Altered membrane fluidity occurs during metabolic impairment of cardiac myocytes.
The purpose of this study was to evaluate the effect of impaired high energy phosphate metabolism on the membrane fluidity of cardiac myocytes. Cultured neonatal rat cardiac myocytes were treated with the metabolic inhibitor, iodoacetic acid (IAA) (30 microM). Membrane lipid fluidity was assessed by the steady-state fluorescence polarization of 1,6-diphenyl 1-1,3,5-hexatriene (DPH). Metabolic inhibition with IAA resulted in a progressive decrease in fluorescence polarization and calculated microviscosity. Microviscosity was decreased by 11% after 60-90 minutes and by 21% after 120-210 minutes, respectively. These changes are consistent with a progressive increase in membrane fluidity. Pretreatment with the experimental phospholipase inhibitor, U26, 384 (5-10 microM) resulted in a slower onset and less change in membrane fluidity after treatment with IAA. Thus, a) metabolic inhibition in cardiac myocytes induces prominent alterations in membrane fluidity which probably contribute to the membrane dysfunction accompanying myocardial injury and b) phospholipid degradation may be a significant factor in the genesis of altered membrane fluidity.
Buja
L M
LM
Department of Pathology and Laboratory Medicine, University of Texas Medical School, Houston 77030.
Miller
J C
JC
Krueger
G R
GR
D000818:Animals; D000831:Animals, Newborn; D002478:Cells, Cultured; D006321:Heart / Q000187:drug effects; D006352:Heart Ventricles; D007461:Iodoacetates / Q000494:pharmacology; D019807:Iodoacetic Acid; D007700:Kinetics; D008560:Membrane Fluidity; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D013050:Spectrometry, Fluorescence
D007461:Iodoacetates; D019807:Iodoacetic Acid