An atropine and glycopyrrolate combination reduces mortality in organophosphate poisoning

Arendse, R.; Irusen, E M

doi:10.1177/0960327109350666

Cited by 24 publications

(17 citation statements)

References 11 publications

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“…Atropine can cause a range of doserelated adverse effects 50 . It crosses the BBB easily and central signs of atropine toxicity are common complications in humans treated with high doses 3 . The very high doses necessary to treat aldicarb poisoning effectively in dogs may result in neurological complications such as drowsiness, ataxia, seizures and respiratory depression.…”

Section: Atropine Sulphatementioning

confidence: 99%

“…Glycopyrrolate Glycopyrrolate could be considered as an alternative drug to atropine for the treatment of aldicarb toxicity 6,33 , or it could also be used in combination with atropine 3 . It is a quaternary ammonium anti-muscarinic agent 33 and is registered for use in dogs and cats as a pre-anaesthetic agent to treat sinus bradycardia, sino-atrial arrest and incomplete atrioventricular (AV) block 50 .…”

Section: Atropine Sulphatementioning

confidence: 99%

“…This may be used to advantage in those patients showing signs of atropine toxicity. A combination of atropine and glycopyrrolate has been used in the treatment of human cases of organophosphate toxicity 3 . The canine LD50 of glycopyrrolate is 25 mg/kg after IV administration 50 .…”

Section: Atropine Sulphatementioning

confidence: 99%

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Treatment rationale for dogs poisoned with aldicarb (carbamate pesticide) : clinical review

Arnot¹,

Veale²,

Steyl³

et al. 2011

J. S. Afr. Vet. Assoc.

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The treatment rationale for dogs poisoned by aldicarb is reviewed from a pharmacological perspective. The illegal use of aldicarb to maliciously poison dogs is a major problem in some parts of the world. In South Africa, it is probably the most common canine poisoning treated by companion animal veterinarians. Aldicarb poisoning is an emergency and veterinarians need to be able to diagnose it and start with effective treatment immediately to ensure a reasonable prognosis. Successful treatment depends on the timely use of an anti-muscarinic drug (e.g. atropine). Additional supportive treatment options, including fluid therapy, diphenhydramine, benzodiazepines and the prevention of further absorption (activated charcoal) should also be considered. Possible complications after treatment are also briefly discussed.

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Section: Atropine Sulphatementioning

confidence: 99%

Section: Atropine Sulphatementioning

confidence: 99%

See 1 more Smart Citation

Treatment rationale for dogs poisoned with aldicarb (carbamate pesticide) : clinical review

Arnot¹,

Veale²,

Steyl³

et al. 2011

J. S. Afr. Vet. Assoc.

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show abstract

“…Atropine has the potential to cause central toxicity which may complicate the management of cardiomyopathy (11). It has been reported that atropine may cause aspiration pneumonia through induction of the swallowing disorder and inhibition of the cough reflex (12), and it is associated with a higher incidence of a transient rash (13).…”

Section: Introductionmentioning

confidence: 99%

E-cadherin and 5-HT alterations in the heart of rats having undergone atropine-induced toxicity

Huang

Liu

2011

Mol Med Report

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Abstract. Atropine-induced heart damage is associated with changes in the expression of various enzymes and proteins. The purpose of this study was to investigate atropine-induced alterations in cardiac E-cadherin and 5-hydroxytryptamine (5-HT) after atropine administration. Male Wistar rats were randomly divided into two groups: a control group and an atropine group. The atropine group intraperitoneally received atropine at a single dose of 15 mg/kg for 7 days; the controls received the same amount of saline via the same route. On Day 8, the rats were anesthetized, and a thoracotomy was performed in all animals. Immunohistochemical analysis was performed to evaluate protein expression of E-cadherin and 5-HT. Sections were analyzed by digital image analysis. Cardiac protein expression of E-cadherin and 5-HT was altered after atropine-induced toxicity in the rat. The expression levels of E-cadherin and 5-HT were significantly decreased after atropine treatment, supported by IOD analysis, when compared with the control (P<0.05). The current findings indicate that such changes would be reflected in abnormal cardiac function, and these proteins may be useful for revealing the mechanisms underlying atropine-induced toxicity and may also provide various clues for further research.

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“…1 Atropine, a frequently used anticholinergic drug in eye clinic, was reported to have adverse effects on human eyes. 7,8 However, little has been known about the effect of atropine on the cornea. In order to provide a reference for secure medication of atropine, the present study was intended to evaluate the cytotoxicity of atropine to HCE cells using an in vitro model of non-transfected HCE cells, verify the cytotoxicity using an in vivo model of cat corneas, and clarify its possible cellular and molecular cytotoxic mechanisms in vitro.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity of atropine to human corneal endothelial cells by inducing mitochondrion-dependent apoptosis

Wen

Fan

Tian

2016

Exp Biol Med (Maywood)

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Atropine, a widely used topical anticholinergic drug, might have adverse effects on human corneas in vivo. However, its cytotoxic effect on human corneal endothelium (HCE) and its possible mechanisms are unclear. Here, we investigated the cytotoxicity of atropine and its underlying cellular and molecular mechanisms using an in vitro model of HCE cells and verified the cytotoxicity using cat corneal endothelium (CCE) in vivo. Our results showed that atropine at concentrations above 0.3125 g/L could induce abnormal morphology and viability decline in a dose-and time-dependent manner in vitro. The cytotoxicity of atropine was proven by the induced density decrease and abnormality of morphology and ultrastructure of CCE cells in vivo. Meanwhile, atropine could also induce dose-and time-dependent elevation of plasma membrane permeability, G1 phase arrest, phosphatidylserine externalization, DNA fragmentation, and apoptotic body formation of HCE cells. Moreover, 2.5 g/L atropine could also induce caspase-2/-3/-9 activation, mitochondrial transmembrane potential disruption, downregulation of anti-apoptotic Bcl-2 and BclxL, upregulation of pro-apoptotic Bax and Bad, and upregulation of cytoplasmic cytochrome c and apoptosis-inducing factor. In conclusion, atropine above 1/128 of its clinical therapeutic dosage has a dose-and time-dependent cytotoxicity to HCE cells in vitro which is confirmed by CCE cells in vivo, and its cytotoxicity is achieved by inducing HCE cell apoptosis via a death receptormediated mitochondrion-dependent signaling pathway. Our findings provide new insights into the cytotoxicity and apoptosisinducing effect of atropine which should be used with great caution in eye clinic.

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An atropine and glycopyrrolate combination reduces mortality in organophosphate poisoning

Cited by 24 publications

References 11 publications

Treatment rationale for dogs poisoned with aldicarb (carbamate pesticide) : clinical review

Treatment rationale for dogs poisoned with aldicarb (carbamate pesticide) : clinical review

E-cadherin and 5-HT alterations in the heart of rats having undergone atropine-induced toxicity

Cytotoxicity of atropine to human corneal endothelial cells by inducing mitochondrion-dependent apoptosis

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