The intrinsic strength of contraction (contractility) of cardiac muscle fibers at a given length can be altered extrinsically by chemical agents known as inotropes (derived from inos, the Greek for strength).
Norepinephrine (noradrenaline), the most important natural inotrope, is released from cardiac sympathetic nerve endings in the ventricle wall. These nerves are part of the efferent limb of the baroreflex already discussed. Binding of norepinephrine to b rreceptors on the myocytes results in an increase in intracellular calcium, and an increase in the proportion of cross-bridges between actin and myosin which are activated and therefore a greater contractile force.
This results in a more rapid increase in ventricular pressure during isovolumetric contraction and a higher arterial pressure. At the same time cardiac fiber shortening is enhanced and velocity of contraction is increased so that the ejection fraction increases. Although this will increase stroke volume initially, it will be limited by the increase in arterial pressure and the reduction in ventricular size (end-diastolic volume) inherent in any increase in ejection fraction.
Increases in stroke volume will only be maintained if there are simultaneous alterations in the peripheral circulation, such as a reduction in peripheral vascular resistance and therefore an attenuation of the increase in arterial pressure.
Positive inotropes, by increasing the strength of myocyte shortening, alter the ventricular function curve. This occurs in two ways: either the curve is shifted upwards or it becomes steeper. This alteration is dose dependent; the greater the inotropic stimulus, the greater is the effect on the ventricular function curve ( Fig 2).
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