Chaudry I H, Sayeed M M, Baue A E
Can J Physiol Pharmacol. 1976 Oct;54(5):750-6. doi: 10.1139/y76-104.
The effect of hemorrhagic shock, hypoxemia, and anoxia on the levels of adenine and pyridine nucleotides of liver and kidney was assessed. ATP levels in liver and kidney of animals in shock or animals subjected to 7 min of anoxia decreased by 85 and 73%, respectively. Under hypoxic conditions (arterial PO2 AT 18 MMHg), the decrease was only 62 and 48% in liver and kidney, respectively. Tissue NAD levels decreased and NADH levels increased during shock but were found to be essentially unaltered during experimental hypoxemia. Thus, shock produced greater alterations in adenine and pyridine nucleotides than did hypoxemia alone, indicating that stagnant hypoxemia due to shock is more deleterious to energy metabolism than is severe hypoxemia with an otherwise normal circulation. The results also suggest that if an anterial PO2 OF 18 MMHg represents the initial stages of tissue hypoxia, then tissue ATP levels are a more sensitive indicator of this than NAD levels.
评估了失血性休克、低氧血症和缺氧对肝脏和肾脏中腺嘌呤和吡啶核苷酸水平的影响。休克动物或缺氧7分钟的动物肝脏和肾脏中的ATP水平分别下降了85%和73%。在低氧条件下(动脉血氧分压为18 mmHg),肝脏和肾脏中的下降分别仅为62%和48%。休克期间组织NAD水平下降而NADH水平升高,但在实验性低氧血症期间发现其基本未改变。因此,休克比单独的低氧血症对腺嘌呤和吡啶核苷酸产生更大的改变,表明休克引起的淤滞性低氧血症比循环正常但存在严重低氧血症对能量代谢更具损害性。结果还表明,如果动脉血氧分压为18 mmHg代表组织缺氧的初始阶段,那么组织ATP水平比NAD水平对此更敏感。