Ankang Hospital of Heilongjiang Public Security Agency

Harbin, China

Ankang Hospital of Heilongjiang Public Security Agency

Harbin, China
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Liang R.,Ankang Hospital of Heilongjiang Public Security Agency | Liang R.,Heilongjiang University | Zhou Y.,Ankang Hospital of Heilongjiang Public Security Agency | Wu F.,Capital Medical University | And 5 more authors.
Toxicology Mechanisms and Methods | Year: 2010

The mechanisms of cardiac toxicity caused by methamphetamine (MA) are poorly understood at present. This study was designed to investigate the effects of MA on ionic currents in myocardial cells. The effects of MA on transient outward potassium current (Ito), inward rectifying potassium current (IK1), and L-type calcium current (ICa-L) in isolated rat ventricular myocytes were studied using the whole-cell patch clamp technique. It was demonstrated that MA inhibited the Ito, IK1, and ICa-L in the rat ventricular myocytes concentration-dependently. MA shifted left the Ito steady-state inactivation curve and shifted down the recovery curve, but had no influence on the steady-state activation curve. MA did not affect the ICa-L steady-state activation curve or steady-state inactivation curve, but shifted down the recovery curve. We concluded that MA had inhibitory effects on the Ito, IK1, and ICa-L in ventricular myocytes, which might be one of the possible electrophysiological mechanisms of cardiac damage caused by MA. © 2010 Informa Healthcare USA, Inc.


PubMed | Ankang Hospital of Heilongjiang Public Security Agency
Type: Journal Article | Journal: Toxicology mechanisms and methods | Year: 2010

The mechanisms of cardiac toxicity caused by methamphetamine (MA) are poorly understood at present. This study was designed to investigate the effects of MA on ionic currents in myocardial cells. The effects of MA on transient outward potassium current (I(to)), inward rectifying potassium current (I(K1)), and L-type calcium current (I(Ca-L)) in isolated rat ventricular myocytes were studied using the whole-cell patch clamp technique. It was demonstrated that MA inhibited the I(to), I(K1), and I(Ca-L) in the rat ventricular myocytes concentration-dependently. MA shifted left the I(to) steady-state inactivation curve and shifted down the recovery curve, but had no influence on the steady-state activation curve. MA did not affect the I(Ca-L) steady-state activation curve or steady-state inactivation curve, but shifted down the recovery curve. We concluded that MA had inhibitory effects on the I(to), I(K1), and I(Ca-L) in ventricular myocytes, which might be one of the possible electrophysiological mechanisms of cardiac damage caused by MA.

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