Summary
The effect of hypoxia on myocardial lipolysis (glycerol release) was investigated in freshly isolated, calcium-tolerant rat ventricular myocytes. Hypoxia was produced by gassing the incubation medium (Joklik-minimum essential medium, supplemented with 1.2 mM MgSO4, 1 mM DL-carnitine, 1.5 mM CaCl2 and 0.6 mM palmitate bound to 0.15 mM fatty acid free bovine serum albumin) with 95% N2−5% CO,. Control (normoxic) incubations were carried out under air-5% CO2 atmosphere. Basal glycerol release increased from 46.6 ± 3.0 nmol/106 cells · 30 min in normoxia to 64.5 ± 4.3 nmol/106 cells · 30 min in hypoxia (p < 0.05). Addition of isoprenaline (10 μM) resulted in a significant (p < 0.05) stimulation of the glycerol release both in normoxia and in hypoxia, but the enhancement above basal rates was apparently lower in hypoxia (8.7 ± 2.5 nmol/106 cells · 30 min) than in normoxia (12.2 ± 2.7 nmol/106 cells · 30 min). Furthermore, whereas the isoprenaline-induced rise in lipolysis both in normoxia and hypoxia was prevented by inclusion of propranolol (10 μM), propranolol did not affect the hypoxia-induced increase in lipolysis. Thus, the above findings suggest that myocardial lipolysis may be stimulated by local non-adrenergic mechanisms during hypoxia.
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Larsen, T.S., Myrmel, T., Skulberg, A. et al. Effects of hypoxia on lipolysis in isolated rat myocardial cells. Mol Cell Biochem 88, 139–144 (1989). https://doi.org/10.1007/BF00223435
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DOI: https://doi.org/10.1007/BF00223435