Brain pH response to hyperventilation in panic disorder: preliminary evidence for altered acid-base regulation.
Brain pH response to hyperventilation in panic disorder: preliminary evidence for altered acid-base regulation.
复制标题
恐慌症中过度换气的大脑 pH 反应：酸碱调节改变的初步证据。
DOI：
10.1176/ajp.2006.163.4.710
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Dager,StephenR
中科院分区：
文献类型：
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作者：
Friedman,SethD;Mathis,CMark;Hayes,Cecil;Renshaw,Perry;Dager,StephenR
目的先前发现过度通气期间惊恐障碍患者脑乳酸过多和呼气末二氧化碳 (pCO2) 恢复延迟，表明酸碱调节发生了改变。提出了两个模型来解释这些结果：1）患有恐慌症的受试者表现出对过度换气更严重的碱中毒，这意味着乳酸增加是直接补偿，或2）患有恐慌症的受试者表现出碱中毒减少或减弱，这意味着乳酸增加是对正常 pH 反应的过度补偿。在这两种模型中，惊恐障碍受试者的 pCO2 恢复延迟可能反映了恢复阶段 pH 正常化速度较慢。方法对患有惊恐障碍的无症状用药患者在调节性过度通气期间进行了研究。每 2 分钟使用磷光谱法测量一次大脑 pH 值。将 9 名惊恐障碍受试者与 11 名健康受试者在基线（5 次扫描）、调节过度通气期间（5 次扫描）和恢复期间（10 次扫描）进行比较。焦虑症状采用标准评分进行评估。结果没有受试者在过度换气之前出现惊恐发作。患有恐慌症的受试者在过度换气期间的 pCO2 较低，而在过度换气后的时间间隔内 pCO2 恢复较慢。尽管惊恐障碍组的呼吸反应不同，但在过度换气期间，大脑 pH 值的增加并没有显着增加，在过度换气期间，pH 值恢复到基线的速度也没有减慢。从健康受试者的数据得出的线性回归模型显示，惊恐障碍组的 pH 值减弱。 结论 尽管惊恐障碍受试者在过度通气期间有更严重的低碳酸血症，但他们观察到的 pH 反应与比较水平相比没有改变，这表明缓冲过度。有人认为乳酸增加可以解释这些发现。
ObjectivePrevious findings of excess brain lactate and delayed end-tidal CO2(pCO2) recovery in subjects with panic disorder during hyperventilation suggested altered acid-base regulation. Two models were posited to explain these results: 1) subjects with panic disorder demonstrate greater alkalosis to hyperventilation, implicating increased lactate as directly compensatory, or 2) subjects with panic disorder demonstrate reduced or blunted alkalosis, implicating increased lactate as overly compensatory to a normal pH response. In both models, delayed pCO2recovery in subjects with panic disorder could reflect slower pH normalization in the recovery phase.MethodAsymptomatic medicated patients with panic disorder were studied during regulated hyperventilation. Phosphorous spectroscopy was used to measure brain pH every 2 minutes. Nine subjects with panic disorder were compared to 11 healthy subjects at baseline (five scans), during regulated hyperventilation (five scans), and across recovery (10 scans). Anxiety symptoms were assessed with standard ratings.ResultsNo subject had a panic attack before hyperventilation. Subjects with panic disorder had lower pCO2during hyperventilation and slower pCO2recovery across the posthyperventilation interval. Despite this different respiratory response in the panic disorder group, brain pH increases were not significantly greater during hyperventilation, nor was pH return to baseline slowed during posthyperventilation. A linear regression model derived from data of healthy subjects showed pH blunting in the panic disorder group.ConclusionsAlthough subjects with panic disorder had greater hypocapnea during hyperventilation, their observed pH response, not altered from comparison levels, implicated exaggerated buffering. It is suggested that increased lactate could account for these findings.