Mochizuki S, Murase T, Yamaoka H, Ishiki M, Tada N, Nagano M
Department of Medicine, Jikei University School of Medicine, Japan.
Basic Res Cardiol. 1987;82 Suppl 1:45-52. doi: 10.1007/978-3-662-08390-1_6.
Myocardial lipoprotein lipase (LPL) activity during ischaemia has not been fully understood, although it plays an important role in regulating myocardial fatty acid metabolism. In this experiment, the effects of ischaemia (Experiment A) and anoxia (Experiment B) on two distinct fractions of LPL, i.e. functional and nonfunctional forms were investigated in isolated, perfused rat heart. In Experiment A, hearts were perfused by Neely-Morgan working heart mode with Krebs Henseleit bicarbonate (KHB) buffer (95% O2:5% CO2), then whole heart ischaemia was induced by using a one-way aortic valve, simultaneously switching to the same buffer but containing heparin (5 mu/ml) for 20 min. In Experiment B, the hearts were perfused by Langendorff method with KHB buffer (95% O2:5% CO2) and the buffer was switched to KHB (95% N2:5% CO2) containing heparin for 20 min. Coronary effluent was collected at 5 min intervals and used for the measurement of functional LPL activities using 3H-glyceryltrioleate. The hearts were quickly frozen at the end of perfusion and homogenized. The suspension was used for the measurement of non-functional LPL activities. In Experiment A, functional LPL activities in ischaemia were significantly lower than in the aerobic condition. On the contrary, the nonfunctional LPL activity in ischaemia was significantly higher than in the aerobic condition. In Experiment B these values were also significantly lower than in the aerobic condition. However, there was no significant difference in non-functional LPL activity between the anoxia and aerobic condition. These results indicate that there is a conversion defect from the precursor of LPL to the functional form of LPL in ischaemia, whereas disturbed LPL synthesis might be involved in anoxic myocardium.
心肌脂蛋白脂肪酶（LPL）在缺血期间的活性尚未完全明确，尽管它在调节心肌脂肪酸代谢中发挥着重要作用。在本实验中，研究了缺血（实验A）和缺氧（实验B）对LPL两种不同组分（即功能性和非功能性形式）的影响，实验对象为离体灌注大鼠心脏。在实验A中，心脏采用Neely-Morgan工作心脏模式，用Krebs Henseleit碳酸氢盐（KHB）缓冲液（95% O₂:5% CO₂）灌注，然后使用单向主动脉瓣诱导全心缺血，同时切换至含有肝素（5μg/ml）的相同缓冲液，持续20分钟。在实验B中，心脏采用Langendorff方法，用KHB缓冲液（95% O₂:5% CO₂）灌注，然后将缓冲液切换至含有肝素的KHB（95% N₂:5% CO₂），持续20分钟。每隔5分钟收集冠状动脉流出液，用于使用³H-甘油三油酸酯测量功能性LPL活性。灌注结束时迅速将心脏冷冻并匀浆。匀浆悬浮液用于测量非功能性LPL活性。在实验A中，缺血时功能性LPL活性显著低于有氧条件。相反，缺血时非功能性LPL活性显著高于有氧条件。在实验B中，这些值也显著低于有氧条件。然而，缺氧和有氧条件下非功能性LPL活性无显著差异。这些结果表明，缺血时存在从LPL前体向功能性LPL形式的转化缺陷，而缺氧心肌可能涉及LPL合成紊乱。
