ABSTRACT
Objective To investigate the effects of pioglitazone on atrial ionic channel remodeling in alloxan-induced diabetic rabbit models.Methods A total of 32 rabbits were randomly (random number) divided into control (CN) group,diabetes mellitus (DM) group,diabetes mellitus + pioglitazone 4 mg/ (d · kg) (DPG) group and diabetes mellitus + double pioglitazone 8 mg/ (d · kg) (DPI) group.The diabetic state was examined by quantitative determination of blood glucose levels of ≥ 14 mmol/L.Langendorff-perfused rabbit hearts were used to isolate single atrial myocyte,and whole-cell patch-clamp technique was used to record action potential duration (APD) and atrial ionic channel currents (ICa,L and INa).Variables with normal distribution were compared with One-way ANOVA and LSD-t test.Results Compared with controls,APD90 and APDS0 of left atrial myocytes were significantly prolonged in DM group (P ＜0.05 vs.CN),and there was no significant difference in APD90 frequency adaptation between them (P ＞0.05 vs.CN).The densities of INa were reduced and the densities of ICa,L were increased in DM group (P ＜ 0.01 vs.CN).The above variables were markedly attenuated in DPG and DPI group.Conclusions Pioglitazone may inhibits atrial ionic channel remodeling in diabetic rabbit models.
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AIM To analyze the mechanism of the adriamycin induced cardiomyopathy. METHODS The patch clamp technique in the whole cell recording was used to study the effect of adriamycin on L type calcium channel current( I Ca L ) in the isolated cardiomyocyte of the guinea pig. RESULTS The current voltage( I U ) curveshowed the bell shape in the control and in 0 1 mmol?L -1 adriamycin. Their peak potentials were about +10 mV. The amlitude of peak calcium current increased from (-0 93?0 05) nA to (-1 31?0 08) nA( P
ABSTRACT
By using the whole-cell clamp-patch technique, the effects of dexamethasone on calcium channel current (Ica) and nicotine receptor channel current (I_(NIC)) were examined. The acute action of glucocorticoid on adrenal medullary chromaffin cell (AMCC) of rats was a significant inhibition of I_(NIC), while no apparent effect was observed on Ica induced by electricity. The results suggest that the acute action of glucocorticoid on catecholamine release in rat AMCC may be directly related to nicotine receptor.