DELAYED (SECONDARY) CEREBRAL ENERGY FAILURE AFTER ACUTE HYPOXIA-ISCHEMIA IN THE NEWBORN PIGLET - CONTINUOUS 48-HOUR STUDIES BY PHOSPHORUS MAGNETIC-RESONANCE SPECTROSCOPY
DELAYED (SECONDARY) CEREBRAL ENERGY FAILURE AFTER ACUTE HYPOXIA-ISCHEMIA IN THE NEWBORN PIGLET - CONTINUOUS 48-HOUR STUDIES BY PHOSPHORUS MAGNETIC-RESONANCE SPECTROSCOPY
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DOI：
10.1203/00006450-199412000-00003
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发表时间：
1994-12-01
影响因子：
3.6
通讯作者：
REYNOLDS, EOR
中科院分区：
文献类型：
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作者：
LOREK, A;TAKEI, Y;REYNOLDS, EOR
严重出生窒息的人类婴儿的大脑中的磷（P-31）光谱在出生第一天通常是正常的。随后，出现脑能量衰竭，预后严重。本研究的主要目的是检验这样的假设：在严重急性逆转脑缺氧缺血损伤后，这种延迟的（“继发性”）能量衰竭可以在新生仔猪中重现。 12 头仔猪接受颈总动脉暂时闭塞和低氧血症 [平均动脉 Po-2 3.1 (SD 0.6) kPa]。平均脑磷酸肌酸浓度[PCr]/无机正磷酸盐浓度[Pi]从1.40 (SD 0.29)下降到0.01 (SD 0.02)，三磷酸核苷酸浓度[NTP]/可交换磷酸盐池浓度[EPP]从0.19 (SD 0.02)下降到0.06 (SD 0.04)(每次下降p < 0.001)。在大脑再灌注和再氧合时，平均[PCr]/[Pi]和[NTP]I[EPP]恢复到基线。接下来 48 小时的持续观察显示，尽管动脉 Po、平均动脉血压和血糖正常，[PCr]/[Pi] 再次下降，24 小时时为 0.62 (SD 0.61) (p < 0.01)，48 小时时为 0.49 (SD 0.37) (p < 0.001)。 [NTP]/[EPP] 也减少，但程度较小。细胞内pH值保持不变。这些发现似乎与出生时窒息的人类婴儿的发现相同。六只对照仔猪的脑代谢物浓度没有发生变化。根据 24-48 小时记录的最低 [PCr]/[Pi] 判断，继发性能量衰竭的严重程度与急性能量消耗的程度直接相关，通过 [NTP]/[EPP] 减少的时间积分获得（p < 0.0001）。这种二次能量衰竭的动物模型可能有助于测试脑保护策略。
Phosphorus (P-31) spectra from the brains of severely birth-asphyxiated human infants are commonly normal on the first day of life. Later, cerebral energy failure develops, which carries a serious prognosis. The main purpose of this study was to test the hypothesis that this delayed (''secondary'') energy failure could be reproduced in the newborn piglet after a severe acute reversed cerebral hypoxicischemic insult. Twelve piglets were subjected to temporary occlusion of the common carotid arteries and hypoxemia [mean arterial Po-2 3.1 (SD 0.6) kPa]. Mean cerebral phosphocreatine concentration [PCr]/inorganic orthophosphate concentration [Pi] decreased from 1.40 (SD 0.29) to 0.01 (SD 0.02), and nucleotide triphosphate concentration [NTP]/exchangeable phosphate pool concentration [EPP] decreased from 0.19 (SD 0.02) to 0.06 (SD 0.04) (p < 0.001 for each decrease). On reperfusion and reoxygenation of the brain, mean [PCr]/[Pi] and [NTP]I[EPP] returned to baseline. Observations continuing for the next 48 h showed that [PCr]/[Pi] again decreased, in spite of normal arterial Po,, mean arterial blood pressure, and blood glucose, to 0.62 (SD 0.61) at 24 h (p < 0.01) and 0.49 (SD 0.37) at 48 h (p < 0.001). [NTP]/[EPP] also decreased, but to a lesser degree. Intracellular pH remained unchanged. These findings appeared identical with those seen in birth-asphyxiated human infants. No changes in cerebral metabolite concentrations took place in six control piglets. The severity of secondary energy failure, as judged by the lowest [PCr]/[Pi] recorded at 24-48 h, was directly related to the extent of acute energy depletion, obtained as the time integral of reduction in [NTP]/[EPP] (p < 0.0001). This animal model of secondary energy failure may prove useful for testing cerebroprotective strategies.