Oliver M F, Opie L H
National Heart and Lung Institute, London, UK.
Lancet. 1994 Jan 15;343(8890):155-8. doi: 10.1016/s0140-6736(94)90939-3.
Evidence for the utilisation of substrates by the ischaemic myocardium and its dependence for viability on a critical supply of glucose was established many years ago. It was recognised that an excess of free fatty acids (FFA) could increase the severity of ischaemic damage and possibly be arrhythmogenic. But metabolic intervention to improve survival during acute myocardial infarction was not regarded as a priority, perhaps because of uncertainty about its value and the advent of trials of beta-blocker and antiarrhythmic drugs. There has never been an adequate trial of the benefit to the ischaemic or infarcting myocardium of increasing local glucose concentrations or reducing the availability of FFA. We have taken into account new knowledge of the effects of fatty acids on cation channels and brought up to date the arguments for metabolic intervention with glucose-insulin solutions or antilipolytic drugs sustained ischaemia.
许多年前就已证实缺血心肌利用底物的情况及其对葡萄糖关键供应的存活依赖性。人们认识到过量的游离脂肪酸（FFA）会加重缺血损伤的严重程度，并可能引发心律失常。但改善急性心肌梗死期间存活率的代谢干预措施未被视为优先事项，这可能是因为其价值存在不确定性，以及β受体阻滞剂和抗心律失常药物试验的出现。从未有过关于提高局部葡萄糖浓度或降低FFA可用性对缺血或梗死心肌益处的充分试验。我们考虑了脂肪酸对阳离子通道影响的新知识，并更新了使用葡萄糖 - 胰岛素溶液或抗脂解药物进行代谢干预以维持缺血的论据。
