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KMID : 0382619900100020651
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Hanyang Journal of Medicine
1990 Volume.10 No. 2 p.651 ~ p.663
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Effect of Artemisia Mongolica Fischer on the Atrial Contractility and Action Potential of the Sinus Node Cells of the Rabbit Heart
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Abstract
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In order to explore electrophysiological effects of Artemisia mongolica Fischer on the cardiac functions, action potentials were recorded in the isolated rabbit sinus node cells by means of the conventional microelectrode technique before and after superfusion with ethanol extract of Artemisia (AEE). Also studied were effects of AEE on the slow channel-mediated action potential (SPA) of the ventricular papillary muscle cells as well as on the atrial contractility in the rabbit heart.
The results obtained were summerized as follows:
1) After superfusion with AEE (0.03, 0.05 & 0.08%)for 5min no significant changes were observed in overshoot potential(OS), maximum diastolic potential (MDP) and action potential duration (APD_(60)) of the sinus node cells. 2) The AEE invariably decreased the rate of spontaneous firing (RSF) from the sinus node cells. Generally the negative chronotropic effect of AEE was observed from 1 to 7 min after onset of superfusion. 3) Following superfusion with AEE amplitude of the SAP of the ventricular papillary muscle decreased and the duration of SAP was shortened. 4) On the other hand AEE invariably decreased atrial contractility in a dose-dependent manner. 5) In the atrial segment treated separately with atropine, propranolol, quinidine and aminophylline, the negative inotropic effect of AEE were not altered. 6) The negative inotropic effect of AEE was not completely abolished by verapamil or ryanodine. 7) And AEE completely abolished atrial aftercontractions induced by electrical stimulation (1Hz-10msec-2T) of atrial muscle segment in the potassium-free Tyrode´s solution.
The results suggest that AEE decreases RSF of the sinus node cells as a result of reduced slow inward current (i_(Ca)) and that the negative inotropic effect of AEE is associated with a decreased release of Ca^(2+) from the sarcoplasmic reticulum.
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