Effects of pressure or volume overload hypertrophy on passive
stiffness in isolated adult mammalian cardiac muscle cells.
Kato, Satoshi, Masaaki Koide, George Cooper, Michael R. Zile.
Gazes Cardiac Research Institute, Cardiology Division of the
Department of Medicine, Medical University of South Carolina, and the
Ralph H. Johnson Department of Veterans Affairs Medical Center,
Charleston, South Carolina
APStracts 3:0277H, 1996.
It has been hypothesized that the changes in myocardial stiffness
induced by chronic hemodynamic overloading are dependent on changes
in the passive stiffness of the cardiac muscle cell (cardiocyte).
However, no previous studies have examined the passive constitutive
properties of cardiocytes isolated from animals with myocardial
hypertrophy. Accordingly, changes in relative passive stiffness of
cardiocytes isolated from animals with chronic pressure or volume
overload hypertrophy were determined by examining the effects of
anisosmotic stress on cardiocyte size. Anisosmotic stress was
produced by altering superfusate osmolarity. Hypertrophied
cardiocytes were enzymatically isolated from 16 adult cats with right
ventricular (RV) pressure overload hypertrophy induced by pulmonary
artery banding (PAB) and from 6 adults cats with right ventricular
volume overload hypertrophy induced by creating an atrial septal
defect (ASD). Left ventricular (LV) cardiocytes from each cat served
as non-hypertrophied, normally loaded, same animal controls.
Superfusate osmolarity was decreased from 305 +/- 3 to 135 +/- 5 mOsm
and increased to 645 +/- 4 mOsm. During anisosmotic stress, there
were no significant differences between hypertrophied RV and normal
LV cardiocytes in pressure overload PAB cats with respect to percent
change in cardiocyte area (47 +/- 2% in RV vs 48 +/- 2% in LV),
diameter (46 +/- 3% in RV vs 48 +/- 2 % in LV), cardiocyte length
(2.4 +/- 0.2% in RV vs 2.0 +/- 0.3% in LV), or sarcomere length (1.5
+/- 0.1% in RV vs 1.3 +/- 0.3 % in LV). Likewise, there were no
significant differences in cardiocyte strain between hypertrophied RV
and normal LV cardiocytes from ASD cats. In conclusion, the presence
of either chronic pressure overload hypertrophy or chronic volume
overload hypertrophy did not alter the cardiocyte response to
anisosmotic stress. Thus, chronic overload hypertrophy did not alter
relative passive cardiocyte stiffness.
Received 1 December 1995; accepted in final form 12 June 1996.
APS Manuscript Number H1118-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996