LOSS OF CANINE MYOCARDIAL NICOTINAMIDE ADENINE DINUCLEOTIDES DETERMINES THE TRANSITION FROM REVERSIBLE TO IRREVERSIBLE ISCHEMIC DAMAGE OF MYOCARDIAL-CELLS
LOSS OF CANINE MYOCARDIAL NICOTINAMIDE ADENINE DINUCLEOTIDES DETERMINES THE TRANSITION FROM REVERSIBLE TO IRREVERSIBLE ISCHEMIC DAMAGE OF MYOCARDIAL-CELLS
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DOI：
10.1007/bf01908051
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发表时间：
1981-01-01
影响因子：
9.5
通讯作者：
SCHAPER, W
中科院分区：
文献类型：
--
作者：
KLEIN, HH;SCHAPER, J;SCHAPER, W
研究了缺血-梗死心肌中烟酰胺辅酶的丢失是否可能是可逆性缺血向不可逆性梗死细胞损伤转变的原因。6只犬的LAD [左前降支]闭塞4 h。在缺血1/2、1、1 1/2、2和4小时后，从缺血-梗死区域取硬膜穿刺活检，并进一步分为心外膜下和心内膜下两半。在每个时间间隔测量烟酰胺辅酶NAD、NADH和NADPH的浓度，并通过EM评估细胞损伤程度。在4只大鼠的脑、心肌、肾和骨骼肌中测定糖水解酶活性（EC 3.2.2.5），该酶分解NAD。缺血1h后，缺血区内膜下NAD和NADH的总和即总NAD开始显著下降。NADPH降解发生较晚。总NAD的损失为0.00000。当EM诊断为不可逆细胞损伤时，60-70%。糖水解酶活性在脑中最高，其次是心肌、肾和骨骼肌，反映了这些组织对缺血的不同耐受性。缺血性损伤的关键机制似乎是组织酸中毒，其激活糖水解酶，导致重要辅酶的损失。
If the loss of nicotinamide coenzymes in ischemic-infarcted myocardium may be responsible for the transition from reversibly ischemic to irreversibly infarcted cell damage was studied. The LAD [left anterior descending artery] was occluded in 6 dogs for 4 h. Transmural needle biopsies were taken from the ischemic-infarcted region after 1/2, 1, 1 1/2, 2 and 4 h of ischemia and further divided into subepicardial and subendocardial halves. At each time interval the concentration of the nicotinamide coenzymes NAD, NADH and NADPH were measured, and the degree of cellular injury was evaluated by EM. The glycohydrolase activity (EC 3.2.2.5), the enzyme which splits NAD, was determined in brain, myocardium, kidney and skeletal muscle of 4 rats. Total NAD, the sum of NAD and NADH, started to decrease significantly in the ischemic subendocardium 1 h after onset of ischemia. Degradation of NADPH occurred later. Loss of total NAD was .apprx. 60-70% when EM diagnosed irreversible cell injury. The glycohydrolase activity was the highest in brain followed by myocardium, kidney and skeletal muscle, reflecting the different tolerances of these tissues towards ischemia. The key mechanism for ischemic injury seems to be the tissue acidosis which activates the glycohydrolase leading to a loss of the vital coenzymes.