Afanas'ev S A, Naryzhnaia N V, Lukavskaia I A, Antonchenko I V, Popov S V, Kozlov B N, Kandinskiĭ M L, Shipulin V M
Department of Experimental Cardiology, Institute of Cardiology, Tomsk Scientific Center, Siberian Division, Russian Academy of Medical Sciences, Kievskaya ul. 111a, Tomsk, 634012 Russia.
Eksp Klin Farmakol. 2003 Nov-Dec;66(6):24-8.
Peculiarities in the extrasystolic and post-extrasystolic contractility of the isolated myocardium of patients suffering from chronic ischemic heart disease (IHD), in comparison to that of intact rats, were studied in the presence of the antiarrhythmic drug amiodarone. The contractility was measured in an isometric mode at an electric stimulation frequency of 0.5 Hz, a temperature of 37 degrees C, and a perfusion rate of 10 ml/min. The extrasystolic action was produced by additional electric pulses generated 25 sec after the base stimulation signal. Amiodarone (1 microgram/ml) reduced the inotropic response of intact rat myocardium to the extrasystolic action, but increased the post-extrasystolic contractility. In the myocardium of IHD patients, the drug also suppressed manifestations of the spontaneous abnormal contractility, while not decreasing the inotropic response to the extrasystolic action. An increase in the post-extrasystolic contractility reached on the average 24% (against 6% in the control). The effect of amiodarone on the post-extrasystolic contractility can be related to a change in the functional state of sarcoplasmic reticulum (SR) and in the content of deposited Ca2+ ions. SR is an important factor of intracellular homeostasis of cardiomyocytes during IHD and can probably influence the antiarrhythmic efficacy of amidarone in IHD patients.
