AJP - Heart Add DOIs to your references at manuscript stage!
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 297: H223-H232, 2009. First published April 24, 2009; doi:10.1152/ajpheart.00992.2008
0363-6135/09 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
297/1/H223    most recent
00992.2008v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Hu, Q.
Right arrow Articles by Canty, J. M.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hu, Q.
Right arrow Articles by Canty, J. M., Jr.

Reductions in mitochondrial O2 consumption and preservation of high-energy phosphate levels after simulated ischemia in chronic hibernating myocardium

Qingsong Hu,2 Gen Suzuki,2,3 Rebeccah F. Young,2 Brian J. Page,1,2,3 James A. Fallavollita,1,2,3 and John M. Canty, Jr.1,2,3,4

1Veterans Affairs Western New York Health Care System; 2Center for Research in Cardiovascular Medicine and Departments of 3Medicine and 4Physiology and Biophysics, University at Buffalo, Buffalo, New York

Submitted 12 September 2008 ; accepted in final form 14 April 2009

We performed the present study to determine whether hibernating myocardium is chronically protected from ischemia. Myocardial tissue was rapidly excised from hibernating left anterior descending coronary regions (systolic wall thickening = 2.8 ± 0.2 vs. 5.4 ± 0.3 mm in remote myocardium), and high-energy phosphates were quantified by HPLC during simulated ischemia in vitro (37°C). At baseline, ATP (20.1 ± 1.0 vs. 26.7 ± 2.1 µmol/g dry wt, P < 0.05), ADP (8.1 ± 0.4 vs. 10.3 ± 0.8 µmol/g, P < 0.05), and total adenine nucleotides (31.2 ± 1.3 vs. 40.1 ± 2.9 µmol/g, P < 0.05) were depressed compared with normal myocardium, whereas total creatine, creatine phosphate, and ATP-to-ADP ratios were unchanged. During simulated ischemia, there was a marked attenuation of ATP depletion (5.6 ± 0.9 vs. 13.7 ± 1.7 µmol/g at 20 min in control, P < 0.05) and mitochondrial respiration [145 ± 13 vs. 187 ± 11 ng atoms O2·mg protein–1·min–1 in control (state 3), P < 0.05], whereas lactate accumulation was unaffected. These in vitro changes were accompanied by protection of the hibernating heart from acute stunning during demand-induced ischemia. Thus, despite contractile dysfunction at rest, hibernating myocardium is ischemia tolerant, with reduced mitochondrial respiration and slowing of ATP depletion during simulated ischemia, which may maintain myocyte viability.

energy metabolism; mitochondrial respiration; stunned myocardium


Address for reprint requests and other correspondence: J. M. Canty, Jr., Biomedical Research Bldg., Rm. 345, Univ. at Buffalo, 3435 Main St., Buffalo, NY 14214 (e-mail: canty{at}buffalo.edu)






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2009 by the American Physiological Society.