Several methods to experimentally induce panic cause profound acid-base disturbances. Evidence suggests that CO(2) inhalations, lactate infusions and, to a certain extent, voluntary hyperventilation can conceivably lead to a common scenario of brain acidosis in the face of disparate intravascular pH alterations. The importance of this event is reflected in data that support a model in which experimental panic attacks, as proxy to those occurring spontaneously, constitute a response to acute brain acidosis. Given that central CO(2)/H(+) chemoreception is an important drive for ventilation, and many chemosensitive neurons are related to respiration and arousal, this model can explain much of the connection between panic and respiration. We propose that the shared characteristics of CO(2)/H(+) sensing neurons overlap to a point where threatening disturbances in brain pH homeostasis, such as those produced by CO(2) inhalations, elicit a primal emotion that can range from breathlessness to panic.
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