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Cardiovascular Research 1997 35(1):113-119; doi:10.1016/S0008-6363(97)00104-1
© 1997 by European Society of Cardiology
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Copyright © 1997, European Society of Cardiology

Undiminished mitochondrial function during stunning in rabbit heart at 28°C

Coert J Zuurbiera,b,* and Johannes H.G.M van Beeka

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


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