Dissociation between adenosine release, cardiac oxygen consumption
and energy status in guinea pig working hearts.
Decking, U. K. M., S. Arens, G. Schlieper, K. Schulze, and J.
Schrader.
Institut f[umlaut]ur Herz und Kreislaufphysiologie, Heinrich-Heine
-Universit[umlaut]at D[umlaut]usseldorf, 40225 D[umlaut]usseldorf and
Abt. Kardiologie, Universit[umlaut]atsklinikum Benjamin Franklin,
12200 Berlin
APStracts 3:0303H, 1996.
Rapid adaptation of ATP formation and coronary flow is required when
cardiac work is altered. Cardiac energy status was proposed to
control both oxygen consumption (MVO2) and release of vasoactive
adenosine (AR). To investigate the hypothesis of a linear relation
between free AMP and AR, 31P NMR was employed in a newly elaborated
guinea pig heart performing pressure-volume work. Under basal
conditions, MVO2 was 7.8+/-1.0 [mu]mol_min-1_[gamma]-1, free AMP
297+/-189 nM and AR 226+/-179 pmol_min-1_[gamma]-1 (n=29). Decreasing
arterial PO2 by 50% reduced MVO2 and increased free AMP by 29%,
however AR rose 3-fold (n=5). Doubling oxygen content of the
perfusion medium (fluorocarbon emulsion) did not alter MVO2, free AMP
and AR (n=6). When afterload was doubled, MVO2 increased (+45%) and
AR decreased (-60%) despite no change in ADP or AMP (n=6). Dobutamine
increased MVO2 (+50%) and AMP (+98%), however AR rose more than
5?times (n=8). Switching substrates from glucose+pyruvate to glucose
diminished MVO2, increased ADP 2-fold and AMP 4-fold while AR
remained constant (n=6). Our findings demonstrate that cardiac energy
status is not the prime regulator of oxidative phosphorylation also
in the isolated heart. Changes in the oxygen supply-to-demand ratio
induced a rise in AR that exceeded by far the increase in free AMP.
Thus, additional factors, possibly inhibition of adenosine kinase,
influence the release of vasoactive adenosine.
Received 5 March 1996; accepted in final form 26 June 1996.
APS Manuscript Number H216-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996