5-HD). Myocardial I/R was induced by 30 min occlusion of left circumflex coronary artery followed by 120 min reperfusion. In group N and N + 5-HD a bolus of nicorandil 100 μg/kg was given iv at 10 min before myocardial ischemia followed by continuous infusion at 10 μg· kg-1 · min-1 until the beginning of myocardial ischemia. In group Ⅳ a bolus of 5-HD 5 mg/kg was injected iv at 20 min before myocardial ischemia.The animals were sacrificed at the end of 120 min reperfusion. The mitochondrial membrane potential was measured by flow cytometry using JC-1 fluorescence probe as indicator. Bcl-2, Bax and cytochrome c protein expression was determined by immuno-histochemistry. Myocardial ultrastructure was examined with transmission electron microscope. Results Red fluovescence intensity indicating normal live cells was significantly higher, the green fluorescence intensity indicating apoptotic cells was lower and red/green fluorescence intensity ratio was higher; the Bcl-2/Bax ratio was significantly higher and cytochrome c protein expression lower in group N than in group I/R.5-HD administration negated the protective effect of nicorandil pretreatment against myocardial I/R injury. Conclusion Nicorandil stabilizes mitochondrial membrane potential, decreases cytochrome c protein releasing, and suppresses mitochondrial apoptotic signal transduction by opening the mito-KATP channels.
RÉSUMÉ
Objective Role of melanocortin receptor 4 (MCAR) in excitatory amino acid release from rat astrocytes in spinal cord. Methods Astrocytes were isolated from the spinal cord of newborn pathogen-free Wistar rats ( 1-3 days after birth) and cultured in serum-free Neurobasal/B27 liquid culture medium. After 4 passages the primary cultured astrocytes were randomly divided into 3 groups (6 wells each): group Ⅰ control (group C); group Ⅱ the astrocytes were exposed to TNF-α 10 μg/L (group T) and group Ⅲ the astrocytes were exposed to TNF-α 10 μg/L and HS014 (selective MC4R antagonist) 1 μmol/L (group TH). The astrocytes were incubated at 37 ℃ for 3 h. The supernatant was collected for determination of glutamic acid (Glu) and aspartic acid (Asp)concentrations by HPLC-MS/MS. Results TNF-α significantly increased Glu and Asp release from astrocytes in group T as compared with group C. The Glu and Asp concentrations were significantly lower in group TH than in group T. Conclusion MG4R is involved in the excitatory amino acid release from astrocytes in the spinal cord.