Larsen T S, Myrmel T, Skulberg A, Severson D L, Mjøs O D
Department of Physiology, University of Tromsø, Norway.
Mol Cell Biochem. 1989;88(1-2):139-44. doi: 10.1007/BF00223435.
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% CO2. Control (normoxic) incubations were carried out under air-5% CO2 atmosphere. Basal glycerol release increased from 46.6 +/- 3.0 nmol/10(6) cells.30 min in normoxia to 64.5 +/- 4.3 nmol/10(6) cells.30 min in hypoxia (p less than 0.05). Addition of isoprenaline (10 microM) resulted in a significant (p less than 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/10(6) cells.30 min) than in normoxia (12.2 +/- 2.7 nmol/10(6) cells.30 min). Furthermore, whereas the isoprenaline-induced rise in lipolysis both in normoxia and hypoxia was prevented by inclusion of propranolol (10 microM), 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.
在新鲜分离的、耐钙的大鼠心室肌细胞中研究了缺氧对心肌脂解（甘油释放）的影响。通过向孵育培养基（Joklik - 最低必需培养基，补充有1.2 mM硫酸镁、1 mM DL - 肉碱、1.5 mM氯化钙和0.6 mM与0.15 mM游离脂肪酸结合的棕榈酸的无脂肪酸牛血清白蛋白）中通入95% N₂ - 5% CO₂来产生缺氧环境。对照（常氧）孵育在空气 - 5% CO₂气氛下进行。基础甘油释放量从常氧状态下30分钟时的46.6±3.0 nmol/10⁶个细胞增加到缺氧状态下30分钟时的64.5±4.3 nmol/10⁶个细胞（p＜0.05）。加入异丙肾上腺素（10 μM）在常氧和缺氧状态下均导致甘油释放量显著增加（p＜0.05），但缺氧状态下高于基础水平的增加量（8.7±2.5 nmol/10⁶个细胞·30分钟）明显低于常氧状态下（12.2±2.7 nmol/10⁶个细胞·30分钟）。此外，虽然普萘洛尔（10 μM）可阻止常氧和缺氧状态下异丙肾上腺素诱导的脂解增加，但普萘洛尔不影响缺氧诱导的脂解增加。因此，上述发现表明在缺氧期间心肌脂解可能受到局部非肾上腺素能机制的刺激。
