Corbett R J, Laptook A R, Sterett R, Tollefsbol G, Garcia D
Ralph Rogers and Mary Nell Magnetic Resonance Center,Department of Radiology, University of Texas Southwestern Medical Center, Dallas 75235-9085, USA.
Pediatr Res. 1996 Mar;39(3):477-86. doi: 10.1203/00006450-199603000-00016.
Newborn and 1-mo-old swine were exposed to identical durations (18 min) and degrees of hypoxia (O2 content = 4 mL/dL), to examine the effects of hypoxia on cerebral energy metabolism and intracellular pH (pHi) in vivo, using 31P and 1H nuclear magnetic resonance spectroscopy. Hypoxia produced the same extent of reductions in phosphocreatine (PCr) (63 +/- 28% and 65 +/- 10%, newborns and 1-mo-olds, respectively) and pHi (6.93 +/- 0.06 and 6.89 +/- 0.06, respectively) for either age group. The magnitude of changes in PCr, lactate, and pHi was larger for subgroups of data collected when cardiovascular instability was present, suggesting that hypotension and possibly reduced cerebral perfusion contributed to cerebral energy failure and lactic-acidosis for either age group. There were no correlations between the blood plasma glucose concentration at 18 min of hypoxia and the extent of change in PCr, lactate, or pHi for either age group. During a subsequent period of complete ischemia induced via cardiac arrest after 20 min hypoxia, the decline in PCr and nucleoside triphosphate (NTP), and increase in lactate followed similar rates compared with previously studied age-matched animals that were normoxic before ischemia. The rate constants for the change in PCr, NTP, and lactate followed similar rates compared with previously studied age-matched animals that were normoxic before ischemia. The rate constants for the change in PCr, NTP, and lactate during ischemia showed no correlation with the blood plasma glucose concentration measured immediately before cardiac arrest. These results suggest that cerebral glycolytic rates and energy utilization during ischemia are unaffected by a preceding interval of hypoxia and that hyperglycemia does not delay cerebral energy failure during hypoxia or combined hypoxic-ischemia.
将新生和1月龄猪暴露于相同时长（18分钟）和程度的低氧环境（氧含量 = 4毫升/分升），以利用31P和1H核磁共振波谱法在体内研究低氧对脑能量代谢和细胞内pH值（pHi）的影响。对于两个年龄组，低氧均使磷酸肌酸（PCr）产生相同程度的降低（新生猪和1月龄猪分别降低63±28%和65±10%）以及pHi产生相同程度的降低（分别为6.93±0.06和6.89±0.06）。当存在心血管不稳定情况时收集的亚组数据中，PCr、乳酸和pHi的变化幅度更大，这表明低血压以及可能的脑灌注减少导致了两个年龄组的脑能量衰竭和乳酸酸中毒。对于两个年龄组，低氧18分钟时的血浆葡萄糖浓度与PCr、乳酸或pHi的变化程度之间均无相关性。在低氧20分钟后通过心脏骤停诱导的随后完全缺血期，与先前研究的缺血前为正常氧合状态的年龄匹配动物相比，PCr和核苷三磷酸（NTP）的下降以及乳酸的增加遵循相似的速率。与先前研究的缺血前为正常氧合状态的年龄匹配动物相比，PCr、NTP和乳酸变化的速率常数遵循相似的速率。缺血期间PCr、NTP和乳酸变化的速率常数与心脏骤停前即刻测量的血浆葡萄糖浓度无相关性。这些结果表明，缺血期间的脑糖酵解速率和能量利用不受先前低氧期的影响，并且高血糖不会延迟低氧或低氧-缺血联合状态下的脑能量衰竭。
