Calcium homeostasis in cardiomyocytes isolated from heat-shocked
rats.
Cornelussen, Richard N, Luc Ver Donck, Greet Verellen, Marcel Borgers,
Ger J Van Der Vusse, Robert S Reneman, and Luc H Snoeckx.
Department of Physiology and Department of Molecular Cell Biology
and Genetics, Cardiovascular Research Institute Maastricht,
University of Limburg, Maastricht, the Netherlands, Department of
Life Sciences, Janssen Research Foundation, Beerse, Belgium
APStracts 3:0256H, 1996.
The cellular mechanism of heat shock-mediated cardioprotection is
still under debate. Since heat pretreatment negatively affects the
normoxic in vitro left ventricular contractile performance when the
extracellular Ca2+-concentration ([Ca2+]o) is relatively low (0.65
-1.25 mM), the intracellular Ca2+-homeostasis was studied in more
detail in cardiomyocytes isolated from adult rats 24 h after heat
stress (42 C for 15 min) or anesthesia (Control). Sensitivity to
Ca2+-overload was assessed by exposure to veratridine (quiescent
cells), or to [Ca2+]o ranging from 0.125 to 20 mM in quiescent and
paced cardiomyocytes. The fraction of irreversibly hypercontracted
cells was not different in both groups. The FURA-2 fluorescence ratio
(i340/i380), which was used as a measure for the cytoplasmic Ca2+
-concentration [Ca2+]i in quiescent cells following exposure to
[Ca2+]o (0.5-10 mM), was also not different between both groups.
Myofilament Ca2+-sensitivity was assessed in paced (0.5 Hz) cells by
measuring simultaneously the [Ca2+]i-transients and cell shortening.
At stepwise increases of [Ca2+]o from 1 to 10 mM, these parameters
were comparable in both groups. The diastolic cell length shortened
progressively and equally in both groups following increasing
[Ca2+]o. However, within 2 min upon return from 10 to 1 mM [Ca2+]o,
cells from heat-shocked rats retained the same length, while cells
from control rats contracted further (p=0.05). These data suggest
that heat stress improves relaxation following challenge with high
[Ca2+]o.
Received 7 November 1995; accepted in final form 15 May 1995.
APS Manuscript Number H1039-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 July 96