Protection of reoxygenated cardiomyocytes against osmotic fragility
by no donors.
Schl[umlaut]uter, K. D., G. Jakob, M. Ruiz-Meana, D. Garcia-Dorado, H.
M. Piper.
Physiologisches Institut, Justus-Liebig-Universit[umlaut]at
Gie[beta]en, Aulweg 129, D-35392 Gie[beta]en, Germany; Servico de
Cardiologia, Hospital General Universitario Vall d Hebron, Paseo Vall
d Hebron 119-129, Barcelona 08035, Spain
APStracts 3:0048H, 1996.
In ischemic-reperfused myocardium, myocardial cells are jeopardized
not only by reoxygenation-induced hypercontracture but also by the
development of a transsarcolemmal osmotic gradient. Here, the
question was addressed whether osmotic fragility of cardiomyocytes
can be reduced by interventions during reoxygenation. Isolated
ventricular cardiomyocytes (from adult rats), exposed to 120 min
hypoxia and subsequent reoxygenation, were used as model. Upon
reoxygenation medium osmolality was reduced from 270 mOsm to 80 mOsm.
Loss of sarcolemmal integrity was characterized by enzyme loss from
cells (creatine kinase, lactate dehydrogenase). Cardiomyocytes
reoxygenated after 120 min hypoxia hypercontracted, but enhanced
enzyme loss was only observed at 80 mOsm. The NO donors SIN-1 (10
mM), sodium nitroprusside (10 mM), S-nitroso-N-acetyl-D,L
-penicillamine (SNAP, 100 [mu]M) and the anti-lipid peroxidant
diphenylphenylenediamine (DPPD, 2.5 [mu]M) reduced enzyme loss upon
hypoosmolal reoxygenation. Agents activating cyclic-GMP dependent
pathways (atrionatriuretic peptide (1 [mu]M), urodilatin (1 [mu]M),
and 8-bromo-cyclo-GMP (10 mM)), the contractile inhibitor 2,3
-butanedione monoxime (10 mM) and the SIN-1 metabolite SIN-1C (10 mM)
did not protect cardiomyocytes against osmotic fragility. The results
show that increased osmotic fragility of isolated adult rat
cardiomyocytes can be prevented at the time of reoxygenation by NO
donors and DPPD, in a cyclic-GMP independent way.
Received 24 February 1995; accepted in final form 17 January
1996.
APS Manuscript Number H176-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 February 96