It is general belied that myocardial ischemia caused an increase of plasma fibrinogen(Fg),but the changes of Fg in ischemic region is not clear.In 17 open chest dogs, an external stenosis or infarction was produced by a micro-meter constrictor on left circumflex coronary artery. The changes of Fg and platelet count(PC) in coronary sinus were observed for 60 min. The results showed that acute myocardial ischemia produed a decrease in Fg when coronary artery stenosis was more than 75%; there was also a decrease in PC when stenosis was more than 90%. The reduced amplitude of PC was more than that of Fg. Histopathologic examination confirmed the presence of damanged endothelial cell, platelet adhesion and aggregation coronary thrombosis and microemboli in ischemic region It is suggested that acute myocardial ischemia lead to a decrease of Fg in the ischemic myocardium, which was associated with platelet aggregation and coronary thrombosis.

AIM: To study the blocking effects of extracellular Cd 2+ on the inward rectifier potassium channel (IRK1) expressed in the Xenopus oocytes METHODS:Two-microelectrode voltage clamp (TEV) method was used RESULTS:Cd 2+ can concentration-, time- and voltage dependently block IRK1 instantaneous currents ( 1 5 ms after voltage applied ) when external Cd 2+ concentration is 0, 0 1, 0 15, 0 3, 0 9, 2 7 or 5 4 mmol/L with K + concentration fixed to 90 mmol/L Cd 2+ almost has no effect on the gating property and outward currents of IRK1 Cd 2+ can concentration-dependently increase the normalized conductance of IRK1 IRK1 can not permeate Cd 2+ because reverse potential did not change Three exponential fitting analyze indicates that time constant is not changed with the change in Cd 2+ concentration This shows that the inhibitory effects of Cd 2+ may be caused by surface potential or the blocking site of Cd 2+ is at the surface of the channel Because external Cd 2+ can not inhibit IRK1 macroscopic currents more powerfully when external Cd 2+ concentration is lower These mean that external Cd 2+ does not work through surface potential mechanism CONCLUSION: Cd 2+ is considered as one of the fast open channel blockers of IRK1 and its blocking site is at the surface of the channel

AIM:To study the blocking effects of extracellular Cd2+ on the inward rectifier potassium channel (IRK1) expressed in the Xenopus oocytes. METHODS：Two-microelectrode voltage clamp (TEV) method was used. RESULTS：Cd2+ can concentration-, time- and voltage dependently block IRK1 instantaneous currents ( 1.5 ms after voltage applied ) when external Cd2+ concentration is 0, 0.1, 0.15, 0.3, 0.9, 2.7 or 5.4 mmol/L with K+ concentration fixed to 90 mmol/L. Cd2+ almost has no effect on the gating property and outward currents of IRK1. Cd2+ can concentration-dependently increase the normalized conductance of IRK1. IRK1 can not permeate Cd2+ because reverse potential did not change. Three exponential fitting analyze indicates that time constant is not changed with the change in Cd2+ concentration. This shows that the inhibitory effects of Cd2+ may be caused by surface potential or the blocking site of Cd2+ is at the surface of the channel. Because external Cd2+ can not inhibit IRK1 macroscopic currents more powerfully when external Cd2+ concentration is lower. These mean that external Cd2+ does not work through surface potential mechanism.CONCLUSION:Cd2+ is considered as one of the fast open channel blockers of IRK1 and its blocking site is at the surface of the channel.

Objective To explore the nechanism of the interaction between K-opioid receptor and ? adrenal receptor. Method The effects of u50 488H on L-type calcium currents in the normal and hypoxic rat ventricular myocytes were studied by using whole-cell patch clamp technique. Results The basal as well as Isoproterenol-stimulated I_ Ca,L were inhibited by U50,488H in a dose-dependent manner in normal rat ventricular myocytes. In the hypoxic rat ventricular myocytes,the inhibitory effect of U50,488H was decreased. U50,488H had no significant effect on Forkolin-stimulated I_ Ca,L . Conclusion The results indicated that the negative modulation of ?-opioid receptor on ?-adrenoceptor was attenuated in the hypoxic ventricular myocytes,and the target of U50,488H on ?-adrenergic system might be situated between ?-adrenoceptor and adenylate cyclase.

Objective To observe the effects of infrasound on rat myocardial cells and to study its underlying mechanism. Methods One hundred Sprague-Dawley rats were divided into a normal control group and a infrasound exposure group, composed of various subgroups subject to exposure to infrasound for 2 hours daily for 1 d,7 d,14 d,21 d,and 28 d, respectively. The ultra-microstructure and apoptosis of the rat myocardial cells were observed, and SOD and MDA were measured. Results After exposure to infrasound, significant ultra-microstructural impairment and increased apoptosis of the myocardial cells were observed in the infrasound exposure group as compared to those of the normal control group,(P

AIM: The present study was to investigate the time course of ?-adrenoceptor desensitization and changes in the calcium transient in rat ventricular myocytes following chronic hypoxia. METHODS: With the spectrofluorometric method, the intracellular calcium( i) transient and its response to ?-adrenoceptor stimulation were determined in the single right ventricular myocytes, loaded with Fura-2.RESULTS: After 2-3 weeks of chronic hypoxia, the amplitudes of electrically induced i transient and caffeine-induced i transient started to decrease and the duration of i transient prolonged. The enhanced electrically induced i transient evoked by isoprotrenol was also decreased. After 3 or 4 weeks of chronic hypoxia, these changes aggravated gradually. After 8 weeks of chronic hypoxia, the changes of all these parameters were convalescent, meanwhile there was no significant difference compared with that of 4 weeks group. CONCLUSIONS: After 2-4 weeks of chronic hypoxia, the ?-adrenoceptor desensitization occurs, the underlying mechanism is related to the decreased function of L-type of calcium channel, ryanodine receptor-operated calcium channel and calcium ATPase, which is responsible for the decreased cardiac functionl. At 8 weeks of hypoxia, the heart is in adaptation and compensatory process.

AIM: To investigate the effects and mechanisms of swainsonine-induced apoptosis on SGC-7901 cells. METHODES: After being treated with swainsonine, effective dose and median inhibition concentration (IC50) of swainsonine to SGC-7901 cells were examined by MTT assay. Cell cycle distribution and apoptotic rates were analyzed by flow cytometry. Expression of p53, c-myc and Bcl-2 were determined by immunocyto- chemical method, and the concentration of Ca2+ intra-cellular ([Ca2+]i ) was measured by the laser scanning confocal microscope (LSCM). RESULTS: Swainsonine inhibited cell growth of SGC-7901 in vitro, IC50 of 24 h was 0.84 μg·ml-l, and complete inhibition concentration of swainsonine was 6.2 μg·ml-l. Treated with swainsonine at the concentrations of 0.5, 1.5 and 4.5 μg·ml-l for 24 h, the expression of apoptosis inhibiting gene p53 and bcl-2 decreased, and apoptotic trigger gene c-myc increased (P<0.05), as well as [Ca2+]i overloading, SGC-7901 cell was induced to apoptosis in the end. The percentage of S phase were 38.8%, 39.7% and 29.6%, respectively (20.0% in control group and 23.2% in 5-Fu group), the percentage of G2/M phase were 4.5%, 1.7% and 5.3%, respectively (5.5% in control group and 9.0% in 5-Fu group), and the percentage of G1/M phase was not altered. SGC-7901 cells were treated by swainsonine at the concentrations of 0.5, 1.5 and 4.5 μg·ml-l for 24 h. Compared with the control group, the percentage of S phase were increased and that of G2/M cells were decreased significantly in treatment groups (P<0.01). CONCLUSION: Swainsonine can inhibit the cell proliferation and induce apoptosis of SGC-7901 cells, the mechanisms of swainsonine-induced apoptosis may related with [Ca2+]i overloading and expression of apoptosis-related genes.

AIM: To observe the changes of NO, ET-1, SOD and MDA levels in plasma of rats exposed to infrasound. METHODS: Using infrasound (frequency: 8 Hz; sound pressure level:130 dB), the rats were exposed for 1 d, 7 d, 14 d, 21 d and 28 d, 2 h daily, then the levels of NO, ET-1, SOD and MDA were measured after exposure. RESULTS: The changes of NO levels in plasma significantly declined at 7 d and 14 d (P0.05). The changes of ET-1 levels in all groups in plasma were significantly increased (P

AIM:To investigate effect of hypoxia on the expression of proliferating cell nuclear antigen(PCNA) a nd phenotype of cardiac fibroblasts(CFs). METHODS: The purif ied cardiac fibro blasts were cultured and divided randomly into there groups :control group, mode rate hypoxia(MH) group and severe hypoxia(SH) group. After 72 h,MTT method was u s ed to investigate the proliferation of CFs, and the ultrastructure of fibroblast s were observed with transmission electron microscopy The expression of PCNA a n d ?-actin in cardiac fibroblasts were measured by the means of immunohistochemi s try and laser scanning confocal microscopy, respectively. RESULTS: MTT A 490 nm value of MH group was significantly higher than that of control group by (18 4?25 0)% ( P

To study the effect of genistein on the proliferation of cardiac fibroblasts(CF), CFs were cultured from neonatal rat hearts, DNA synthesis of the cells was determined by incorporation of ［3H］TdR into DNA, the cell cycle was measured by flow cytometric analysis. Genistein(0.5－50 μmol*L-1) attenuated 2.5% fetal calf serum-induced proliferation of CF in concentration-dependent manner. Genistein(50 μmol*L-1) arrested CF cell progression at G2/M phase. The results suggest that genistein be a potential substance for treatment of cardiac fibrosis.