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Mudanpi, a herbal medicine prepared from the root bark of Paeonia Suffruticosa, was traditionally used for thousands of years to 'remove pathogenic heat from blood'. Previous studies showed that Mudanpi has a significant cardioprotective effect against cardiac ischemia (Ma et al 1984), and its active component, paeonol, inhibits the pacemaker potential of cultured myocytes (Ma et al 1986) suggesting that paeonol might influence the activity of cardiac ion channels. Further studies indeed showed that paeonol has a significant effect on the ion channels of cardiac myocytes (Ma et al 2006). We present here the findings obtained over many years from the East to the West; data were collected from heart ischemic model to ion channel activities of the isolated cardiac myocytes using patch clamp electrophysiological method. The cardiac ischemic model was established by coronary artery occlusion in canines; extract of mudanpi was infused intravenously. The epicardial ECG were recorded by applying 30 electrodes to predetermined epicardial sites. The electrodes were connected to an amplifier, and the epicardial ECG recorded. The elevation of S-T segments were used as a measure of the degree of ischemia. Aterial pressure, heart rate and heart oxygen consumption were recorded. The actions of paeonol on ionic channel were studied using the standard whole-cell configuration of the patch-clamp technique in isolated guinea-pig ventricular myocytes. The effects of paeonol on the action potential (AP) and a variety of ion channels were studied, and the possible mechanisms underlying the alteration of ion channel function were analysed. The results showed that Mudanpi had a significant protective effect against acute ischemic injury by reducing myocardial oxgen consumption, reducing cardiac arrhythmic risk, lowering blood pressure and heart rate. The main effect of paeonol on the ventricular myocytes was to shorten the AP duration, suppress the AP upstroke velocity and amplitude, actions associated with the blockade of the voltage-gated, fast sodium current. The shortening effect of paeonol on the AP duration was independent of the blockade of the fast sodium current, and the blockage of calcium current, nor did it activate ATP-sensitive potassium current or chloride current. However, paeonol did block the slowly inactivating sodium current, and blockade of this current is known to result in AP shortening. Using the Noble Heart computational model (Noble et al 1998) we predicted that paeonol inhibits ADP of the AP, a strong indication of antiarrhythmic action. These findings suggest that paeonol, and therefore Mudanpi, may possess antiarrhythmic activity, which may confer their cardioprotective effects. [ABSTRACT FROM AUTHOR]