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Biomedical subjects

J W Smudski

Publications and source records attributed to J W Smudski.

8 recordsLinked to original sources
PubMed1979

Diphenylhydantoin induced gingival hyperplasia in ferrets: a precautionary note.

Diphenylhydantoin appears to modify the tissue response in ferrets to a gingival irritant. In the present study, ferrets were tested for the tissue response to a local irritant in their maxillary right quadrant, while their maxillary left quadrant was the control. A low incidence of hyperplasia was induced only in irritated gingival tissue of animals receiving DPH. The problems encountered in comparing the hyperplasia produced in ferrets and humans were also discussed.

Animals↗
PubMed1977

Lidocaine's influence on the accumulation and depletion rates of mouse brain amines.

Mouse brain was analyzed for serotonin, norepinephrine, and dopamine. Pargyline plus lidocaine treatment caused an increased accumulation rate of serotonin over one hour compared to pargyline controls. alpha Methyl-p-tyrosine plus lidocaine treatment caused a decreased depletion rate of dopamine over four hours compared to rates of alpha methyl-p-tyrosine controls, and no difference for norepinephrine.

Animals↗
PubMedDate not supplied

Effects of short-term and long-term administration of procaine hydrochloride and mepivacaine hydrochloride on hexobarbital-induced sleeping times in mice.

Investigations were performed to determine the effects of short-and long-term pretreatment with procaine and mepivacaine on hexobarbital-induced sleeping times in mice. It was found that short-term preadministration with procaine (40 mg/kg) and mepivacine (40 and 60 mg/kg) significantly increased hexobarbital-induced sleeping time, but long-term pretreatment had no effect.

Animals↗
PubMedDate not supplied

Lidocaine's influence on brain amines in mice.

This series of experiments suggests that a relationship exists between convulsive doses of lidocaine and central depletion of 5-HT and DA. Since DA and usually 5-HT are regarded as central inhibitory transmitters, this study further supports the postulate that lidocaine's convulsive activity is by inhibition of central inhibitory pathways-possibly a dopaminergic or tryptaminergic pathway or both.

Animals↗