Corbett R J, Laptook A R
Department of Radiology, University of Texas Southwestern Medical Center, Dallas, TX 75235-9071.
J Neurochem. 1990 Apr;54(4):1208-17. doi: 10.1111/j.1471-4159.1990.tb01950.x.
The purpose of this study was to investigate neonatal brain energy metabolism, acid, and lactate homeostasis in the period immediately following partial ischemia. Changes in brain buffering capacity were quantified by measuring mean intracellular brain pH, calculated from the chemical shift of Pi, in response to identical episodes of hypercarbia before and after ischemia. In addition, the relationship between brain buffer base deficit and intracellular pH was compared during and following ischemia. Thus, in vivo 31P and 1H nuclear magnetic resonance spectra were obtained from the brains of seven newborn piglets exposed to sequential episodes of hypercarbia, partial ischemia, and a second episode of hypercarbia in the postischemic recovery period. For the first episode of hypercarbia, brain buffering was similar to values reported for adult animals of other species (percentage pH regulation = 54 +/- 16%). During ischemia, the brain base deficit per unit change in pH was -19 +/- 5 mM/pH unit, which is similar to values reported for adult rats. By 20-35 min postischemia, brain acidosis partly resolved in spite of a net increase in lactate concentration. Therefore, the consumption of lactate could not explain acid homeostasis in the first 35 min following ischemia. We conclude that H+/HCO3- or other proton equivalent translocation mechanisms must be sufficiently developed in piglet brain to support acid regulation. This is surprising, because a substantial body of evidence implies these processes would be less active in immature brain. The second episode of hypercarbia, from 35 to 65 min postischemia, resulted in a smaller decrease in brain pH compared with the first episode, a result indicating an increase in brain buffering capacity (percentage pH regulation = 79 +/- 29%). This was associated with a parallel decrease in brain lactate content, and therefore acid regulation could be attributed to either continued ion translocation or the consumption of lactate. A mild decrease in brain pH and content of energy metabolites was observed, a finding suggesting that the metabolic consequences of severe postischemic hypercarbia are neither particularly dangerous or beneficial.
本研究的目的是调查局部缺血后即刻新生儿脑能量代谢、酸和乳酸稳态。通过测量平均细胞内脑pH值来量化脑缓冲能力的变化，该值由无机磷酸盐（Pi）的化学位移计算得出，以响应缺血前后相同的高碳酸血症发作。此外，还比较了缺血期间和缺血后脑缓冲碱缺乏与细胞内pH值之间的关系。因此，从七只新生仔猪的大脑中获得了体内31P和1H核磁共振谱，这些仔猪在缺血后恢复期经历了连续的高碳酸血症、局部缺血和第二次高碳酸血症发作。对于第一次高碳酸血症发作，脑缓冲与其他物种成年动物报道的值相似（pH调节百分比 = 54 ± 16%）。在缺血期间，每单位pH变化的脑碱缺乏为 -19 ± 5 mM/pH单位，这与成年大鼠报道的值相似。缺血后20 - 35分钟，尽管乳酸浓度净增加，但脑酸中毒部分得到缓解。因此，乳酸的消耗不能解释缺血后最初35分钟内的酸稳态。我们得出结论，仔猪脑中H⁺/HCO₃⁻或其他质子等效转运机制必须充分发育以支持酸调节。这令人惊讶，因为大量证据表明这些过程在未成熟脑中活性较低。缺血后35至65分钟的第二次高碳酸血症发作导致脑pH值下降幅度小于第一次发作，这一结果表明脑缓冲能力增加（pH调节百分比 = 79 ± 29%）。这与脑乳酸含量的平行下降相关，因此酸调节可归因于持续的离子转运或乳酸的消耗。观察到脑pH值和能量代谢物含量有轻微下降，这一发现表明严重缺血后高碳酸血症的代谢后果既不是特别危险也不是特别有益。
