Respiratory patterning following cerebral ventricular administration of cocaine

Intravenous (IV) cocaine in the conscious cat causes extreme tachypnea and reduction in breath-to-breath variability. In this study, we examined respiratory patterning following administration of cocaine into the cerebral ventricles. Intraventricular cocaine elicited a tachypnea that was nearly identical to that for IV cocaine. At the high dose, peak respiratory rate increased by 380%. Breath-to-breath variability was dramatically reduced by cocaine, especially in the early stages of the intoxication; during these stages, the tachypnea was occasionally interrupted by prolonged inspiratory efforts. Procaine was administered as a control for the anestetic effects of cocaine and caused an initial tachypnea that was similar to that for cocaine. For both cocaine and procaine, the mean ratios of inspiratory to expiratory durations were unaffected, indicating that the tachypnea was accomplished by approximately equal reductions in inspiratory and expiratory durations. We conclude that the tachypnea following cocaine administration results principally from central rather than peripheral mechanism. In addition, the data suggest that anesthetic actions mediate the principal respiratory effects of cocaine.