The Compensatory Mechanisms in The Course of the Diastolic Dysfunction Development at Stress Cardio-myopathy.

Abstract

Aim     To study the activation sequence of compensatory mechanisms during the development of diastolic dysfunction.Material and methods            The study was performed on rats with stress cardiomyopathy induced by high doses of isoproterenol (120 mg/kg twice a day). Heart function was studied 3-5 and 8-10 days after the injection by echocardiography and left ventricular (LV) catheterization. The content, isoform composition of the sarcomeric protein connectin (titin) and its mRNA content were also measured.Results            The early period was characterized by the presence of systolic dysfunction evident as a decrease in the minute volume due to impaired myocardial  LV contractility, and slower LV filling and relaxation. Compensatory changes at this stage were manifested as increases in the left atrial volume and diastolic pause duration due to reduced contraction rate and arterial elasticity. The content of the more compliant N2BA connectin isoform and its mRNA was increased. These changes facilitated increases in LV filling and ejection. In the second period, diastolic dysfunction developed, when the minute volume, contraction rate and LV contractility became normal, although the left atrial pressure remained elevated, and the aortic diameter and LV wall thickness increased. The increased content of the N2BA isoform remained, and this was associated with stable slowing of LV relaxation.Conclusion      The study showed that in the initial period, compensation is achieved by urgent mobilization of the circulatory system, while the improvement in myocardial contractility is secondary.