AHEART July 46/1

Kohzuki, Hisaharu, Hiromi Misawa, Susumu Sakata, Yoshimi Ohga, Hiroyuki Suga, and Miyako Takaki. Energy expenditure by Ba21 contracture in rat ventricular slices derives from cross-bridge cycling. Am. J. Physiol. 276 (Heart Circ. Physiol. 45): H74–H79, 1999.—To clarify the energy-expenditure mechanism during Ba21 contracture of mechanically unloaded rat left ventricular (LV) slices, we measured myocardial O2 consumption (V̇O2) of quiescent slices in Ca21-free Tyrode solution and V̇O2 during Ba21 contracture by substituting Ca21 with Ba21. We then investigated the effects of cyclopiazonic acid (CPA) and 2,3butanedione monoxime (BDM) on the Ba21 contracture V̇O2. The Ca21-free V̇O2 corresponds to that of basal metabolism (2.32 6 0.53 ml O2·min ·100 g LV21). Ba21 increased the V̇O2 in a dose-dependent manner (from 0.3 to 3.0 mmol/l) from 110 to 150% of basal metabolic V̇O2. Blockade of the sarcoplasmic reticulum (SR) Ca21 pump by CPA (10 μmol/l) did not at all decrease the Ba21-activated V̇O2. BDM (5 mmol/l), which specifically inhibits cross-bridge cycling, reduced the Ba21activated V̇O2 almost to basal metabolic V̇O2. These energetic results revealed that the Ba21-activated V̇O2 was used for the cross-bridge cycling but not for the Ca21 handling by the SR Ca21 pump.