AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 292: H2791-H2797, 2007. First published January 19, 2007; doi:10.1152/ajpheart.01384.2006
0363-6135/07 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
292/6/H2791    most recent
01384.2006v1
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 ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Banas, M. D.
Right arrow Articles by Fallavollita, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Banas, M. D.
Right arrow Articles by Fallavollita, J. A.

Determinants of contractile reserve in viable, chronically dysfunctional myocardium

Michael D. Banas,1,3,4 Sunil Baldwa,1,2,3,4 Gen Suzuki,3,4 John M. Canty, Jr.,1,3,4,5 and James A. Fallavollita1,3,4

1Veterans Affairs Western New York Health Care System, Buffalo; 2Canandaigua Veterans Affairs Medical Center, Canandaigua, New York; and 3Center for Research in Cardiovascular Medicine, 4Department of Medicine, and 5Department of Physiology and Biophysics, University at Buffalo, Buffalo, New York

Submitted 20 December 2006 ; accepted in final form 19 January 2007

There is considerable variability in the sensitivity of inotropic reserve to identify viability in chronically dysfunctional myocardium. This is partially related to the underlying pathophysiology, with more frequent contractile reserve in chronically stunned (with normal resting perfusion) than hibernating myocardium (with reduced flow). This study was undertaken to determine the physiological responses to transient and graded stimulation in chronically stunned and hibernating myocardium to define the relative roles of acute catecholamine desensitization and biphasic responses. Pigs were chronically instrumented with a fixed left anterior descending artery stenosis that resulted in chronically stunned myocardium after 2 mo. One month later, hibernating myocardium was confirmed by regional dysfunction (wall thickening, 3.2 ± 0.3 vs. 5.5 ± 5 mm in remote, P = 0.01) with reduced resting flow (0.70 ± 0.07 vs. 0.92 ± 0.09 ml·min–1·g–1 in remote, P = 0.01) without infarction. Wall thickening in dysfunctional regions significantly increased during both graded and transient epinephrine stimulation in chronically stunned (from 3.6 ± 0.3 to 5.6 ± 0.5 and 4.9 ± 0.5 mm, respectively) and hibernating myocardium (from 3.3 ± 0.3 to 5.4 ± 0.6 and 5.0 ± 0.7 mm, respectively) and returned to baseline within 15 min. Although a biphasic response during graded stimulation was common, the subsequent decrement in function was small and similar in both groups (stunned, 0.7 ± 0.2 mm; hibernating, 1.1 ± 0.3 mm, P = 0.25). We conclude that 1) the extent of contractile reserve during beta-adrenergic stimulation is similar in chronically stunned and hibernating myocardium, 2) there are no significant differences between the responses to transient compared with graded catecholamine stimulation, and 3) submaximal catecholamine stimulation does not induce additional stunning in either chronically stunned or hibernating myocardium.

inotropic reserve; catecholamine; viability; stunned myocardium; hibernating myocardium



Address for reprint requests and other correspondence: J. A. Fallavollita, Biomedical Research Bldg., Rm. 349, Dept. of Medicine/Cardiovascular Medicine, Univ. at Buffalo, 3435 Main St., Buffalo, NY 14214 (e-mail: jaf7{at}buffalo.edu)







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2007 by the American Physiological Society.