Microtubule Depolymerization Normalizes In Vivo Myocardial Contractile Function in Dogs With Pressure-Overload Left Ventricular Hypertrophy
Author(s) -
Masaaki Koide,
Masayoshi Hamawaki,
Takahiro Narishige,
Hiroshi Sato,
Shintaro Nemoto,
Gilberto DeFreyte,
Michael R. Zile,
George Cooper,
Blasé A. Carabello
Publication year - 2000
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.102.9.1045
Subject(s) - pressure overload , in vivo , medicine , cardiology , muscle hypertrophy , ventricular pressure , contraction (grammar) , microtubule , endocrinology , hemodynamics , biology , microbiology and biotechnology , cardiac hypertrophy
Because initially compensatory myocardial hypertrophy in response to pressure overloading may eventually decompensate to myocardial failure, mechanisms responsible for this transition have long been sought. One such mechanism established in vitro is densification of the cellular microtubule network, which imposes a viscous load that inhibits cardiocyte contraction.
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