Autonomic responses of blood vessels and sweat glands in patients with schizophrenia treated with olanzapine or clozapine

Citation
M. Mueck-weymann et al., Autonomic responses of blood vessels and sweat glands in patients with schizophrenia treated with olanzapine or clozapine, PSYCHOPHAR, 157(4), 2001, pp. 368-372
Citations number
10
Categorie Soggetti
Neurosciences & Behavoir
Journal title
Volume
157
Issue
4
Year of publication
2001
Pages
368 - 372
Database
ISI
SICI code
Abstract
Rationale: Data comparing, the in vivo effects on autonomic nervous system function of standard clinical doses of olanzapine and clozapine are sparse. Objective: The coal of this study was to compare the skin conductance resp onse (which is peripherally mediated via muscarinic m(3)-receptors) and the inspiratory gasp response (which is peripherally mediated via adrenergic r eceptors) between healthy controls and schizophrenics treated with clozapin e or olanzapine. Methods: Twenty patients with schizophrenia (according to DSM-III-R criteria) treated with either clozapine (200-500 mg/day) or olanz apine (10-20 mg/day) as well as ten matched controls underwent simultaneous recordings of the skin conductance response (SCR) of sweat glands and of t he inspiratory gasp response (IGR) of acral blood vessels. A single, deep i nspiration was used as the stimulus. Group differences for the SCR amplitud es and the post-IGR redilation times were compared using the Mann-Whitney t est. Results: Both clozapine- and olanzapine-treated patients showed a sign ificant SCR reduction compared to controls. Interestingly, the reduction in SCR was significantly larger in the clozapine croup compared to the olanza pine group (P <0.05). Moreover, only clozapine-treated patients showed a st atistical trend towards a longer IGR redilation time compared to controls. Conclusion: The significantly stronger SCR reduction amongst clozapine-trea ted compared to olanzapine-treated patients suggests that olanzapine at a s tandard clinical dose exhibits a significantly smaller anticholinergic effe ct at peripheral m(3)-receptors in vivo compared to clozapine. The prolonga tion of IGR redilation can be explained by a prolonged release of noradrena line due to the alpha (2)-antagonistic effect of clozapine.