Vary T C, Randle P J
Adv Myocardiol. 1985;6:473-81.
The effect of ischemia on the concentration of active pyruvate dehydrogenase (PDH) complex has been investigated in glucose-perfused hearts of normal rats fed a normal diet or a high-fat diet or starved for 48 hr and in hearts from alloxan-diabetic rats. Global ischemia induced by low flow (approximately equal to 1 ml/min) lowered the concentration of active complex under most conditions employed. Parallel studies of the effect of anoxia and of potassium arrest of the heart indicated that the effect of low-flow ischemia may result from decreased mechanical activity of the heart as a consequence of tissue hypoxia; the enzymatic mechanism may be activation of PDH kinase by increased reduction of mitochondrial NAD. In hearts of normal rats fed a normal diet, global ischemia induced by zero flow increased the concentration of active complex. Evidence is given that this may result from a combination of anoxia and acidosis. In aerobic perfusions, concentrations of active complex were ranked in the order: normal diet greater than high-fat diet greater than 48-hr starved greater than alloxan-diabetic. This order was maintained when the concentration of active complex was lowered by global ischemia induced by zero flow.
在喂食正常饮食、高脂饮食或饥饿48小时的正常大鼠以及四氧嘧啶糖尿病大鼠的心脏中，研究了缺血对活性丙酮酸脱氢酶（PDH）复合体浓度的影响。在大多数实验条件下，低流量（约1毫升/分钟）诱导的整体缺血降低了活性复合体的浓度。对缺氧和心脏钾停搏影响的平行研究表明，低流量缺血的影响可能是由于组织缺氧导致心脏机械活动降低所致；酶促机制可能是线粒体NAD还原增加激活了PDH激酶。在喂食正常饮食的正常大鼠心脏中，零流量诱导的整体缺血增加了活性复合体的浓度。有证据表明，这可能是缺氧和酸中毒共同作用的结果。在有氧灌注中，活性复合体的浓度排序为：正常饮食＞高脂饮食＞饥饿48小时＞四氧嘧啶糖尿病。当通过零流量诱导的整体缺血降低活性复合体浓度时，这一顺序保持不变。
