Decreased energy metabolism in brain stem during central respiratory depression in response to hypoxia
Decreased energy metabolism in brain stem during central respiratory depression in response to hypoxia
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DOI：
10.1152/jappl.1996.81.4.1772
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发表时间：
1996-10-01
影响因子：
3.3
通讯作者：
Cherniack, NS
中科院分区：
文献类型：
--
作者：
LaManna, JC;Haxhiu, MA;Cherniack, NS
在缺氧诱导的呼吸抑制发生时测量脑干的代谢变化。在迷走神经切断的麻醉大鼠中，通过记录膈肌肌电图活动监测，平均在11分钟内（范围5-27分钟），用8%氧气进行的Eucapnic通气导致呼吸驱动停止，推测是通过中枢神经系统机制。当时，脑干被原位冷冻用于代谢分析。通过使用20 μ m冷冻固定的脑干冻干切片，对1）背细胞核和锥体旁核的腹侧部分; 2）疑核的致密部分和腹侧部分; 3）中线神经元; 4）孤束核;和5）三叉神经脊束核的ATP、磷酸肌酸、乳酸和细胞内pH进行了微区域分析。在呼吸抑制时，所有区域的乳酸均升高三倍。ATP和磷酸肌酸分别降低至对照组的50%和25%。在这些区域，细胞内pH值更酸性0.2-0.4单位，但在腹侧和背侧髓质表面附近的化学敏感区域相对保存。这些结果表明，缺氧诱导的呼吸抑制伴随着呼吸和心血管控制相关脑干区域内的代谢变化。因此，在缺氧引起的呼吸抑制发生后，脑干中似乎存在显著的能量缺乏。
Metabolic changes in the brain stem were measured at the time when oxygen deprivation-induced respiratory depression occurred. Eucapnic ventilation with 8% oxygen in vagotomized urethan-anesthetized rats resulted in cessation of respiratory drive, monitored by recording diaphragm electromyographic activity, on average within II min (range 5-27 min), presumably via central depressant mechanisms. At that time, the brain stems were frozen in situ for metabolic analyses. By using 20-mu m lyophilized sections from frozen-fixed brain stem, microregional analyses of ATP, phosphocreatine, lactate, and intracellular pH were made from 1) the ventral portion of the nucleus gigantocellularis and the parapyramidal nucleus; 2) the compact and ventral portions of the nucleus ambiguus; 3) midline neurons; 4) nucleus tractus solitarii; and 5) the spinal trigeminal nucleus. At the time of respiratory depression, lactate was elevated threefold in all regions. Both ATP and phosphocreatine were decreased to 50 and 25% of control, respectively. Intracellular pH was more acidic by 0.2-0.4 unit in these regions but was relatively preserved in the chemosensitive regions near the ventral and dorsal medullary surfaces. These results show that hypoxia-induced respiratory depression was accompanied by metabolic changes within brain stem regions involved in respiratory and cardiovascular control. Thus it appears that there was significant energy deficiency in the brain stem after hypoxia-induced respiratory depression had occurred.