[The acute electrophysiological effects of amiodarone on normal and hypertrophied rat myocytes].
OBJECTIVE
The aim of the present study was to investigate the acute action of amiodarone (AM) on the inward currents I(Na), I(Ca-L) and outward currents I(k), I(k1), I(to) in hypertrophied and normal rat ventricular myocytes.


METHODS
The pressure overload hypertrophy rat model was established by partial ligation of ascending aorta for 4 weeks. Ventricular myocytes were exposed to 0.01, 0.1, 1, 10 and 50 micromol/L AM and whole cell patch clamp technique was used to study the acute effects of AM on the inward currents I(Na), I(Ca-L) and outward currents I(k), I(k1), I(to).


RESULTS
(1) Compared with the normal ventricular myocytes, the current density of I(k), I(ks), I(to) and I(k1) were all decreased in hypertrophied myocytes, but I(Na) and I(Ca-L) remained unchanged. (2) I(Ca-L) was blocked by 59.0% +/- 4.4% in normal myocytes but only blocked by 16.7% +/- 8.0% in hypertrophied myocytes after 50 micromol/L AM application; IC(50) of I(Na) were 9.2 micromol/L and 5.9 micromol/L in normal and in hypertrophied myocytes, respectively; I(to) was blocked by 55.9% +/- 5.5% in normal myocytes and 23.0% +/- 2.8% in hypertrophied myocytes after 50 micromol/L AM application. I(k1) was not affected by AM in both normal and hypertrophied myocytes; I(ks) was blocked by 21.6% +/- 5.6% in normal myocytes and 42.7% +/- 9.2% in hypertrophied myocytes after 10 micromol/L AM application.


CONCLUSIONS
Our results show that the sensitivity of hypertrophied myocytes to AM on I(Na), I(ks) were higher than that of normal myocytes, while the sensitivity on I(Ca-L), I(k1), I(to) were lower than that of normal myocytes favoring the use of AM on hypertrophied myocardium for antiarrhythmic therapy.
Zhou
Lin
L
Department of Cardiology, First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Jiang
Bin
B
Li
Hong-xia
HX
Chen
Tan
T
Cheng
Xu-jie
XJ
Jiang
Wen-ping
WP
D000638:Amiodarone / Q000494:pharmacology*; D000818:Animals; D002312:Cardiomyopathy, Hypertrophic / Q000503:physiopathology*; D004195:Disease Models, Animal; D007473:Ion Channels; D032383:Myocytes, Cardiac / Q000187:drug effects*; D018408:Patch-Clamp Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D020257:Ventricular Remodeling
D007473:Ion Channels; D000638:Amiodarone