© 1997 by European Society of Cardiology
Copyright © 1997, European Society of Cardiology
Undiminished mitochondrial function during stunning in rabbit heart at 28°C
aLaboratory for Physiology, Institute for Cardiovascular Research, Vrije Universiteit (ICaR-VU), van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands
bCenter for Bioengineering, University of Washington, Box 357962, Seattle, WA 98195-7962, USA
* Corresponding author. Tel.: +1 (206) 685-2840; fax: +1 (206) 685-2651; e-mail: coert@nsr.bioeng.washington.edu
Objective: To investigate effect of brief ischemia on mitochondrial function in intact myocardium, rather than in isolated mitochondria. Methods: The mitochondrial response was characterized by the mean response time (tmito) of cardiac mitochondrial O2 consumption to steps in heart rate. Isolated isovolumic rabbit hearts were perfused at 28°C with a constant flow of Tyrode solution containing 11 mM glucose. O2 consumption and tmito were determined before ischemia and after 25 min of no-flow global ischemia during which hearts were either paced (I+P, n = 8) or unpaced (I–P, n = 8). A non-ischemic control group (n = 8) was also examined. Results: At 20 min reperfusion, developed left ventricular pressure (DLVP) after I+P was decreased to 47±3% (mean±s.e.m.; P<0.05) of control DLVP without significant changes in venous creatine kinase efflux, indicating contractile stunning. In contrast, complete contractile recovery was observed after I–P. Before ischemia, tmito was 11.2±0.6 and 14.9±0.7 s for heart rate steps from 60 to 70 and from 60 to 120 beats/min, respectively. The tmito was lower (P<0.05) for the corresponding downward steps (10.5±0.6 and 12.4±0.6 s, respectively). An increase (P<0.05) in tmito was observed in the course of the experiment for upward (1.2±0.3 s) and downward steps (1.4±0.3 s), but the change was similar after ischemia to that in time-matched controls (P >0.05, both for I–P and I+P vs. control). Oxygen consumption, compared at fixed levels of the ratexpressure product, was unchanged after ischemia (P >0.05, for both I–P and I+P vs. controls), suggesting undiminished efficiency of mitochondrial ATP production. Conclusions: Twenty-five minutes ischemia does not affect mitochondrial function in rabbit hearts at 28°C, even when contractile stunning resulted.
KEYWORDS Ischemia; Stunning; Pacing; Mitochondrial function, 28°C; Rabbit, heart
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  W. D. Gao, T. Dai, and D. Nyhan Increased cross-bridge cycling rate in stunned myocardium Am J Physiol Heart Circ Physiol, February 1, 2006; 290(2): H886 - H893. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. A.I.P. Trines, C. J. Slager, T. A.M. Onderwater, J. M.J. Lamers, P. D. Verdouw, and R. Krams Oxygen wastage of stunned myocardium in vivo is due to an increased oxygen cost of contractility and a decreased myofibrillar efficiency Cardiovasc Res, July 1, 2001; 51(1): 122 - 130. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. H. G. M. van Beek, M. H. van Wijhe, M. H. J. Eijgelshoven, and J. B. Hak Dynamic adaptation of cardiac oxidative phosphorylation is not mediated by simple feedback control Am J Physiol Heart Circ Physiol, October 1, 1999; 277(4): H1375 - H1384. [Abstract] [Full Text] [PDF]
|
|