Influence of acute myocardial depression on left ventricular stiffness and its elastic and viscous components.

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Abstract
The influence of acute myocardial depression on ventricular stiffness and on its elastic and viscous components was studied in 19 dogs. After the animals were placed on cardiopulmonary bypass, stiffness was measured by sinusoidally injecting volume changes of 0.5 ml (deltaV) at 22 Hz into paced, isovolumically (deltaP) of the sinusoidal pressure response. Stiffness was linearly related to pressure (P) throughout the cardiac cycle, so that deltaP/delta V = alpha P + beta, where alpha and beta are constants. Myocardial depression was induced in one of three different ways: by coronary artery ligation, by administration of propranolol (Inderal), or by administration of pentobarbital. All three interventions caused significant increases in the slope, alpha, of the stiffness-pressure relationship, while the intercept, beta, remained unchanged. Release of the coronary occlusion or administration of acetylstrophantidin partially reversed depression and the change in alpha; Approximation of the mechanical nature of the left ventricle in terms of a linear second-order mechanical system permitted the division of stiffness into its elastic and viscous components. Like total stiffness, both the elastic and the viscous components were linearly related to ventricular pressure. Elastic stiffness was not changed, but the slope of the line relating viscous stiffness to pressure was significantly increased during ischemic depression, indicating that a change in viscosity was primarily responsible for the increase in total ventricular stiffness.

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