Interaction of diphenhydramine with cholinesterase inhibitors in mice

Mohammad, F. K.; Abdul-Latif, A.R.; Al-Kassim, N. A. H.

doi:10.1016/0378-4274(87)90137-8

Cited by 8 publications

(4 citation statements)

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“…19 In rats, administration of diphenhydramine (1.0 to 3.0 mg/kg [0.45 to 1.36 mg/lb], IV) elicits abnormally increased wakefulness and motor activity and a cocaine-like stimulation pattern of dopamine transmission in the nucleus accumbens. This finding was consistent with the results of other studies 19,20 that involved rodents and chickens.…”

Section: Discussionmentioning

confidence: 99%

Diphenhydramine exposure in dogs: 621 cases (2008–2013)

Worth¹,

Wismer²,

Dorman³

2016

javma

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OBJECTIVE To characterize the signalment, dose response, and clinical signs of diphenhydramine toxicosis in dogs. DESIGN Retrospective case series. ANIMALS 621 dogs with diphenhydramine exposure. PROCEDURES The electronic medical record database for an animal poison control center was reviewed from January 2008 through December 2013 to identify dogs that had ingested or been injected with diphenhydramine. Information extracted from the records and evaluated included the signalment, clinical signs observed, and estimated exposure dose of diphenhydramine. Clinical signs were categorized as none, mild, moderate, and severe. RESULTS The mean ± SEM age of dogs was 3.6 ± 0.1 years (range, 0.1 to 16 years). Diphenhydramine exposure was by ingestion for 581 (93.6%) dogs and injection for 40 (6.4%) dogs. Only 146 (23.5%) dogs developed ≥ 1 clinical signs of toxicosis, the most common of which were associated with the nervous (lethargy, hyperactivity, agitation, hyperthermia, ataxia, tremors, and fasciculations) or cardiovascular (tachycardia) systems, and 3 dogs died. Although the presence and extent of clinical signs varied greatly among dogs, the exposure dose of diphenhydramine was positively associated with the severity of clinical signs in a dose-dependent manner regardless of the route of exposure (ingestion or injection). CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that dogs exposed to diphenhydramine developed clinical signs of toxicosis fairly infrequently, and those clinical signs were generally mild and primarily affected the neurologic and cardiovascular systems. Supportive treatment for diphenhydramine toxicosis should be administered on the basis of the clinical signs observed.

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Section: Discussionmentioning

confidence: 99%

Diphenhydramine exposure in dogs: 621 cases (2008–2013)

Worth¹,

Wismer²,

Dorman³

2016

javma

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“…We have used doses of diphenhydramine up to 20 mg/kg, i. m. in chicks without showing clinically overt adverse effects; and these doses were found to antagonize organophosphate poisoning in Mohammad et al: Neurobehavioral Effects of Diphenhydramine in Chicks chicks (unpublished observations). Similarly, mice or rats can tolerate diphenhydramine up to 30 mg/kg, given intraperitoneally or subcutaneously (Mohammad et al, 1987;1989;Faris and Mohammad, 1996a;Al-Baggou and Mohammad, 1998;. However, the reported LD0 values of diphenhydramine (mg/kg) in rats are 500, orally and 475, subcutaneously, whereas in mice it is 164, orally and 127, subcutaneously (Barnes and Eltherington, 1973).…”

Section: Discussionmentioning

confidence: 99%

“…These doses are much higher than the doses of the drug used in the chicks of the present study. Similarly, doses of diphenhydramine ＞30 mg/kg were reported to produce stimulatory effects in mice or rats (Mohammad et al, 1987;1989;Faris and Mohammad, 1996a;Al-Baggou and Mohammad, 1998). In the present study, the signs of diphenhydramine toxicosis also included excitatory responses.…”

Section: Discussionmentioning

confidence: 99%

“…Diphenhydramine enhances morphine-induced hyperactivity in mice (Sansone et al, 1987) and causes amnesia in mice (Galeotti et al, 2003). Mice or rats pretreated with relatively high protective doses of diphenhydramine (≥30 mg/kg, intraperitoneally or subcutaneously) prior to intoxication with anticholinesterases manifested nervousness, jumping behavior and hyperactivity (Mohammad et al, 1987;1989;Faris and Mohammad, 1996a;. Acute neurotoxic effects of diphenhydramine in mice are characterized by hyperactivity in the open-field test and increased stereotyped behavior of head bobbing, sniffing as well as biting and licking .…”

Section: Introductionmentioning

confidence: 99%

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Acute Toxicity and Neurobehavioral Effects of Diphenhydramine in Chicks

2012

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The present study was undertaken to examine the acute toxicity (LD50) and neurobehavioral manifestations in the open-field activity and tonic immobility tests in 7-14 day-old chicks treated with the H1-receptor antagonist diphenhydramine. Plasma and whole brain cholinesterase activities were also determined in the chicks. The LD50 of diphenhydramine in chicks was 49.3 mg/kg, intramuscularly (i.m.). The signs of diphenhydramine toxicosis in the chicks which appeared within one hour after injection included excitation, jumping, whole body tremor, ataxia, gasping, frequent defecation, paralysis and recumbency. Fifteen minutes after i.m. injection, diphenhydramine at 2.5 and 5 mg/kg decreased the general locomotor activity of the chicks in the 5-min open-field activity test, as seen by a significant increase in the latency to move from the center of the open-field arena and decreases in the numbers of lines crossed and escape jumps in comparison with control values. Diphenhydramine significantly decreased the frequencies of pecking and defecation only at 5 mg/kg when compared with respective control values. Diphenhydramine treatments at 2.5 and 5 mg/kg also significantly increased the durations of tonic immobility of the chicks and decreased their whole brain cholinesterase activity by 33 and 30%, respectively, in comparison with the control values. In conclusion, the data suggest that diphenhydramine induces central nervous system depression in chicks at doses below the LD50 value of the drug which is reported here for the first time.

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