Decline of contraction after CO₂ acidosis is influenced by overexpression of SERCA2a and muscle length in mouse myocardium

Abstract

Cardiac muscle contraction is controlled by intracellular Ca transients (CaT) and muscle length. In the present study, we observed the effects of Ca delivery to contractile elements and muscle length on the recovery of contraction after CO₂ acidosis. We used the left ventricular papillary muscle obtained from C57BL/6 mice and from SERCA2a-overexpressed mice. We simultaneously measured CaT and tension in both preparations during and after CO₂ acidosis using the aequorin method (30°C).The length of the preparation was changed from Lmax, in which developed tension reached maximum, to 92%Lmax and 84%Lmax. At each length, tension decreased and CaT increased in CO₂ acidosis. After CO₂ acidosis, tension and CaT did not fully recover at Lmax. However, at shorter lengths, tension and CaT after CO₂ acidosis were well maintained compared to those before acidosis. We also measured CaT and tension at Lmax after CO₂ acidosis using SERCA2a-overexpressed transgenic myocardium (TG). In TG, CaT was significantly higher than that in non-TG during and after CO₂ acidosis. After acidosis, tension and CaT were well recovered compared to those in non-TG myocardium. Thus, sufficient Ca delivery to the myofilaments and muscle length are important factors for the recovery from pathophysiological conditions, in particular from CO₂ acidosis. [Jpn J Physiol 54 Suppl:S97 (2004)]