Mitochondrial function is not decreased in stunned papillary muscle at 20 degrees C

It is unclear to what extent mitochondrial function in vivo is changed after brief anoxia. Heat measurements allow evaluation of mitochondrial function within intact cardiac muscle. Heat production was determined using fast metal-film thermopiles, during contraction and post-contractile recovery in control and stunned superfused rabbit papillary muscles at 20 degrees C. Heat rate was measured for a train of ten twitches (0.2 Hz) before anoxia and after 40 min anoxia followed by 2 h of normoxic recovery. During anoxia muscles were stimulated at 0.2 Hz (group A) or at 1.0 Hz (group B). A normoxic control group C was stimulated at 0.2 Hz. After 2 h recovery, tension was 77 +/- 5% (S.E.M.), 72 +/- 7% and 94 +/- 3% of initial values, for group A, B and C respectively, indicating stunning by anoxia. The economy of contraction or the ratio of recovery heat to initial heat did not change significantly in groups A and B when compared with control, indicating that stunning with this protocol is not associated with mitochondrial uncoupling. Post-contractile recovery heat initially decayed exponentially with time constant 24.9 +/- 2.2 s for all groups and with 22.7 +/- 1.1, 22.0 +/- 0.8 and 41.7 +/- 4.4 s at the end for group A, B and C respectively. The cause of the remarkable slowing of the recovery rate over time in controls is unknown, but is mimicked by blocking fatty acid utilization. No slowing of metabolic recovery is observed in the stunned papillary muscles. We conclude that stunning is not associated with a decrease in mitochondrial function or oxidative capacity in cardiac muscle.