Impairment of the Ca2+-binding activity of the sarcoplasmic reticulum is a cause of depressed left ventricular diastole in volume-overloaded canine hearts.
Should not yet influence management of diastolic dysfunction; extends preclinical evidence on SR Ca2+ handling in volume-overload models.
The relationship between the active Ca2+-binding function of the cardiac sarcoplasmic reticulum (SR) and left ventricular (LV) relaxation was studied in various stages of chronically volume overloading canine hearts induced by complete atrio-ventricular (A-V) block. Rapid kinetic measurement of the Ca2+-binding activity of SR was made using a dual-beam spectrophotometric assay procedure. LV hemodynamics, especially diastolic indexes, were evaluated by the pressure-volume relationship using a trans-epicardial echo-cardiographic technique. In this study the maximum Ca2+-binding capacity and the initial Ca2+-binding rate of SR were impaired in eccentric hypertrophied hearts and failing hearts induced by volume overload. However, there was no significant difference of SR functional defect between the hypertrophied and the failing hearts. LV systolic properties were not influenced even by chronic volume overload. Its diastolic properties, however, were reduced with the progress of eccentric hypertrophy, and were estimated to respond more sensitively to the abnormalities of cardiac function compared with systolic properties. There was a close interrelation between the Ca2+-binding activity of SR on the molecular level and diastolic parameters, especially the time constant T, on the ventricular chamber level. In conclusion, the impairment of the Ca2+-binding activity of SR is a cause of depression of LV diastole. However, the role of SR in the occurrence of heart failure could not be clarified in this study.
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Takashi Maeba (1985) studied this question.
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