Anesthetic Doses Of Ketamine Research Articles

KETAMINE CATALEPSY AND ANESTHESIA IN DOGS PRETREATED WITH ANTISEROTONERGIC OR ANTIDOPAMINERGIC NEUROLEPTICS OR WITH ANTICHOLINERGIC AGENTS

Summary Pretreatment with methiothepin or chlorpromazine prevents catalepsy, prolongs duration of anesthesia and recovery, prevents apneustic respiration, and favors disappearance of limb-withdrawal and jaw reflexes in dogs injected intramuscularly with a minimum anesthetic dose of ketamine. These effects relate to degree of sedation produced by the neuroleptics, and therefore may be nonspecific. A subsedative dose of pimozide antagonizes ketamine anesthesia and potentiates catalepsy, respiratory apneusis, and emergent delirium. Sedative doses of pimozide are less effective in these regards. Mecamylamine enhances ketamine catalepsy and respiratory apneusis, and lightens (but does not shorten) anesthesia. Atropine prevents ketamine catalepsy and antagonizes respiratory apneusis, but potentiates muscle jerking, prolongs recovery time, and greatly prolongs emergent delirium. The results seem to implicate dopaminergic, nicotinic cholinoceptive, and muscarinic cholinoceptive mechanisms in a complex system of mediation and modulation of canine responses to ketamine. This system is different from one previously proposed for the cat. Weingarten (1972) postulated that ketamine catalepsy might be due to stimulation of the monoaminergic component of a balanced cholinergic-monoaminergic system in the brain. In rabbits, the anticholinergic agent procyclidine enhanced ketamine catalepsy ( Authier & others, 1972 ). In cats, the antiserotonergic neuroleptic agent methiothepin ( Monachon & others, 1972 ) prevented ketamine catalepsy, but pimozide 9an antidopaminergic neuroleptic, Anden & others, 1970 ) and chlorpromazine 9a neuroleptic of mixed antimonoamine activity) did not affect ketamine catalepsy ( Hatch, 1973 ). Thus, it appeared that ketamine catalepsy may indeed relate to a cholinergic-monoaminergic imbalance, and that the monoamine of interest in this regard might be serotonin. The purpose of the present study was to examine the validity of the proposed cholinergic-serotonergic mechanism of ketamine catalepsy in dogs. This species is particularly susceptible to the cataleptic and deliriant effects of ketamine.

PREVENTION OF KETAMINE CATALEPSY AND ENHANCEMENT OF KETAMINE ANESTHESIA IN CATS PRETREATED WITH METHIOTHEPIN

Summary Cats pretreated with methiothepin and then injected intramuscularly with a minimum anesthetic dose of ketamine become anesthetized sooner, sleep longer, and take longer to recover than control animals. Instead of muscle tonus and limb rigidity, muscle flaccidity is seen. Limb-withdrawal and jaw reflexes disappear. Respiration loses its irregular, apneustic character. These effects are dose-dependent and are not produced by a sedative dose of chlorpromazine or pimozide. Pimozide prevents the sporadic stimulus-induced paw twitching typical of ketamine, but neither methiothepin nor chlorpromazine do this. The results suggest serotonergic mechanisms may function to partly offset or adapt to the depressant effects of ketamine, to mediate ketamine catalepsy, and to produce respiratory irregularity and apneusis. Stimulus-induced muscle twitching due to ketamine may be a dopaminergic phenomenon.

Prevention of ketamine catalepsy and enhancement of ketamine anesthesia in cats pretreated with methiothepin

Summary Cats pretreated with methiothepin and then injected intramuscularly with a minimum anesthetic dose of ketamine become anesthetized sooner, sleep longer, and take longer to recover than control animals. Instead of muscle tonus and limb rigidity, muscle flaccidity is seen. Limb-withdrawal and jaw reflexes disappear. Respiration loses its irregular, apneustic character. These effects are dose-dependent and are not produced by a sedative dose of chlorpromazine or pimozide. Pimozide prevents the sporadic stimulus-induced paw twitching typical of ketamine, but neither methiothepin nor chlorpromazine do this. The results suggest serotonergic mechanisms may function to partly offset or adapt to the depressant effects of ketamine, to mediate ketamine catalepsy, and to produce respiratory irregularity and apneusis. Stimulus-induced muscle twitching due to ketamine may be a dopaminergic phenomenon.