attack intensity were not affected by the drug. In discussion of the experiment the authors mention that the baseline panic attack frequency and disability scores were significantly higher in the antagonist than in placebo group. The authors suggest several explanations to the unexpectedly poor response to L-365,260. Like Bradwejns group, they mention unclear locus of action of this CCK-B antagonists, and therefore possibility of inadequate distribution of L-365,260 to the appropriate regions. Secondly the measured 1-hour plasma levels might have been insufficient for blockage of endogenous panic attacks, though they proved to be adequate for blockage of CCK-4 induced panic attacks. The study shows that at the particular dose of 120 mg/day L-365,260 did not prove to be clinically useful in relieving panic attacks, but the outcome of the higher doses could have been different. Also, the through levels of the drug were not measured in the study. It is worth mentioning that Westenberg and den Boer in their review article on panic disorder treatments noticed that in Balenger study that Kramer and co-authors used as the guideline, alprazepam proved to be clinically effective in much higher doses than it was used for General Anxiety disorder9. It is also not known whether CCK-4 is the main component of endogenous panic attack, to what stage of its development it contributes and how it interacts with other neurotransmitter. Future prospectsEight years has passed since De Montegny proved CCK-4 to possess anxiogenic qualities in humans. Its panicogenic effect is replicated in the studies described in this review, and now CCK-4 is a proven panic-inducing agent, along with sodium lactate, carbon dioxide and yohimbine. It satisfies four out of seven criteria for an ideal panicogenic agent, and therefore can serve an extremely useful tool in investigation of panic disorder.3 Besides being of great help to researchers, the potential useful...
