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Chinese Medical Journal ; (24): 1834-1839, 2018.
Article in English | WPRIM | ID: wpr-773968


Background@#Pressure overload-induced myocardial hypertrophy is a key step leading to heart failure. Previous cellular and animal studies demonstrated that deteriorated excitation-contraction coupling occurs as early as the compensated stage of hypertrophy before the global decrease in left ventricular ejection fraction (LVEF). This study was to evaluate the cardiac electromechanical coupling time in evaluating cardiac systolic function in the early stage of heart failure.@*Methods@#Twenty-six patients with Stage B heart failure (SBHF) and 31 healthy controls (CONs) were enrolled in this study. M-mode echocardiography was performed to measure LVEF. Tissue Doppler imaging (TDI) combined with electrocardiography (ECG) was used to measure cardiac electromechanical coupling time.@*Results@#There was no significant difference in LVEF between SBHF patients and CONs (64.23 ± 8.91% vs. 64.52 ± 5.90%; P = 0.886). However, all four electromechanical coupling time courses (Qsb: onset of Q wave on ECG to beginning of S wave on TDI, Qst: onset of Q wave on ECG to top of S wave on TDI, Rsb: top of R wave on ECG to beginning of S wave on TDI, and Rst: top of R wave on ECG to top of S wave on TDI) of SBHF patients were significantly longer than those of CONs (Qsb: 119.19 ± 35.68 ms vs. 80.30 ± 14.81 ms, P < 0.001; Qst: 165.42 ± 60.93 ms vs. 129.04 ± 16.97 ms, P = 0.006; Rsb: 82.43 ± 33.66 ms vs. 48.30 ± 15.18 ms, P < 0.001; and Rst: 122.37 ± 36.66 ms vs. 93.25 ± 16.72 ms, P = 0.001), and the Qsb, Rsb, and Rst time showed a significantly higher sensitivity than LVEF (Rst: P =0.032; Rsb: P = 0.003; and Qsb: P = 0.004).@*Conclusions@#The cardiac electromechanical coupling time is more sensitive than LVEF in evaluating cardiac systolic function.

Adult , Echocardiography , Echocardiography, Doppler , Electrocardiography , Female , Humans , Male , Middle Aged , Systole , Ventricular Function, Left
Acta Physiologica Sinica ; (6): 203-209, 2010.
Article in Chinese | WPRIM | ID: wpr-337758


Voltage-dependent potassium channels (Kv) are involved in proliferation and transformation in mammary epithelial cells. In previous studies, several groups have detected various potassium channels in breast cancer cells, and they assumed that potassium channels are related to the development of breast carcinoma, although the precise mechanisms are still unknown. We have previously reported that 4-aminopyridine (4-AP), one kind of potassium channel (K(+) channel) blocker, could affect the proliferation of MCF10A cells. The aim of the present study is to explore the expression and properties of K(+) channels in human mammary epithelial cells (MCF10A) and whether Kv channels are required for the proliferation of MCF10A cell. Electrophysiological, MTT analysis, PCR and Western blot methods were used to identify a K(+) conductance which is involved in tumorigenesis and not yet be described in MCF10A cells. A voltage-dependent, outward rectification and 4-AP-sensitive K(+) current was observed in these cells. The perfusion of 5 mmol/L 4-AP significantly decreased the amplitude of Kv current from (912.5+/-0.6) pA to (275+/-0.8) pA (n=5, P<0.01), when cells were recorded using 800 ms voltage steps from a holding potential of -60 mV to voltage ranging from -60 mV to +60 mV. PCR analysis demonstrated that Kv1.1, Kv1.2, Kv1.3, and Kv1.5 were all expressed in MCF10A and MCF7 cells. Furthermore, the expression of Kv1.5 was much higher in MCF10A than that in MCF7. Inhibitory effect of 4-AP on cell proliferation was dosage-dependent. Incubation with 5 mmol/L 4-AP reduced MCF10A cell proliferation to 25.29% in 48 h. Western blot analysis showed the activation of ERK1/2 which related to cell proliferation was enhanced, while p38 activation was decreased by 4-AP treatment for 10 min. These data provided the first evidence of the Kv channels expression in MCF10A cell and 4-AP could inhibit the proliferation of MCF10A through blocking the potassium channels, and the mechanism may be related to regulating the activity of different members of cell proliferation signaling pathway of MEK/ERK.

4-Aminopyridine , Pharmacology , Cell Line , Cell Proliferation , Epithelial Cells , Physiology , Humans , Potassium Channel Blockers , Pharmacology , Potassium Channels, Voltage-Gated , Physiology
Acta Physiologica Sinica ; (6): 175-182, 2007.
Article in English | WPRIM | ID: wpr-258673


To test the hypothesis that AMP-activated protein kinase (AMPK) is possibly the downstream signaling molecule of certain subtypes of adrenergic receptor (AR) in the heart, we evaluated AMPK activation mediated by ARs in H9C2 cells, a rat cardiac source cell line, and rat hearts. The AMPK-alpha subunit and the phosphorylation level of Thr(172)-AMPK-alpha subunit were subjected to Western blot analysis. Osmotic minipumps filled with norepinephrine (NE), phenylephrine (PE) or vehicle [0.01% (W/V) vitamin C solution] were implanted into male Sprague-Dawley rats subcutaneously. The pumps delivered NE or PE continuously at the rate of 0.2 mg/kg per hour. After 7-day infusion, the activity of AMPK was examined following immunoprecipitation with anti-AMPK-alpha antibody. At the cellular level, we found that NE elevated AMPK phosphorylation level in a dose- and time-dependent manner, with the maximal effect at 10 micromol/L NE after 10-minute treatment. This effect was insensitive to propranolol, a specific beta-AR antagonist, but abolished by prazosin, an alpha(1)-AR antagonist, suggesting that alpha(1)-AR but not beta-AR mediated the phosphorylation of AMPK. Moreover, the results from rat models of 7-day-infusion of AR agonists demonstrated that the activity of AMPK was significantly higher in NE (7.4-fold) and PE (6.0-fold) infusion groups than that in the vehicle group (P<0.05, n=6). On the other hand, no obvious cardiac hypertrophy and tissue fibrosis changes were observed in PE-infused rats. Taken together, our results demonstrate that alpha(1)-AR stimulation enhances the activity of AMPK, indicating an important role of alpha(1)-AR stimulation in the regulation of AMPK in the heart. Understanding the activation of AMPK mediated by alpha(1)-AR might have clinical implications in the therapy of heart failure.

AMP-Activated Protein Kinases , Metabolism , Animals , Cell Line , Heart Ventricles , Male , Myocardium , Cell Biology , Metabolism , Norepinephrine , Pharmacology , Phenylephrine , Pharmacology , Phosphorylation , Rats , Rats, Sprague-Dawley , Receptors, Adrenergic, alpha , Physiology
Article in Chinese | WPRIM | ID: wpr-680013


Objective To evaluate the effectiveness of minimally invasive therapy on treating hypertensive cerebral hemorrhage.Methods 40 cases hypertensive cerebral hemorrhage were randomly divided into two groups, 20 cases were received the minimally invasive drainage therapy and 20 cases medicine therapy.Results Effective rate was high(P