Maddock R J
Department of Psychiatry, University of California Davis School of Medicine, 95817, USA.
J Neuropsychiatry Clin Neurosci. 2001 Winter;13(1):22-34. doi: 10.1176/jnp.13.1.22.
Panic patients consistently show exaggerated lactic acid response to alkalosis, whether produced by hyperventilation or by sodium lactate infusion. Understanding why this occurs may provide important clues to the pathogenesis of panic disorder. Although brain hypoxia from excessive hypocapnia-induced cerebral vasoconstriction is often cited as the mechanism of elevated brain lactic acid in panic disorder, studies of brain metabolism show that hypocapnia rarely leads to brain hypoxia. Increased lactic acid production is a normal response to intracellular alkalosis and to intracellular cyclic AMP. Thus, other possible mechanisms of the exaggerated lactic acid response in panic disorder include a disturbance of mechanisms regulating intracellular pH and factors increasing intracellular cyclic AMP. Both mechanisms are consistent with the suffocation false alarm theory of panic disorder. This review suggests a theoretical framework for future magnetic resonance spectroscopy studies that can test some of the predictions of these competing models.
惊恐障碍患者对碱中毒的乳酸反应始终表现出过度增强，无论这种碱中毒是由过度通气还是输注乳酸钠引起的。弄清楚为何会出现这种情况，可能为惊恐障碍的发病机制提供重要线索。尽管因过度低碳酸血症引起脑血管收缩导致的脑缺氧常被认为是惊恐障碍中脑乳酸升高的机制，但脑代谢研究表明，低碳酸血症很少导致脑缺氧。乳酸生成增加是对细胞内碱中毒和细胞内环磷酸腺苷（cAMP）的正常反应。因此，惊恐障碍中乳酸反应过度增强的其他可能机制包括调节细胞内pH值机制的紊乱以及增加细胞内环磷酸腺苷的因素。这两种机制均与惊恐障碍的窒息假警报理论相符。本综述为未来的磁共振波谱研究提出了一个理论框架，该研究能够检验这些相互竞争模型的一些预测。
