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Constitutive properties of hypertrophied myocardium: cellular contribution to changes in myocardial stiffnessRecent studies have suggested that pressure overload hypertrophy (POH) alters the viscoelastic properties of individual cardiocytes when studied in isolation. However, whether these changes in cardiocyte properties contribute causally to changes in the material properties of the cardiac muscle as a whole is unknown. Accordingly, a selective, isolated, acute change in cardiocyte constitutive properties was imposed in an in vitro system capable of measuring the resultant effect on the material properties of the composite cardiac muscle. POH caused an increase in both myocardial elastic stiffness, from 20.5 +/- 1.3 to 28.4 +/- 1.8, and viscous damping, from 15.2 +/- 1.1 to 19.8 +/- 1.5 s (normal vs. POH, P < 0.05), respectively. Recent studies have shown that cardiocyte constitutive properties could be acutely altered by depolymerizing the microtubules with colchicine. Colchicine caused a significant decrease in the viscous damping in POH muscles (19.8 +/- 1.5 s at baseline vs. 14.7 +/- 1.3 s after colchicine, P < 0.05). Therefore, myocardial material properties can be altered by selectively changing the constitutive properties of one element within this muscle tissue, the cardiocyte. Changes in the constitutive properties of the cardiocytes themselves contribute to the abnormalities in myocardial stiffness and viscosity that develop during POH.
Document ID
20040088330
Acquisition Source
Legacy CDMS
Document Type
Reprint (Version printed in journal)
Authors
Harris, Todd S.
(and Gazes Cardiac Research Institute, Medical University of South Carolina and Veterans Administration Medical Center Charleston, South Carolina 29401, United States)
Baicu, Catalin F.
Conrad, Chester H.
Koide, Masaaki
Buckley, J. Michael
Barnes, Mary
Cooper, George 4th
Zile, Michael R.
Date Acquired
August 21, 2013
Publication Date
June 1, 2002
Publication Information
Publication: American journal of physiology. Heart and circulatory physiology
Volume: 282
Issue: 6
ISSN: 0363-6135
Subject Category
Life Sciences (General)
Funding Number(s)
CONTRACT_GRANT: P01-HL-48788
CONTRACT_GRANT: R01-HL-55444-03
Distribution Limits
Public
Copyright
Other
Keywords
Non-NASA Center
NASA Discipline Cardiopulmonary

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