Effects of pethidine on cardiac electrophysiological properties.
- Author:
Xiong ZHANG
1
;
Lin-lin WANG
;
Yue-min DING
;
Yuan LU
;
Qiang XIA
Author Information
- Publication Type:Journal Article
- MeSH: Action Potentials; drug effects; Animals; Heart; drug effects; physiology; Heart Block; chemically induced; Heart Rate; drug effects; In Vitro Techniques; Ion Channels; antagonists & inhibitors; Male; Meperidine; pharmacology; Rats; Rats, Sprague-Dawley; Receptors, Opioid; physiology
- From: Journal of Zhejiang University. Medical sciences 2003;32(3):207-211
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of pethidine on electrophysiological properties of the isolated ventricular myocytes and the underlying mechanism.
METHODSLangendorff was applied to perfuse rat heart model and whole-cell current clamp and voltage clamp techniques were used.
RESULTSPethidine decreased heart rate (HR) in a concentration dependent manner and caused severe atrioventricular block (AVB) at >or=250 micromol/L. Pethidine reduced action potential amplitude and maximal rate of depolarization, prolonged action potential duration. Pethidine at 100 micromol/L decreased sodium currents (I(Na)), transient outward potassium currents (I(to)), delayed rectifier potassium currents (I(k)) and L-type calcium currents (I(Ca.L)) to (60.7+/-6.9)%, (55.4+/-5.6)%, (65.1+/-8.0)% and (67.4+/-10.1)% of control levels,respectively. These effects could be recovered by washout. Naloxone, an opioid receptor antagonist, could not abolish the effects of pethidine on ionic currents.
CONCLUSIONPethidine decreased HR and induced AVB, which may be related to the inhibition of I(Na), I(to), I(k) and I(Ca-L) of heart. The depression of cardiac currents is not mediated by opioid receptor.
