MITOCHONDRIAL-FUNCTION IS NOT DECREASED IN STUNNED PAPILLARY-MUSCLE AT 20-DEGREES-C

Citation
Cj. Zuurbier et al., MITOCHONDRIAL-FUNCTION IS NOT DECREASED IN STUNNED PAPILLARY-MUSCLE AT 20-DEGREES-C, Journal of Molecular and Cellular Cardiology, 29(1), 1997, pp. 347-355
Citations number
35
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
00222828
Volume
29
Issue
1
Year of publication
1997
Pages
347 - 355
Database
ISI
SICI code
0022-2828(1997)29:1<347:MINDIS>2.0.ZU;2-Q
Abstract
It is unclear to what extent mitochondrial function in vivo is changed after brief anoxia. Heat measurements allow evaluation of mitochondri al function within intact cardiac muscle. Heat production was determin ed using fast metal-film thermopiles, during contraction and post-cont ractile recovery in control and stunned superfused rabbit papillary mu scles at 20 degrees C. Heat rate was measured for a train of ten twitc hes (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 (gr oup A) or at 1.0 Hz (group B). A normoxic control group C was stimulat ed 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 respective ly, indicating stunning by anoxia. The economy of contraction or the r atio of recovery heat to initial heat did not change significantly in groups A and B when compared with control, indicating that stunning wi th this protocol is not associated with mitochondrial uncoupling. Post -contractile recovery heat initially decayed exponentially with time c onstant 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. T he cause of the remarkable slowing of the recovery rate over time in c ontrols is unknown, but is mimicked by blocking fatty acid utilization . No slowing of metabolic recovery is observed in the stunned papillar y muscles. We conclude that stunning is not associated with a decrease in mitochondrial function or oxidative capacity in cardiac muscle. (C ) 1997 Academic Press Limited