OBJECTIVETo investigate the effects of docosahexaenoic acid (DHA) on sodium channel current (I(Na)) and transient outward potassium channel current (I(to)) in rat ventricular myocytes and to evaluate potential anti-arrhythmic mechanisms of DHA.

METHODSI(Na) and I(to) of individual ventricular myocytes were recorded by patch-clamp technique in whole-cell configuration at room temperature. Effects of DHA at various concentrations (0, 20, 40, 60, 80, 100 and 120 micromol/L) on I(Na) and I(to) were observed.

RESULTS(1) I(Na) was blocked in a concentration-dependent manner by DHA, stably inactivated curves were shifted to the left, and recover time from inactivation was prolonged while stably activated curves were not affected by DHA. At -30 mV, I(Na) was blocked to (1.51 ± 1.32)%, (21.13 ± 4.62)%, (51.61 ± 5.73)%, (67.62 ± 6.52)%, (73.49 ± 7.59)% and (79.95 ± 7.62)% in the presence of above DHA concentrations (all P < 0.05, n = 20), and half-effect concentration (EC(50)) of DHA on I(Na) was (47.91 ± 1.57)micromol/L. (2) I(to) were also blocked in a concentration-dependent manner by DHA, stably inactivated curves were shifted to the left, and recover time from inactivation was prolonged with increasing concentrations of DHA, and stably activated curves were not affected by DHA. At +70 mV, I(to) was blocked to (2.61 ± 0.26)%, (21.79 ± 4.85)%, (63.11 ± 6.57)%, (75.52 ± 7.26)%, (81.82 ± 7.63)% and (84.33 ± 8.25)%, respectively, in the presence of above DHA concentrations (all P < 0.05, n = 20), and the EC(50) of DHA on I(to) was (49.11 ± 2.68)micromol/L.

CONCLUSIONThe blocking effects of DHA on APD and I(to) may serve as one of the anti-arrhythmia mechanisms of DHA.

Animals ; Cells, Cultured ; Docosahexaenoic Acids ; pharmacology ; Heart Ventricles ; cytology ; Myocytes, Cardiac ; metabolism ; physiology ; Patch-Clamp Techniques ; Potassium Channels ; drug effects ; Rats ; Rats, Sprague-Dawley ; Sodium Channels ; drug effects

OBJECTIVETo analyze the echocardiographic standardized myocardial segmentation features in patients with left ventricular noncompaction (LVNC).

METHODSEchocardiographic characteristics of 9 patients with LVNC were analyzed and the localization of lesions were determined according to the standardized myocardial segmentation (SMS) recommended by American Heart Association (AHA).

RESULTSLoose trabeculation in the myocardial lesions were evidenced in all LVNC patients. Communication between deep intertrabecular recess and LV cavity was evident with color flow imaging. According to SMS of AHA, noncompaction of ventricular myocardium was localized in apical segment in all 9 patients, in apical segment of the inferior wall (IW) in 9 patients, in apical segment of the lateral wall (LW) in 7 patients, in middle segment (MS) of IW in 7 patients, in MS of LW in 6 patients. One NC segment was also evidenced in apical segment and MS of septal ventricular wall, basal segment of IW and LW and right ventricular apex, respectively. NC was not found in left ventricular anterior wall.

CONCLUSIONEchocardiographic standardized myocardial segmentation is helpful to diagnose LVNC and NC was mostly localized in the apical segments of LVNC patients.

Adolescent ; Adult ; Aged ; Cardiomyopathies ; diagnosis ; diagnostic imaging ; Child ; Child, Preschool ; Echocardiography ; methods ; Female ; Humans ; Male ; Middle Aged ; Myocardium ; pathology ; Reference Standards ; Ventricular Dysfunction, Left ; diagnosis ; diagnostic imaging ; Young Adult

OBJECTIVETo investigate the effects of docosahexaenoic acid (DHA) on large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels and voltage-dependent K(+) (K(V)) channels in rat coronary artery smooth muscle cells (CASMCs), and evaluate the vasorelaxation mechanisms of DHA.

METHODSBK(Ca) and K(V) currents in individual CASMC were recorded by patch-clamp technique in whole-cell configuration. Effects of DHA at various concentrations (0, 10, 20, 40, 60 and 80 µmol/L) on BK(Ca) and K(V) channels were observed.

RESULTS(1) DHA enhanced IBK(Ca) and BK(Ca) tail currents in a concentration-dependent manner while did not affect the stably activated curves of IBK(Ca). IBK(Ca) current densities were (68.2 ± 22.8), (72.4 ± 24.5), (120.4 ± 37.9), (237.5 ± 53.2), (323.6 ± 74.8) and (370.6 ± 88.2)pA/pF respectively (P < 0.05, n = 30) with the addition of 0, 10, 20, 40, 60 and 80 µmol/L DHA concentration, and half-effect concentration (EC(50)) of DHA was (36.22 ± 2.17)µmol/L. (2) IK(V) and K(V) tail currents were gradually reduced, stably activated curves of IK(V) were shift to the right, and stably inactivated curves were shifted to the left in the presence of DHA. IK(V) current densities were (43.9 ± 2.3), (43.8 ± 2.3), (42.9 ± 2.0), (32.3 ± 1.9), (11.7 ± 1.5) and (9.6 ± 1.2)pA/pF respectively(P < 0.05, n = 30)post treatment with 0, 10, 20, 40, 60 and 80 µmol/L DHA under manding potential equal to +50 mV, and EC(50) of DHA was (44.19 ± 0.63)µmol/L.

CONCLUSIONDHA can activate BK(Ca) channels and block K(V) channels in rat CASMCs, the combined effects on BK(Ca) and K(V) channels lead to the vasodilation effects of DHA on vascular smooth muscle cells.

Animals ; Coronary Vessels ; cytology ; drug effects ; metabolism ; Docosahexaenoic Acids ; pharmacology ; Female ; Large-Conductance Calcium-Activated Potassium Channels ; metabolism ; Male ; Myocytes, Smooth Muscle ; drug effects ; metabolism ; Patch-Clamp Techniques ; Potassium Channels, Calcium-Activated ; metabolism ; Rats ; Rats, Sprague-Dawley