Hypothermic Action of Chlorpromazine in Monkeys

Chai, C. Y.; Fann, Y.D.; Lin, Mao Tsun

doi:10.1111/j.1476-5381.1976.tb07654.x

Cited by 18 publications

(5 citation statements)

References 24 publications

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“…The representative central nervous system depressant chlorpromazine showed no effect on respiratory function, in spite of causing CNS depressive signs such as reduction in spontaneous locomotor activity. Chai et al (1976) also reported no change in respiration even after administering chlorpromazine to Taiwan monkeys (Macaca cyclopsis, a congeneric species with cynomolgus monkeys) at 2 mg/kg, i.v. No respiratory side-effects with chlorpromazine have been noted in the pharmacology literature (Baldessarini, 1996).…”

Section: Discussionmentioning

confidence: 99%

Measurement of respiratory function using whole-body plethysmography in unanesthetized and unrestrained nonhuman primates

et al. 2010

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-Extended term, continuous measurement and observation of drug responses were performed to examine the feasibility of a custom-made whole-body plethysmograph for measuring respiratory function in unanesthetized, unrestrained monkeys. Using this apparatus, respiratory function (respiration rate, tidal volume, and minute volume) was observed for 23 hr in unanesthetized, unrestrained cynomolgus monkeys (Macaca fascicularis). The respiration rate, tidal volume, and minute volume in the light period (7:00 to 19:00) reached approximately 30% to 50% higher values than in the dark period (19:00 to 7:00), thus clearly exhibiting circadian variation in the cynomolgus monkey respiratory functions. Administration of morphine (10 mg/kg, s.c.) resulted in sustained reduction in tidal volume and minute volume, and ketamine (30 mg/kg [sub-anesthetic dose], i.m.) also produced sustained reduction in respiration rate, tidal volume, and minute volume. With dimorpholamine (1 mg/kg, i.v.) or caffeine (10 mg/kg, s.c.), respiration rate, tidal volume, and minute volume increased. Physiological saline (1 ml/kg, s.c. and 0.1 ml/ kg, i.v.) and chlorpromazine (10 mg/kg, s.c.) produced no clear-cut changes in respiration rate, tidal volume, or minute volume. From the above results, we conclude that our custom-made whole-body plethysmograph is useful for measuring respiratory function in unanesthetized and unrestrained monkeys.

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Section: Discussionmentioning

confidence: 99%

Measurement of respiratory function using whole-body plethysmography in unanesthetized and unrestrained nonhuman primates

et al. 2010

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“…Other reported effects include reduced action of serotonin, 9 α‐adrenergic blockade, inhibition of acetylcholinesterase, and a weak antihistamine effect 8 . Phenothiazines can cause arterial hypotension generally attributed to vasodilation, 10,11 hypothermia due to depletion of catecholamines in the hypothalamus, 12,13 and decreased PCV and hemoglobin concentration potentially due to splenic sequestration of red blood cells 8 . Frequently administered phenothiazines used in dogs include ACE (as an anxiolytic and sedative) and chlorpromazine (as an antiemetic).…”

Section: Discussionmentioning

confidence: 99%

Administration of acepromazine maleate to 31 dogs with a history of seizures

McConnell¹,

Kirby²,

Rudloff³

2007

J Vet Emergen Crit Care

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Objective: To retrospectively evaluate the incidence of seizures in dogs presenting with a history of seizures that were treated with acepromazine (ACE) during hospitalization. Design: Retrospective study. Setting: Privately owned emergency and referral hospital. Animals: Thirty‐one client‐owned dogs. Interventions: Administration of ACE. Measurements and main results: The medical records from dogs with an acute or chronic seizure history that received ACE were reviewed. Factors evaluated included presenting complaint, seizure history, ACE dosage, duration of observation, seizure activity, and other medications used. Thirty‐one dogs qualified for the study: 20 males and 11 females. Age range was 3 months to 14.9 years. Presenting complaint was seizure in 28/31 dogs. There was a prior history of seizures in 22/31 dogs, and 15/22 were currently on antiseizure medication. ACE was given 1–5 times per dog. Mean ACE dose was 0.029 mg/kg IV (range: 0.008–0.057 mg/kg; n=46), 0.036 mg/kg IM (range: 0.017–0.059 mg/kg; n=14), 0.53 mg/kg PO (n=2). Twenty‐seven dogs did not seizure after administration of ACE within the observation period (mean: 16.4 hours, range: 0.25–66 hours). Twenty‐five dogs received antiseizure medication before ACE. Eight seizure episodes occurred in 4 dogs (all of whom presented for seizures) within 0.3–10 hours after ACE administration. Conclusions: There was no observed correlation between ACE administration in dogs with a seizure history and the recurrence of seizure activity during hospitalization. The time from ACE administration to seizure activity was greater than expected for measurable effects to be seen in 1 dog (10 hour). Further studies with a larger group and alternative ACE doses are needed to more thoroughly evaluate the safety of short‐term ACE use in dogs with a seizure history.

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“…Recent evidence has suggested that the temperature regulating system may include central nervous structures other than POAH, e.g., medulla oblongata and spinal cord (Hellon, 1971;Chai & Lin, 1973;Lin & Chai, 1974;Simon, 1974). Indeed, two distinct structures in the brain stem, namely, the POAH and medulla oblongata, have been found responsible for the Cpz 6 hypothermia (Chai et aL, 1976). Furthermore, present results also showed a dose-dependent hypothermia in response to the direct injections of Cpz into third or fourth cerebral ventricle.…”

Section: Discussionmentioning

confidence: 99%

“…They discovered that systemic administration of N-methyl Cpz (a quarternary analogue of Cpz), a substance which supposedly has difficulty penetrating the blood-brain barrier, also produces hypothermia. On the other hand, direct injection of this drug (Cpz) into the preoptic anterior hypothalamus (POAH) has been shown to produce dose-dependent hypothermia in monkeys (Chai, Fann & Lin, 1976) and in hamsters (Reigle & Wolf, 1971). …”

Section: Introductionmentioning

confidence: 99%

The Enhancement of Chlorpromazine‐induced Hypothermia by Lesions in the Anterior Hypothalamus

Chai

Lin

1977

British J Pharmacology

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I Administration of chlorpromazine (Cpz), either systemically or centrally, to unanaesthetized rats at an environmental temperature of 230C caused dose-dependent hypothermia. 2 In order to achieve equivalent hypothermia, intraventricular administration required a total dose of 20 1tg Cpz and intraperitoneal administration a dose of 9.7 mg/kg body weight. Accordingly, the doseratio between intraventricular and intraperitoneal administration was 1 to 110. Cpz apparently exerts its hypothermic effect by acting directly on central nervous structures rather than through peripheral sites. 3 Cpz-induced hypothermia was potentiated by preoptic anterior hypothalamic (POAH) lesions but not by lesions of the ventromedial nucleus (VMN) of the hypothalamus. It was found that Cpz induced hypothermia most readily in rats with large POAH lesions (-10.40C), less so in rats with spinal lesions (-5.5°C) at least with control rats (-2.9°C).

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Hypothermic Action of Chlorpromazine in Monkeys

Cited by 18 publications

References 24 publications

Measurement of respiratory function using whole-body plethysmography in unanesthetized and unrestrained nonhuman primates

Measurement of respiratory function using whole-body plethysmography in unanesthetized and unrestrained nonhuman primates

Administration of acepromazine maleate to 31 dogs with a history of seizures

The Enhancement of Chlorpromazine‐induced Hypothermia by Lesions in the Anterior Hypothalamus

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