Comparative effects of diazepam and midazolam on paraoxon toxicity in rats*1, *2

Krutak-Krol, H.; Domino, Edward F.

doi:10.1016/0041-008x(85)90425-9

Cited by 31 publications

(7 citation statements)

References 10 publications

(6 reference statements)

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“…SE is diagnosed according to the established criteria of continues seizures for 30 min or longer or several seizures occurring with impairment of consciousness between seizures. 6,7,11,12 Initial SE consists of the first 10-20 min of the epileptic state, during which physiological mechanisms This study aimed to determine the etiology, treatment protocol and outcome of convulsive status epilepticus (SE) in children. An institutional treatment protocol using benzodiazepines (diazepam and midazolam) was assessed in a retrospective case study.…”

Section: Subjects/methodsmentioning

confidence: 99%

Convulsive status epilepticus in children: Etiology, treatment protocol and outcome

Saz

Karapınar

Özçetin

et al. 2011

Seizure

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This study aimed to determine the etiology, treatment protocol and outcome of convulsive status epilepticus (SE) in children. An institutional treatment protocol using benzodiazepines (diazepam and midazolam) was assessed in a retrospective case study. The treatment protocol (Ege Pediatric Status Epilepticus Protocol or EPSEP) was developed based on an operational definition of pediatric SE according to the duration of seizure activity. Pediatric SE is divided into three categories: initial SE (20-30 min), established SE (30-60 min) and refractory SE (>60 min). Eight (30%) of the studied episodes were initial SE, 10 (37%) were established SE, and 9 (33%) were refractory SE. With respect to the etiological spectrum of SE, 11 (40%) children had meningitis or encephalitis. Febrile SE was identified in 7 (26%) patients. Only 2 episodes of initial SE (7.5%) were controlled with first step of the protocol (two concomitant-doses of rectal diazepam). Midazolam bolus and infusions (up to 1.2 μg/kg/min) were used to treat 22 episodes of SE (9 refractory SE, 10 established SE and 3 initial SE). Complete arrest of convulsive SE was achieved in 21 of 22 (95%) episodes with midazolam infusion. We concluded that the combined use of benzodiazepines (diazepam+midazolam) was safe and effective in the treatment of convulsive SE in children.

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Section: Subjects/methodsmentioning

confidence: 99%

Convulsive status epilepticus in children: Etiology, treatment protocol and outcome

Saz

Karapınar

Özçetin

et al. 2011

Seizure

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“…It seems that a more lipophilic antimuscarinic drug would be more effective than atropine (23). Krutak-Krol and Domino (24) found that the atropine dose of 10 mg/kg im is optimal in experimental studies. The minimum absolute lethal dose of OPCs is 1.3 LD 50 (25).…”

Section: Discussionmentioning

confidence: 99%

Dose-Dependency of Toxic Signs and Outcomes of Paraoxon Poisoning in Rats

Maksimović

Škrbić

Stojiljković

2022

Acta Med. (Hradec Kralove, Czech Repub.)

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Organophosphorus compounds induce irreversible inhibition of acetylcholinesterase, which then produces clinically manifested muscarinic, nicotinic and central effects. The aim of the study was to analyse the clinical signs of acute paraoxon poisoning in rats and to determine the relationship between the intensity of signs of poisoning and the dose of paraoxon and/or the outcome of poisoning in rats. Animals were treated with either saline or atropine (10 mg/kg intramuscularly). The median subcutaneous lethal dose (LD50) of paraoxon was 0.33 mg/kg and protective ratio of atropine was 2.73. The presence and intensity of signs of poisoning in rats (dyspnoea, lacrimation, exophthalmos, fasciculations, tremor, ataxia, seizures, piloerection, stereotypic movements) were observed and recorded for 4 h after the injection of paraoxon. Intensity of these toxic phenomena was evaluated as: 0 – absent, 1 – mild/moderate, 2 – severe. Fasciculations, seizures and tremor were more intense at higher doses of paraoxon and in non-survivors. In unprotected rats piloerection occurred more often and was more intense at higher doses of paraoxon as well as in non-survivors. In atropine-protected rats, piloerection did not correlate with paraoxon dose or outcome of poisoning. The intensity of fasciculations and seizures were very strong prognostic parameters of the poisoning severity.

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“…Moreover, a dose of 100 mg/kg was significantly less effective than the dose of 10 mg/kg. 25 Repeated lower doses of atropine over time might potentially give better results. 26 The presence, time of occurrence and intensity of paraoxon poisoning signs were examined.…”

Section: B) Survivalmentioning

confidence: 99%

Onset rate and intensity of signs of organophosphate poisoning related to paraoxon dose and survival in rats

Maksimović¹,

Duka²,

Bednarčuk³

et al. 2021

Scripta Medica

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Introduction: Oganophosphorus compounds (OP) bind to acetylcholinesterase (AChE) and inactivate it. In the synaptic cleft, undestroyed and accumulated acetylcholine produce the acute cholinergic effects. The aim of this study was to determine the frequency, speed of onset and intensity of certain signs of paraoxon poisoning depending on dose and outcome of poisoning. Methods: The study was conducted in adult Wistar rats. The median lethal dose (LD50) of paraoxon as well as protective ratio (PR) of atropine (10 mg/kg intramuscularly) was determined. Clinical signs of poisoning were observed: fasciculations, tremor, seizures, ataxia, piloerection, lacrimation, exophthalmos, bizzare/stereotypic behaviour and dyspnoea. The time from paraoxon injection to the first appearance of the sign of poisoning was recorded as well as the intensity of poisoning with evaluation at 10 time intervals throughout the 4 h observational period. Results: The LD50 of paraoxon was 0.33 mg/kg (subcutaneously) and PR of atropine was 2.73. Dose-dependent, piloerection occurred more often (p = 0.009) and at higher intensity (p = 0.016) at higher doses. Fasciculations, tremor, seizures and ataxia occurred significantly earlier at higher doses of paraoxon (p = 0.015, 0.002, 0.021 and 0.016, respectively), as well as the intensity of seizure, tremor and fasciculation. Piloerection (p = 0.002) and seizures occurred more frequently (p = 0.009) in non-survivors. Fasciculations, tremor, seizures and ataxia occurred significantly earlier and at higher intensity in non-survivors (p < 0.001, for all parameters), as well as dyspnoea (p = 0.009 and p = 0.048). In atropine-protected rats, nicotinic effects persevered, so they were the prognostic parameter of the severity of the poisoning. Conclusion: Seizures and fasciculations followed by tremor were strong prognostic parameters of the probability of lethal outcome of paraoxon poisoning. Also, the mentioned poisoning signs were with their intensity and speed of occurrence in a clear positive correlation with the administered dose of paraoxon. Even at high doses of paraoxon, atropine blocked the muscarinic (but not nicotinic) effects and somewhat mitigated the CNS toxic effects.

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Comparative effects of diazepam and midazolam on paraoxon toxicity in rats1, 2

Cited by 31 publications

References 10 publications

Convulsive status epilepticus in children: Etiology, treatment protocol and outcome

Convulsive status epilepticus in children: Etiology, treatment protocol and outcome

Dose-Dependency of Toxic Signs and Outcomes of Paraoxon Poisoning in Rats

Onset rate and intensity of signs of organophosphate poisoning related to paraoxon dose and survival in rats

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