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An animal model of nicotinic-acid-induced vasodilation: effect of haloperidol, caffeine and nicotine upon nicotinic acid response

Authors
Journal
Schizophrenia Research
0920-9964
Publisher
Elsevier
Publication Date
Volume
50
Issue
3
Identifiers
DOI: 10.1016/s0920-9964(00)00082-7
Keywords
  • Caffeine
  • Neuroleptic
  • Nicotine
  • Nicotinic Acid
  • Schizophrenia
  • Vasodilation

Abstract

Abstract Background: The normal vasodilatory response to ingestion of nicotinic acid (NA) is impaired in some patients with schizophrenia. It is unclear whether the impairment is a feature of the disorder itself or to a confounding factor such as neuroleptics, caffeine or nicotine use. Methods: To address this question in a controlled manner, we have developed an animal (rat) model of NA-induced vasodilation, in which response is monitored by measuring change in skin temperature. Results: We observed that (i) acute administration of acetylsalicylic acid (100 mg/kg), caffeine (2.5 mg/kg) and haloperidol (0.1 or 0.5 mg/kg) and (ii) chronic administration of haloperidol (0.2 mg/kg/day) significantly inhibited NA (30 mg/kg) response, whereas neither acute (0.25 mg/kg) or chronic (0.5 mg/kg/day for 14 days) administration of nicotine, or chronic administration of caffeine (5 mg/kg/day for 14 days) had any significant effect upon NA response. Conclusions: Our data suggest that at least one drug commonly used to treat schizophrenia (haloperidol) can interfere with the vasodilatory response to NA. Studies using non-medicated patients with schizophrenia are required to determine whether reduced vasodilatory response to NA in schizophrenia is a feature of the disorder or a consequence of treatment.

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