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Cardiovascular Research 1999 42(3):567-570; doi:10.1016/S0008-6363(99)00027-9
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Respiratory control in normal and hypertrophic hearts

C. Gibbs

Department of Physiology, Monash University, Clayton, VIC 3168 Australia

Received 10 December 1998; accepted 14 January 1999

The first 150 words of the full text of this article appear below.

See article of Bache et al. [1] (pages 616–626) in this issue.

In a paper in the current issue of Cardiovascular Research, Bache, Zhang, Murakami, Zhang, Cho, Merkle, Gong, Fraser and Ugurbil [1] look at the proposition that the exaggerated depletion of PCr (phosphocreatine) and accumulation of inorganic phosphate (Pi) that occurs in left ventricular hypertrophy (LVH) is the result of impaired myocyte oxygenation. Using 31P- and 1H-NMR spectroscopy to determine myocardial high energy phosphate (HEP) levels and myoglobin desaturation the authors show convincingly that even at high work loads the exaggerated depletion of PCr and the increase in Pi are not the result of inadequate cellular oxygenation. They also conclude that the greater loss of PCr in the hypertrophic hearts during high work rates is probably caused by alterations in the regulation of myocardial oxidative phosphorylation. Their conclusion of adequate cellular oxygenation would receive support from earlier in . . . [Full Text of this Article]


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