Myocardial infarction alters myofilament calcium sensitivity and
mechanical behavior of myocytes.
Li, Peng, Polly A. Hofmann, Baosheng Li, Ashwani Malhotra, Wei Cheng,
Edmund H. Sonnenblick, Leonard G. Meggs, and Piero Anversa.
Departments of Medicine, New York Medical College, Valhalla, New
York 10595, Albert Einstein College of Medicine, New York, New York
10461, and Department of Physiology and Biophysics, University of
Tennessee College of Medicine, Memphis, Tennessee 38163
APStracts 3:0317H, 1996.
To determine whether myocardial infarction leads to alterations in
myofilament isometric tension as a function of [Ca2+], unloaded
shortening velocity, VMAX, and sarcomere compliance, these properteis
were examined in skinned myocytes 7 days after coronary artery
occlusion. Changes in myofilament proteins were also evaluated.
Myocardial infarction was characterized by a 10-15% reduction in
myofilament isometric tension at submaximum Ca2+ levels in the
physiologic range. However, developed tension at maximum activation
was unaltered. Conversely, VMAX was decreased by 31% in the remaining
viable cells, while resting tension was increased by 30-40%. The
regulatory protein troponin I (TnI) content was reduced, but
phosphorylation of TnI and troponin T (TnT) was increased. Myosin
isoenzymes and TnT contents were not altered. In conclusion,
molecular responses occurred acutely after myocardial infarction and
these adaptations may depress the mechanical behavior of the
unaffected cells, contributing to acute impairment in global cardiac
pump function beyond that resulting from myocyte loss.
Received 7 May 1996; accepted in final form 8 July 1996.
APS Manuscript Number H408-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 21 August 1996