Why the study?
Do alterations in beta-adrenergic tone and left ventricular asynchrony affect the systolic load dependency of LV relaxation rate in anesthetized dogs?
Do alterations in beta-adrenergic tone and left ventricular asynchrony affect the systolic load dependency of LV relaxation rate in anesthetized dogs?
Beta-adrenergic tone and ventricular asynchrony significantly modify the load-dependent relaxation of the left ventricle, highlighting the role of temporal dispersion in disturbed relaxation.
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Alters load-dependent LV relaxation in dogs; leaves open relevance to human diastolic dysfunction and requires prospective validation.
We studied the effect of left ventricular (LV) asynchrony and alterations in beta-adrenergic tone on the systolic load (pressure) dependency of LV isovolumic relaxation rate in anesthetized dogs. The time constant (T) of isovolumic exponential pressure decline was used as an index of relaxation rate. Variably afterloaded LV contractions resulted in a progressive increase in LV end-systolic pressure from 124 +/- 6 in the control beat to 176 +/- 11 mmHg in the third beat and a progressive lengthening of T from 19 +/- 2 to 30 +/- 4 ms. The direct relation between LV end-systolic pressure and T was nearly linear (r = 0.98), and the slope (k) of this relation was taken to reflect the systolic load dependency of T. Administration of isoproterenol (n = 6) produced a decrease in k from 0.11 +/- 0.02 to 0.08 +/- 0.02 (P less than 0.05); with propranolol (n = 6), k increased from 0.08 +/- 0.02 to 0.27 +/- 0.04 (P less than 0.01). Right ventricular epicardial pacing (n = 6) produced an asynchronous LV contraction and an increase in k from 0.09 +/- 0.02 (atrial pacing) to 0.25 +/- 0.04 (P less than 0.01). These studies confirm the dependency of LV relaxation rate on systolic loads and indicate that this form of load-dependent relaxation can be modified by alterations in beta-adrenergic tone and LV asynchrony. The observed alterations suggest the importance of temporal dispersion of the contraction-relaxation sequence as a mechanism responsible for disturbed relaxation.
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Blaustein et al. (1983) studied this question.
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