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At least 199 records · Page 11Linked to original sources
PubMed1987

Carbamate poisoning: the 'other' insecticide.

A 16-month-old child who ingested rat poison, according to her parents, was noted to have signs of cholinergic poisoning. In the emergency department, the child was intubated and given atropine via the endotracheal tube until venous access was established. Phytonadione (vitamin K) and pralidoxime (2-PAM) were also administered. The child recovered after an uneventful hospital course. The toxic agent was determined to be a carbamate insecticide, for which treatment with pralidoxime is considered controversial. Treatment of cholinergic poisoning due to unknown or mixed agents and poisoning caused by known carbamate insecticides are discussed.

Antidotes↗
PubMed2000

[Comparison on effects between concentrated-dose and non-concentrated-dose pralidoxime chloride on respiratory muscle paralysis in acute organophosphorus pesticide poisoning].

OBJECTIVE: To compare the effects between concentrated-dose and non-concentrated-dose pralidoxime chloride on respiratory muscle paralysis(RMP) in acute organophosphorus pesticide poisoning(AOPP). METHODS: 76 cases of RMP due to AOPP were involved in a retrospective study. All the patients were poisoned through ingestion. According to the administered dose of pralidoxime chloride within the first three days after the onset, the patients were divided into two groups: Group A consisted 30 patients; they were given pralidoxime chloride 10.0-25.8 grams (with an average of 11.4 grams) everyday in the first three days after the onset. Group B included 46 patients; the dose of pralidoxime chloride used daily in the first three days ranged from 3.3 to 8.6 grams (average 6.3). RESULTS: The curative rate and the death rate in group A were 73.3% and 26.7% respectively, while those in group B were 21.7% and 78.3% respectively. The curative rate in group A was significantly higher than that in group B (chi 2 = 19.83, P < 0.005). CONCLUSION: Concentrated-dose pralidoxime chloride was more effective than non-concentrated-dose for patients with RMP due to AOPP and this kind of administration could remarkably improve the prognosis in such patients.

Adolescent↗
PubMedDate not supplied

Severe organophosphate poisoning complicated by alcohol and turpentine ingestion.

A 52-year-old comatose white male was admitted to the hospital with what was later learned to be severe poisoning by a turpentine solution of dicrotophos, an organophosphorous insecticide he had ingested while drunk. The patient was treated effectively with atropine and pralidoxime chloride and required the largest doses of both agents reported to data. The case was complicated by difficulty in evaluating the response to therapy because of the effects of alcohol and turpentine. The patient was discharged from the hospital on the thirty-third day with no apparent sequelae.

Alcoholic Intoxication↗
PubMed1989

Preventable acute organophosphate poisoning deaths.

Poisoning with cholinesterase inhibiting insecticides such as organophosphates (OP) is a major health problem in Sri Lanka, with over 10,000 hospital admissions and over 1,000 hospital deaths annually. Atropine and pralidoxime are the most useful antidotes in the treatment of OP poisoning. Three cases of fatal OP poisoning are described where although the initial diagnosis and therapy were correct, patients did not survive due to inadequate atropine therapy. The need for continuous monitoring and administering adequate doses of atropine in OP poisoning for several days is stressed.

Acute Disease↗
PubMedDate not supplied

The effect of pralidoxime chloride in the assay of acetylcholinesterase using 5,5'-dithio-bis(2-nitrobenzoic acid) (Ellman's reagent).

Pralidoxime chloride (PAM) hydrolyzes acetylthiocholine, the substrate used in the assay of red cell cholinesterase. The thiocholine that is produced forms a yellow complex when Ellman's reagent is used in the assay. This was tested in blood samples of patients who were treated with PAM after organophosphorus (OP) poisoning and after the observation of an immediate increase in absorption of light at 412 nm.

Acetylcholinesterase↗
PubMed1988

Effects of organophosphorus agents on sarcoplasmic reticulum in skinned skeletal muscle fibers.

These experiments were designed to determine whether skinned skeletal muscle fibers could be useful in screening new antidotes to organophosphorus poisons. Isometric force and fiber diameter were measured in mechanically skinned fibers from mice and frogs. Fibers were depleted of calcium and placed in a calcium loading solution that contained 0.5 mM EGTA with pCa 6.25. The elapsed time (zero time) before a contracture began and the maximum rate of force development (slope) were measured and divided by the square of the diameter (normalized zero time, normalized slope). The zero time was assumed to be the time required for the sarcoplasmic reticulum to attain a threshold concentration for calcium-induced calcium release, and the slope was assumed to indicate primarily the rapidity of the release of calcium from the sarcoplasmic reticulum. Organophosphorus agents, sarin, soman, tabun, and VX were also placed in the loading solutions. Only sarin failed to shorten the normalized zero times of mouse fibers compared to controls, and all agents decreased the normalized slopes. The normalized zero times of frog fibers were not altered by the agents, but the normalized slopes were altered by some agents. Pralidoxime chloride (PAM) and 3-Cl-2,5,6-trimethylbenzoic acid (TBA) were also added to the loading solution for mouse fibers; PAM was marginally effective in moderating some actions of the organophosphates. Because the effects of the agents on the fibers were so definite, we concluded that the skinned muscle fiber might indeed be useful as a screening tool for developing and testing new antidotes to organophosphorus poisons.

Animals↗
PubMed1992

Protection against the effects of anticholinesterases on the latencies of action potentials in mouse skeletal muscles.

1. Adult male albino mice were injected subcutaneously with an organophosphorous anticholinesterase to initiate excessive variability in the latency of indirectly elicited muscle action potentials (jitter) when assessed 5 days later. 2. Pretreatment of the mice with a single dose of pyridostigmine prevented the development of jitter after subsequent dosing with an organophosphate. 3. Treatment with one dose of pralidoxime (2PAM) prevented the development of jitter if given less than 1 h after treatment with ecothiopate, a reactivatable inhibitor of cholinesterase. Similar treatment with 2PAM after a non-reactivatable inhibitor did not prevent the development of jitter. The repeated administration of 2PAM over 12 h did ameliorate jitter. 4. Pretreatment of mice orally with alpha-tocopherol and N-acetylcysteine, known to prevent ecothiopate-induced myopathy, did not prevent the development of jitter after ecothiopate. 5. It is concluded that the development of jitter was a consequence of the inhibition of acetylcholinesterase, and although jitter did not develop acutely, the potential for the full development of jitter was achieved about 1 h after intoxication with ecothiopate. The development of jitter did not involve the generation of free radicals. Reduction of the early effects of intoxication with anticholinesterases by pyridostigmine or 2PAM prevented the development of jitter.

Acetylcholinesterase↗
PubMed2004

Ultrastructural changes in rat liver treated with pralidoxime following acute organophosphate poisoning.

We investigated the ultrastructural effects of methamidophos and the positive effects of 2-pralidoxime (2-PAM) on the liver. Male Wistar-albino rats were assigned to 4 groups and all were treated per os: Group 1 (n=10) received 30 mg/kg methamidophos; Group 2 (n=7) (serving as controls for Group 1) received physiologic NaCl; Group 3 (n=10) received 30 mg/kg methamidophos and was treated with 2-PAM and atropine when cholinergic symptoms were noted; and Group 4 (n=7) (serving as controls for Group 3) was treated with physiologic NaCl. Plasma cholinesterase was measured using radioimmunoassay. Liver tissues were prepared for electron microscopic studies. Methamidophos treatment of Group 1 led to serious changes in hepatocytes and organelles. These changes were not detected in Group 3. In Group 1, the chromatin content of some hepatocyte nuclei and cytoplasmic density increased; these cells also became vacuolar in appearance as a result of lysis in the mitochondrial matrices. In some cells, the lipid content constituted the majority of the cytoplasm. Furthermore, these cells were surrounded by glycogen accumulation. In some areas of the perisinusoidal zone, collagen fibers had increased to form bands. None of these changes were noted in Group 3. These findings suggest that acute organophosphate poisoning causes serious histopathological effects in rat liver, but that these changes are reversible with appropriate treatment strategies.

Acute Disease↗
PubMed2004

[Three cases of organophosphate poisoning treated with pralidoxime iodide and whole-bowel irrigation].

We encountered three cases of organophosphate poisoning treated with pralidoxime iodide (PAM) and whole-bowel irrigation without atropine sulfate. All patients recovered without persistence or recurrence of toxic symptoms and without any somatic after effects. In case 1, a 48-year-old woman ingested approximately 5 g of ethylthiometon in a suicide attempt. She was transferred to the hospital because of cardiopulmonary arrest. After resuscitation, she was transferred to our center. She was placed on a ventilator and received i.v. PAM and polyethylene glycol-electrolyte through a nasojejunal tube for whole-bowel irrigation. Six days later, serum ChE was improved. In case 2, a 51-year-old man ingested approximately 30 g of malathion in a suicide attempt and was transferred to our center because of dyspnea. He was treated with PAM and whole-bowel irrigation, but did not require a respirator. Serum ChE already showed improvement the following day. In case 3, a 31-year-old man ingested approximately 50 g of DEP in a suicide attempt and was transferred to our center because of unconsciousness. He was treated with a respirator, PAM and whole-bowel irrigation. Serum ChE improved within two days. These cases suggest the possibility that preferential whole-bowel irrigation without atropine sulfate prevents the persistence or recurrence of the toxic effects of organophosphate.

Adult↗
PubMedDate not supplied

Protective agents in acute high-dose organophosphate exposure: comparison of ranitidine with pralidoxime in rats.

Weak and reversible inhibitors of cholinesterase, when coadministred in excess with a more potent inhibitor such as organophosphates, can act in a protective manner. Ranitidine (RAN) is a clinically widely used histamine type 2 (H2) receptor blocker. Ranitidine is also the most potent inhibitor of acetylcholinesterase among H2 blockers (inhibitory constant K in the low micromolar range) but roughly three orders of magnitude less potent than paraoxon. This study evaluates RAN-conferred protection in acute high-dose organophosphate (paraoxon, POX) exposure in rats in direct comparison with the therapeutic gold-standard pralidoxime (PRX). Group 1 received 1 microM POX, group 2 received 50 microM RAN, group 3 received 50 microM PRX, group 4 received 1 microM POX + 50 microM RAN and group 5 received 1 microM POX + 50 microM PRX. All substances were applied intraperitoneally. The animals were monitored for 48 h and mortality was recorded at 30 min and 1, 2, 3, 4, 24 and 48 h. Blood was taken for red blood cell acetylcholinesterase (RBC-AChE) measurements at baseline, 30 min and 24 and 48 h. Mortality occurred mainly in the fi rst 30 min after POX administration, with minimal changes occurring thereafter. Mortality (in %) at 30 min in groups 1, 4 and 5 was 52 +/- 18, 37 +/- 20 and 17 +/- 18, respectively, and mortality at 48 h was 59 +/- 12, 39 +/- 20 and 28 +/- 20, respectively. The RBC-AChE activities (in % of baseline values) at 30 min in groups 1, 4 and 5 were 18 +/- 16, 47 +/- 23 and 48 +/- 20, respectively. At 24 h the values were 46 +/- 16, 65 +/- 24 and 86 +/- 17, respectively, and at 48 h the values were 71 +/- 19, 78 +/- 21 and 110 +/- 27, respectively. Coadministration of PRX significantly decreases mortality in the described model at all points in time. Coadministration of RAN statistically significantly decreases mortality at 24 and 48 h. The extent of protection conferred by RAN is less (but not statistically significantly so) than that conferred by the gold-standard PRX. Coadministration of PRX statistically significantly increases RBC-AChE activities in the described model at all points in time. Ranitidine confers a statistically significant protection for the enzyme at 30 min only. We conclude that RAN is potentially of clinical use in reducing mortality in acute high-dose organophosphate exposure. Further studies involving different organophosphates and dosages, as well as different animal species, will be needed both to con fi rm these initial findings and to address the issue of the optimal timing for RAN preadministration.

Animals↗