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Objective: To investigate the effects of cardiac resynchronization therapy (CRT) on left ventricular (LV) diastolic function measured by speckle tracking imaging (STI) in patients with dilated cardiomyopathy (DCM)., Methods: CRT was performed in 21 DCM patients [15 male, mean age: 61.2 ± 11.2 (49-82) years].LV synchronization, LV systolic function and LV diastolic function were evaluated with conventional echocardiography, tissue Doppler imaging and STI before and 6 months after CRT.NYHA heart function was also assessed. Clinic Response to CRT was defined as improvement of more than 1 NYHA class.Response to CRT in echocardiography was defined as ≥ 15% reduction in LV end systolic volume at 6 months post CRT., Results: There were 16 responders and 5 non-responders at 6 months post CRT.In terms of diastolic function, conventional echocardiography derived deceleration time was both prolonged in non-responders and responders. At 6 months post CRT, STI derived LV isovolumetric diastolic strain rate [(0.19 ± 0.11) /s vs.(0.14 ± 0.09)/s, P < 0.001] was significantly increased while early diastolic mitral valve blood flow velocity/left ventricular isovolumetric diastolic strain rate (680 ± 600 vs.787 ± 690, P < 0.04) was significantly reduced in responder group while remained unchanged in non-responder group.Furthermore, left ventricular isovolumetric diastolic strain rate negatively correlated with plasma brain natriuretic peptide level (r = -0.68, P < 0.05)., Conclusion: In CRT responders of DCM patients, LV diastolic function is significantly improved and this change could be detected more effectively by STI derived LV diastolic function parameters.

Objective: To investigate the changes of open probability (Po) of large conductance Ca(2+)-activated K(+) channel (BK channel) in diabetic coronary smooth muscle cells and elucidate the underlying cellular electrophysiology mechanisms of coronary dysfunction., Methods: Rat coronary smooth muscle cells were isolated from control group and diabetic group. BK single channel currents were recorded by patch clamp technique in inside-out configuration. Open probabilities were calculated and compared between two groups. After exposure to DHS-1, a specific BK channel activator, Po at 0.2 and 1 µmol/L free Ca(2+) were compared between control and diabetic groups., Results: In the presence of 0.2 µmol/L free Ca(2+), the Po at baseline was significantly lower in diabetic rats than in control rats (0.0032 ± 0.0012 vs. 0.095 ± 0.036, P < 0.05). Cytoplasmic application of DSH-1 significantly increased the Po to 0.335 ± 0.096 (P < 0.05 vs. baseline) in control rats, whereas DSH-1 had no effect in diabetic rats (Po = 0.022 ± 0.018, P > 0.05 vs. baseline). In the presence of 1 µmol/L free Ca(2+), the Po at baseline was also significantly lower in diabetic rats than in control rats (0.210 ± 0.055 vs. 0.458 ± 0.077, P < 0.05). Cytoplasmic application of DHS-1 further robustly enhanced Po to 0.823 ± 0.019 (P < 0.05 vs. baseline) in control rats and to 0.446 ± 0.098 in diabetic rats (P < 0.05 vs. baseline of diabetic rats; P < 0.05 vs. control rats with DHS-1)., Conclusion: The decrease of Po of BK single channel in coronary smooth muscle cells may be a potential cause for coronary dysfunction in diabetic rats.

Objective: To evaluate left ventricular (LV) function and twist in patients with diabetic cardiovascular autonomic neuropathy (CAN) by two-dimensional speckle tracking imaging (STI)., Methods: STI was performed in 56 subjects with type 2 diabetes mellitus (DM) (35 with DM only: group A, 21 with CAN: group B) and 34 normal subjects (Control) from LV short-axis view. LV peak systolic, peak early (E') and peak late (A') diastolic circumferential strain in 18 myocardial segments were measured at the levels of mitral annulus, papillary muscle and apex and the rotation at mitral annulus and apex levels were also measured. LV peak systolic and the ratio of E' and A' of global and three levels, twist, untwisting rate and untwisting half-time were calculated., Results: In group A, compared with control group, LV peak systolic radial circumferential strain has no significant difference (P > 0.05), E'/A' was reduced (P < 0.05), twist at aortic valve closure and twist at mitral valve opening were significantly increased (P < 0.05), untwisting rate reduced, and untwisting half time delayed. In group B, compared with control group and group A, circumferential strain parameters [(-12.64 ± 6.49)% vs. (-19.11 ± 9.98)% and (-21.14 ± 10.13)%, P < 0.05] and E'/A' [(0.90 ± 0.35) vs. (1.24 ± 0.47) and (1.98 ± 0.63), P < 0.05] were significantly decreased, twist at aortic valve closure [(19.08 ± 5.62)° vs. (16.57 ± 2.84)° and (14.36 ± 4.06)°, P < 0.05] and twist at mitral valve opening [(13.99 ± 2.31)° vs. (11.36 ± 2.63)° and (9.04 ± 5.63)°, P < 0.05] were significantly increased, untwisting rate [(0.40 ± 0.28)%/ms vs. (0.46 ± 0.14)%/ms and (0.53 ± 0.21)%/ms, P < 0.05] reduced, and untwisting half time [(489.61 ± 97.14) ms vs. (445.21 ± 54.53) ms and (410.60 ± 50.23) ms, P < 0.05] delayed., Conclusion: Speckle tracking imaging could be used to evaluate early changes on LV twist deformation and LV systolic function in patients with type 2 diabetes mellitus.

Objective: To investigate the mechanism of enhanced large conductance calcium-activated potassium channel currents (BK) in coronary smooth muscle cells (SMCs) by docosahexaenoic acid (DHA)., Methods: Coronary SMCs were isolated by enzyme digestion. Potassium channels in coronary SMCs were identified by applications of different potassium blockers. Effects of DHA and its metabolite 16, 17-epoxydocosapentaenoic acid (16, 17-EDP) on BK channels in the absence and presence of cytochrome P450 epoxygenase inhibitor SKF525A were studied by patch clamp in whole-cell configuration., Results: BK channels were widely distributed in SMCs, and BK currents in normal SMCs accounted for (64.2 ± 2.7)% of total potassium currents (n = 20). DHA could activate BK channels, and its 50% effective concentration (EC(50)) was (0.23 ± 0.03) µmol/L, however, the effect of DHA on BK channels was abolished after SMCs were incubated with cytochrome P450 epoxygenase inhibitor SKF525A. 16, 17-EDP, a metabolite of DHA, could reproduce the effects of DHA on BK channels, and its EC(50) was (19.7 ± 2.8) nmol/L., Conclusion: DHA and metabolites can activate BK channels and dilate coronary arteries through activating cytochrome P450 epoxygenase pathway.

Objective: to investigate the regulation in vascular tension of diabetic coronary artery by large conductance Ca(2+)-activated K(+) channel (BK channel) and to elucidate the mechanisms of coronary dysfunctions due to diabetes., Methods: regulation of vascular tension in normal coronary artery was evaluated by videomicroscopy system. Streptozotocin-induced rat diabetic animal model was established successfully by intraperitoneal injection. Coronary smooth muscle cells were isolated by enzyme digestion. The BK currents in control and diabetic groups were recorded by patch clamp technique in whole cell configuration. Changes of vascular tension in normal and diabetic coronary arteries were assayed by multi-wire myograph system., Results: more than 50% was contracted in inner diameters of coronary arteries when 100 nmol/L IBTX, a specific BK channel blocker, was applied. In comparison with normal group, the BK current densities in diabetic group significantly decreased when test potentials were more than 60 mV (P < 0.05). The BK current densities at 150 mV in normal group and diabetic group were (275 ± 40) pA/pF and (70 ± 10) pA/pF respectively. When 100 mmol/L KCl was washed out, vascular tensions of normal and diabetic coronary artery were (398 ± 38) mg and (390 ± 35) mg respectively (P > 0.05); however, when 100 nmol/L IBTX was added, the vascular tensions of normal and diabetic coronary artery were (395 ± 40) mg and (50 ± 7) mg (P < 0.05)., Conclusion: BK channels play an important role in the regulation of coronary vascular tension, whereas BK channels in diabetic coronary artery are dysfunction, BK currents decrease and vascular tensions increase.

Objective: To determine the feasibility on the left ventricular systolic synchronism and cardiac function evaluation in patients with permanent cardiac pacing by real-time three-dimensional echocardiography., Methods: Fifteen patients with sick sinus syndrome post dual-chamber pacemaker implantation were enrolled in this study. Pacemakers were programmed to AAI, DDD, and VVI respectively. After pacing for 5 minutes in each mode, participants were examined with real-time three-dimensional echocardiography. Images in different pacing modes were obtained and analyzed by the off-line Qlab 4.2 software. Parameters including global and 17-segmental volume-time curves (VTCs), dispersion of time to minimal regional volume for 16, 12, and 6 left ventricular segments (Tmsv16-s, Tmsv12-s, Tmsv6-s), and maximal difference of time to minimal regional volume for l6, 12 and 6 left ventricular segments (Tmsv16-dif, Tmsv12-dif, Tmsv6-dif), end diastolic volume (EDV), end systolic volume (ESV), left ventricular ejection fraction (LVEF) were measured respectively. Parameters of peak filling rate (PFR), regional end diastolic volume (rEDV), regional end systolic volume (rESV), and regional ejection fraction (rEF) were also calculated., Results: Left ventricular systolic synchronism as reflected by VTCs, Tmsv16-s, Tmsv12-s, Tmsv6-s, Tmsv16-dif, Tmsv12-dif and Tmsv6-dif as well as parameters reflecting ventricular function, i.e., LVEF, PFR were significantly better in AAI mode than in DDD and VVI models (all P < 0.05). All above indexes were similar between DDD and VVI models (all P > 0.05). rEFs of left inferior wall in base, septum in base and apex were significantly lower in DDD and VVI models compared that in AAI mode (P < 0.05)., Conclusion: Real-time three-dimensional echocardiography can objectively and accurately evaluate left ventricular systolic synchronism and cardiac function in patients with permanent cardiac pacing and AAI mode is superior to DDD and VVI models.

Objective: To investigate the role of P-type Na+ -K+ -ATPase in the mechanism of migraine., Methods: nitroglycerin induced migraine Twenty Sprague-Dawley rats, 10 male and 10 female, were randomly divided into 2 groups: model group, undergoing subcutaneous injection of nitroglycerin 10 mg/kg once a week for 4 weeks so as to establish migraine model, and control group, undergoing subcutaneous injection of normal saline. Then the rats were killed with their trigeminal ganglia, trigeminocervical complex, and cortex of frontal lobe taken out. RT-PCR and Western-blotting were used to detect the mRNA and protein expression of P-type Na+ -K+ -ATPase. Immuno-precipitation assay was conducted to observe the Na+ -K+ -ATPase activity. The concentration of intracellular Ca2+ was investigated by Fluo-3/AM fluorometric method., Results: The mRNA and protein expression levels and activity of P-type Na+ -K+ -ATPase in the trigeminal ganglion and trigeminocervical complex of the model group were 0.72 +/- 0.05, 0.59 +/- 0.05, and 5.21 +/- 0.51 respectively, and the mRNA and protein expression levels and activity of P-type Na+ -K+ -ATPase in the cortex of frontal lobe of the model group were 0.70 +/- 0.05, 0.60 +/- 0.05, and 3.61 +/- 0.49 respectively, all significantly lower than those of the control group (0.83 +/- 0.10, 0.67 +/- 0.06, 6.53 +/- 0.73, 0.81 +/- 0.08, 0.71 +/- 0.09, and 6.61 +/- 0.73 respectively, all P < 0.05). The concentration of intracellular Ca2 in trigeminal ganglion and trigeminocervical complex and the concentration of Ca2+ in the cortex of frontal lobe of the model group were 211,182 +/- 12,973 and 186,511 +/- 18,297 respectively, both significantly higher than those of the control group (135,243 +/- 18,105 and 143,289 25,175 respectively, both P < 0.01)., Conclusion: P-type Na+ -K+ -ATPase may infect the pathogenesis of migraine by its expression and activity.