Calcium and myocardial cell injury. An appraisal in the cardiomyopathic hamster

Abstract

The heart muscle is very compliant within a wide range of physiologic impulses. The adaptive energy of the myocardium depends, however, upon adequate oxygen supply and the functional state of the plasmalemma. These limitations have been well demonstrated in a number of experimental models with emphasis on the essential role of Ca²⁺ transmembrane movements for maintenance of heart functions and its viability. This postulate appeared quite important when we found that Ca²⁺ slow channel blockers could prevent necrotic changes in hamster hereditary cardiomyopathy. However, the effectiveness of β-adrenoagonists when given in low doses seems more difficult to interpret since these agonists can only promote Ca²⁺ transmembrane movements. We can only surmise that Ca²⁺ accumulation in cardiomyopathic hearts does not derive from a primary defect of the plasmalemma but rather from an exhausted hypokinetic state that favours Ca²⁺ accumulation with progressive deterioration of the structural proteins. It is thus inferred that Ca²⁺ mediates rather than initiates the degradation process which characterizes this inherited cardiomyopathy.