Abstract

Cardiac contractility is defi ned as the intrinsic ability of cardiac muscle fi bers to contract at a given fi ber length. Changes in the ability to produce strong contractions result from different degrees of binding between myosin and actin fi laments that depend in turn on the concentration of calcium ions in the cytosol of cardiac muscle cells. This is controlled by the action of noradrenaline and acetylcholine, neurotransmitters of the autonomic nervous system. The inotropic state of the heart is evaluated using the Left Ventricular Pressure (LVP) signal as an indirect measure of the force of ventricular myofi ber contraction. From the LVP, we can also derive useful parameters such as the maximum rate of ventricular pressure increase (dP/dt Max), the maximum rate of ventricular pressure decrease (dP/dt Min), and the Ejection Time (the duration of blood ejection from the left ventricle, beginning with opening of the aortic valve and ending with closing of the aortic valve). The aim of this study was to validate a chronic model of telemetered dog, thus allowing the evaluation of cardiac contractility by the recording of LVP in conjunction with ABP and ECG (Fig. 1) after oral administration of three known inotropic compounds.

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