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There is evidence that the failing human left ventricle in vivo subjected to additional preload is unable to use the Frank-Starling mechanism. The present study compared the force-tension relation in human nonfailing and terminally failing (heart transplants required because of dilated cardiomyopathy) myocardium. Isometric force of contraction of electrically driven left ventricular papillary muscle strips was studied under various preload conditions (2 to 20 mN). To investigate the influence of inotropic stimulation, the force-tension relation was studied in the presence of the cardiac glycoside ouabain. In skinned-fiber preparations of the left ventricle, developed tension was measured after stretching the preparations to 150% of the resting length. To evaluate the length-dependent activation of cardiac myofibrils by Ca2+ in failing and nonfailing myocardium, the tension-Ca2+ relations were also measured. After an increase of preload, the force of contraction gradually increased in nonfailing myocardium but was unchanged in failing myocardium. There were no differences in resting tension, muscle length, or cross-sectional area of the muscles between both groups. Pretreatment with ouabain (0.02 mumol/L) restored the force-tension relation in failing myocardium and preserved the force-tension relation in nonfailing tissue. In skinned-fiber preparations of the same hearts, developed tension increased significantly after stretching only in preparations from nonfailing but not from failing myocardium. The Ca2+ sensitivity of skinned fibers was significantly higher in failing myocardium (EC50, 1.0; 95% confidence limit, 0.88 to 1.21 mumol/L) compared with nonfailing myocardium (EC50, 1.7; 95% confidence limit, 1.55 to 1.86 mumol/L). After increasing the fiber length by stretching, a significant increase in the sensitivity of the myofibrils to Ca2+ was observed in nonfailing but not in failing myocardium. These experiments provide evidence for an impaired force-tension relation in failing human myocardium. On the subcellular level, this phenomenon might be explained by a failure of the myofibrils to increase the Ca2+ sensitivity after an increase of the sarcomere length.
R H Schwinger, and
M Böhm, and
A Koch, and
U Schmidt, and
I Morano, and
H J Eissner, and
P Uberfuhr, and
B Reichart, and
E Erdmann
February 1998,
Cardiovascular research,
R H Schwinger, and
M Böhm, and
A Koch, and
U Schmidt, and
I Morano, and
H J Eissner, and
P Uberfuhr, and
B Reichart, and
E Erdmann
August 1996,
Circulation,
R H Schwinger, and
M Böhm, and
A Koch, and
U Schmidt, and
I Morano, and
H J Eissner, and
P Uberfuhr, and
B Reichart, and
E Erdmann
December 2015,
American journal of physiology. Heart and circulatory physiology,
R H Schwinger, and
M Böhm, and
A Koch, and
U Schmidt, and
I Morano, and
H J Eissner, and
P Uberfuhr, and
B Reichart, and
E Erdmann
March 1989,
Giornale italiano di cardiologia,
R H Schwinger, and
M Böhm, and
A Koch, and
U Schmidt, and
I Morano, and
H J Eissner, and
P Uberfuhr, and
B Reichart, and
E Erdmann
September 2006,
Biophysical journal,
R H Schwinger, and
M Böhm, and
A Koch, and
U Schmidt, and
I Morano, and
H J Eissner, and
P Uberfuhr, and
B Reichart, and
E Erdmann
October 2002,
News in physiological sciences : an international journal of physiology produced jointly by the International Union of Physiological Sciences and the American Physiological Society,
R H Schwinger, and
M Böhm, and
A Koch, and
U Schmidt, and
I Morano, and
H J Eissner, and
P Uberfuhr, and
B Reichart, and
E Erdmann
January 2005,
Journal of muscle research and cell motility,
R H Schwinger, and
M Böhm, and
A Koch, and
U Schmidt, and
I Morano, and
H J Eissner, and
P Uberfuhr, and
B Reichart, and
E Erdmann
January 2012,
American journal of physiology. Heart and circulatory physiology,
R H Schwinger, and
M Böhm, and
A Koch, and
U Schmidt, and
I Morano, and
H J Eissner, and
P Uberfuhr, and
B Reichart, and
E Erdmann
October 1993,
The American journal of physiology,
R H Schwinger, and
M Böhm, and
A Koch, and
U Schmidt, and
I Morano, and
H J Eissner, and
P Uberfuhr, and
B Reichart, and
E Erdmann
December 1986,
The American journal of physiology,
