Effect of Arachidonic Acid on the Rate of Oxygen Consumption in Isolated Cardiomyocytes from Intact Rats and Animals with Ischemic or Diabetic Injury to the Heart

• Published in: Bulletin of experimental biology and medicine 2015-12, Vol.160 (2), p.190-192
• Main Authors: Egorova, M. V., Kutsykova, T. V., Afanas’ev, S. A., Popov, S. V.
• Format: Article
• Language: English
• Subjects: Animals; Arachidonic acid; Arachidonic Acid - pharmacology; Biomedical and Life Sciences; Biomedicine; Cell Biology; Diabetes mellitus; Diabetes Mellitus, Experimental - metabolism; Heart attack; Heart cells; Internal Medicine; Laboratory Medicine; Male; Mitochondria - drug effects; Mitochondria - metabolism; Myocardial Infarction - metabolism; Myocardium - metabolism; Myocytes, Cardiac - drug effects; Myocytes, Cardiac - metabolism; Oxygen Consumption - drug effects; Pathology; Rats; Rats, Wistar; Streptozocin; Unsaturated fatty acids
• ISSN: 0007-4888; 1573-8221
• DOI: 10.1007/s10517-015-3124-1

We studied the rate of oxygen consumption by isolated cardiomyocytes from intact rats and animals with experimental myocardial infarction or streptozotocin-induced diabetes mellitus. The measurements were performed in standard incubation medium under various conditions of oxygenation and after addition of arachidonic acid (20 μmol/liter). Under normoxic conditions, arachidonic acid improves respiration of cardiomyocytes from intact animals, but reduces this parameter in cells isolated from animals with pathologies. The intensity of O 2 consumption by cardiomyocytes from intact rats and animals with pathologies was shown to decrease during hypoxia. Addition of arachidonic acid aggravated inhibition of respiration for cardiomyocytes from intact rats and specimens with myocardial infarction, but had no effect in diabetes mellitus. The effect of arachidonic acid on oxygen consumption rate is probably mediated by a nonspecific mechanism realized at the mitochondrial level.