Early reversal of acidosis and metabolic recovery following ischemia.
Early reversal of acidosis and metabolic recovery following ischemia.
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DOI：
10.3171/jns.1994.81.4.0567
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发表时间：
1994-10
影响因子：
4.1
通讯作者：
Trevor L. Hoffman;Joseph LaManna;S. Pundik;Warren R. Selman;T. Whittingham;R. Ratcheson;W. Lust
中科院分区：
文献类型：
--
作者：
Trevor L. Hoffman;Joseph LaManna;S. Pundik;Warren R. Selman;T. Whittingham;R. Ratcheson;W. Lust
组织酸中毒被认为是神经组织缺血性损伤的关键因素。本研究的目的是确定持续性缺血后酸中毒或酸中毒的程度是否会影响缺血事件后的代谢恢复。细胞内pH值（pHi），腺苷三磷酸，磷酸肌酸，和乳酸水平在大脑皮层中测量在再灌注的早期阶段，无论是5或10分钟的全脑缺血在normo和高血糖沙鼠。向总共130只沙鼠注射含有1.5 ml中性红（1%）（+/-2.5 gm/kg葡萄糖）的溶液; 30分钟后，将沙鼠置于氟烷麻醉下，并将颈动脉闭塞5或10分钟。在再灌注后0、15、30、60和120秒，将脑冷冻在液氮中;将它们切片，并对块面拍照，以通过使用中性红组织光度法测定pHi。在缺血结束时，所有组中的pHi均从对照值7.05 +/- 0.03（平均值+/-平均值的标准误差）显著降低。在血糖正常的大脑中，缺血5分钟和10分钟后，pHi值分别降至6.71 +/- 0.04和6.68 +/- 0.11。高血糖的大脑更酸;在缺血5分钟和10分钟后，数值分别下降到6.57 +/- 0.10和6.52 +/- 0.24。在血糖正常的大脑中，乳酸水平大约是对照组织的5倍，而在高血糖的大脑中，乳酸水平增加了8倍。三磷酸腺苷和磷酸肌酸水平在所有组的缺血结束时耗尽。在2分钟的再流活动后，正常和高血糖脑中的pHi水平在5分钟缺血组中恢复到对照值，而pHi水平在10分钟缺血组中仍然显著降低。无论缺血持续时间如何，血糖正常的大脑中高能磷酸盐的恢复是相似的，在2分钟时恢复到仅为对照组织中恢复的20%。然而，在高血糖的大脑中，在5分钟的缺血后，通过2分钟的再流活动，高能磷酸盐完全恢复。将高血糖大脑的缺血时间延长至10分钟，代谢恢复速度减慢至正常血糖大脑中观察到的速度。结果表明，回流期允许快速恢复的pHi水平基本上在正常化的主要含能化合物。（摘要400字处截断）
Tissue acidosis is believed to be a key element in ischemic injury of neural tissue. The goal of this study was to determine whether persisting postischemic acidosis or the extent of acidosis would affect metabolic recovery following an ischemic event. Intracellular pH (pHi), adenosine triphosphate, phosphocreatine, and lactate levels were measured in the cerebral cortex during the early stages of reperfusion, following either 5 or 10 minutes of global ischemia in both normo- and hyperglycemic gerbils. A total of 130 gerbils were injected with a solution containing 1.5 ml Neutral Red (1%) (+/- 2.5 gm/kg glucose); 30 minutes later, the gerbils were placed under halothane anesthesia, and the carotid arteries were occluded for either 5 or 10 minutes. The brains were frozen in liquid nitrogen at 0, 15, 30, 60, and 120 seconds after reperfusion; they were sectioned and the block face was photographed to determine the pHi by using Neutral Red histophotometry. At the conclusion of the ischemia, the pHi in all groups had decreased significantly from a control value of 7.05 +/- 0.03) (mean +/- standard error of the mean). In normoglycemic brains, the pHi values fell to 6.71 +/- 0.04 and 6.68 +/- 0.11 after 5 and 10 minutes of ischemia, respectively. Hyperglycemic brains were more acidotic; values fell to 6.57 +/- 0.10 and 6.52 +/- 0.24 after 5 and 10 minutes of ischemia, respectively. Lactate levels were approximately fivefold greater than those of control tissue in normoglycemic brains, while lactate levels in hyperglycemic brains were increased eightfold. The adenosine triphosphate and phosphocreatine levels were depleted at the end of ischemia in all groups. After 2 minutes of reflow activity, the pHi levels in both normo- and hyperglycemic brains were restored to those of control values in the '5-minute ischemic group, while the pHi levels remained significantly depressed in the 10-minute ischemic group. Restoration of high-energy phosphates was similar in normoglycemic brains regardless of ischemic duration, recovering to only 20% of the restoration obtained in control tissue at 2 minutes. In hyperglycemic brains, however, there was complete recovery of high-energy phosphates by 2 minutes of reflow activity following 5 minutes of ischemia. Extending the ischemic period to 10 minutes in hyperglycemic brains slowed the rate of metabolic recovery to that observed in normoglycemic brains. The results indicate that the reflow period permits the rapid restoration of pHi levels substantially before the normalization of primary energetic compounds.(ABSTRACT TRUNCATED AT 400 WORDS)