This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Armstrong, S. C. Articles by Ganote, C. E. Search for Related Content PubMed PubMed Citation Articles by Armstrong, S. C. Articles by Ganote, C. E.

American Journal of Pathology, Vol 138, 545-555, Copyright © 1991 by American Society for Investigative Pathology

REGULAR ARTICLES

Effects of the phospholipase inhibitor mepacrine on injury in ischemic and metabolically inhibited adult isolated myocytes

SC Armstrong and CE Ganote
Department of Pathology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City 37614.

The phospholipase inhibitor mepacrine has been shown to delay cell death of metabolically inhibited cultured cardiomyocytes. The present study was initiated to determine if mepacrine also delays cell death and development of osmotic fragility of both metabolically inhibited and ischemic adult rat cardiomyocytes. Isolated myocyte suspensions were incubated with 3 mmol/l (millimolar) iodoacetic acid and 6 mmol/l amytal (inhibited) or were pelleted into a slurry and layered with oil (ischemic) in the presence and absence of 10 or 50 mumol/l (micromolar) mepacrine. Rates of contracture, cell viability as determined by trypan blue permeability, cell viability after osmotic swelling in 170 mOsm media (osmotic fragility), and cell morphology were monitored. Mepacrine had no effects on rates of contracture, but was found to significantly delay cell death during isotonic incubations of both metabolically inhibited and ischemic cells. In contrast, mepacrine had no effect on the development of osmotic fragility. Incubation of metabolically inhibited myocytes in calcium-free media did not delay contracture or cell injury, but did attenuate the protective effects of mepacrine. This study confirms previous reports that mepacrine protects cells from injury, extends the observations of protection to ischemic isolated adult myocytes, but shows that development of osmotic fragility is not inhibited by mepacrine.

This article has been cited by other articles:

				R. J. Diaz and G. J. Wilson Studying ischemic preconditioning in isolated cardiomyocyte models Cardiovasc Res, May 1, 2006; 70(2): 286 - 296. [Abstract] [Full Text] [PDF]

				T. Okada, H. Otani, Y. Wu, S. Kyoi, C. Enoki, H. Fujiwara, T. Sumida, R. Hattori, and H. Imamura Role of F-actin organization in p38 MAP kinase-mediated apoptosis and necrosis in neonatal rat cardiomyocytes subjected to simulated ischemia and reoxygenation Am J Physiol Heart Circ Physiol, December 1, 2005; 289(6): H2310 - H2318. [Abstract] [Full Text] [PDF]

				T. Okada, H. Otani, Y. Wu, T. Uchiyama, S. Kyoi, R. Hattori, T. Sumida, H. Fujiwara, and H. Imamura Integrated pharmacological preconditioning and memory of cardioprotection: role of protein kinase C and phosphatidylinositol 3-kinase Am J Physiol Heart Circ Physiol, August 1, 2005; 289(2): H761 - H767. [Abstract] [Full Text] [PDF]

				R. J. Diaz, C. Zobel, H. Cheol Cho, M. Batthish, A. Hinek, P. H. Backx, and G. J. Wilson Selective Inhibition of Inward Rectifier K+ Channels (Kir2.1 or Kir2.2) Abolishes Protection by Ischemic Preconditioning in Rabbit Ventricular Cardiomyocytes Circ. Res., August 6, 2004; 95(3): 325 - 332. [Abstract] [Full Text] [PDF]

				J. P. Fabisiak, V. E. Kagan, Y. Y. Tyurina, V. A. Tyurin, and J. S. Lazo Paraquat-induced phosphatidylserine oxidation and apoptosis are independent of activation of PLA2 Am J Physiol Lung Cell Mol Physiol, May 1, 1998; 274(5): L793 - L802. [Abstract] [Full Text] [PDF]