Calcium elevation in cultured heart cells: its role in cell injury

• Published in: The American journal of physiology Vol. 245; no. 5 Pt 1; p. C316
• Main Authors: Murphy, E, Aiton, J F, Horres, C R, Lieberman, M
• Format: Journal Article
• Language: English
• Published: United States 01-11-1983
• Subjects: Adenosine Triphosphate - metabolism; Animals; Biological Transport, Active - drug effects; Calcium - metabolism; Calcium - toxicity; Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone - pharmacology; Cells, Cultured; Chick Embryo; Heart - drug effects; Heart - physiology; L-Lactate Dehydrogenase - metabolism; Mitochondria, Heart - metabolism; Myocardium - pathology; Potassium - metabolism; Sodium - metabolism
• ISSN: 0002-9513
• DOI: 10.1152/ajpcell.1983.245.5.c316

Inhibition of the Na+-K+ pump in cultured embryonic chick heart cells promotes the elevation of intracellular Ca2+ and is a useful manipulation to study the relationship between Ca2+ and myocardial cell injury. One hour of Na+-K+ pump inhibition resulted in a fourfold increase in cell Na+, a 50% decline in cell K+, and a 5- to 10-fold increase in cell Ca2+, 45% of which is mitochondrial. The degree of cell injury induced by Ca2+ loading was evaluated by monitoring the content of adenosine 5'-triphosphate (ATP) and the release of the intracellular enzyme lactate dehydrogenase (LDH). Under these conditions ATP content declined by 25-30% and LDH release increased from 1 to 1.4% of the total LDH. Furthermore, cells subjected to 1 h of Na+-K+ pump inhibition and returned to control solution for 5 h showed that Ca2+ decreased to near control levels and ATP content was restored. Although inhibition of Na+-K+ transport caused a large increase in cell Ca2+, neither Na+-K+ pump inhibition nor elevation in total cell Ca2+ per se resulted in irreversible myocardial cell injury.