Shortterm Modulation Of Ventricular Function

Heart Rate

The ventricle has a positive FFR with an optimal frequency that parallels the myocardial FFR.7475 As indicated earlier, this is an important means of modulating ventricular function that is intimately connected with changes in adrenergic stimulation. Changes in contraction frequency also influence relaxation and filling. There is some shortening of relaxation in conjunction with the positive FFR even without concurrent increases in adrenergic stimulation.73 Moreover, with increased HR, diastole is shortened much more than systole, especially the slow-filling phase.

Paracrine Modulation of Ventricular Function

This has been discussed previously in the section on cellular control of contractility. It is important to emphasize that the significance of these factors with respect to norma1 ventricular function is not established. In the ventricle, these factors tend to have more prominent effects on relaxation than on contraction.161 NO and endothelial-dependent vasodilators cause very modest depression of systolic function and an earlier onset of ventricular relaxation. Substances whose effects are mediated by the IP3 second-messenger system (ET-1, ^-adrenergic agonists) have more or less opposite effects.

Neurohumoral Responses

The most important short-term neurohumoral modulation occurs as a result of variations in sympathetic and parasympathetic stimulation caused by both cardiac neural activity and circulating catecholamines. Stimulation of ^-adrenergic receptors results in increased HR and contractility and more rapid relaxation. These effects are due to the influence of adrenergic stimulation on the sinus node and specialized conduction system and, within the myocyte, activation of adenyl cyclase with increases in cyclic AMP. Increases in HR also allow the heart to use the FFR. Adrenergic stimulation interacts with the FFR not only by increasing HR but also by increasing the gain of the relationship.75 There are many other myocyte cell surface receptors (e.g., a-adrenergic, dopaminergic, histaminergic, angiotensin II, and endothelin receptors), but none has a clearly delineated, significant role in normal, short-term modulation of ventricular function. Vagal stimulation, of course, has profound HR slowing effects as well as modest negative effects on contractility. Correspondingly, vagal withdrawal is an integral component of HR responses during exercise and other stresses.

The heart participates in a number of reflexes that modulate HR and ventricular function in the short term.162-165 These typically result in coordinated changes in parasympathetic and sympathetic stimulation. Thus the heart is a component of the efferent limb of arterial baro- and chemoreceptors. Acute increases in systemic arterial pressure result in slowing of HR due to increased vagal stimulation and decreased sympathetic neural stimulation with attendant effects on contractility; the reverse occurs with decreased arterial pressure. Vagal responses occur very rapidly, on a beat-to-beat basis, whereas changes in sympathetic neural stimulation take somewhat longer to take effect. Pulmonary stretch receptors are largely responsible for normal sinus arrhythmia. Atrial stretch receptors also may modulate HR via the Bainbridge reflex, resulting in tachycardia with increased intravascular volume. Ventricular mechanoreceptors that discharge with deformation are activated when volume decreases. Discharge results in vagally mediated bradycardia and hypotension and appears to be involved in vasovagal syncope. Chemoreceptors on the ventricular epicardium also connect to vagal efferents and may discharge in response to prostaglandins secreted into the pericardial sac.

Ventricular Interaction

Diastolic ventricular interaction has been discussed previously. The ventricles also interact during systole. Left-to-right systolic interaction was mentioned earlier. There is also a modest amount of right-to-left interaction.119 As a result, an abrupt increase in PA pressure results in a small increase in LV contractile performance. Both diastolic and systolic ventricular interaction function as internal feedback mechanisms that modulate SV on a beat-to-beat basis to ensure that left- and right-side heart outputs remain equal over time. Obviously, even tiny differences in output summated over time would have disastrous consequences.

Coronary Perfusion

Changes in coronary perfusion pressure and/or flow per se can influence ventricular function.166,167 Increases augment systolic performance and may cause some decrease in passive compliance. Modest decreases insufficient to cause myocardial ischemia likely have opposite effects. A component of the influence of coronary perfusion on ventricular function is related to turgor. In addition to modulation of diastolic compliance, stretching of myocardial tissue due to increased turgor appears to augment the Frank-Starling effect. It is also possible that stretch-activated Ca channels!68 open as turgor increases with resulting increased activation of the myocardium. Because of coronary autoregulation, these effects of coronary perfusion are probably of minor importance under normal physiologic conditions.

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