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PROTOPAM CHLORIDE.

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Atropine↗
PubMed1965

PARATHION POISONING FROM FLANNELETTE SHEETS.

Two small boys were admitted to the Lions Gate Hospital in coma and acute respiratory distress. They improved and the first boy was sent home; after two nights he was back in hospital in a worsened state. Poisoning with organic phosphate was suspected, and after investigation some flannelette sheets were taken from his home for testing. They proved to have been contaminated with parathion ("nerve gas") in the hold of a ship sailing from Antwerp to Vancouver; the parathion had been offloaded in California. The remainder of the sheets were traced. The symptomatology and treatment of organic phosphate ester poisoning and the chemical testing of parathion are discussed.

Atropine↗
PubMed2002

[The activity of blood cholinesterase in rats exposed to dimethypo after drug intervention].

OBJECTIVE: To investigate the activity of ChE in rats poisoned by dimehypo and then treated with pralidoxime methylchloride or unithiol. METHOD: Rats were divided into control group (dimehypo); intervention groups [dimehypo plus pralidoxime methylchloride or dimehypo plus unithiol (sodium dimercaptopropanesulphonate)]. Rats were dosed with 4 different doses of dimehypo: 1/16, 1/8, 1/4 and 1/2 of LD50 respectively(the LD50 of dimehypo is 342 mg/kg). After being poisoned with dimehypo orally, rats were immediately injected intramuscularly with pralidoxime methylchloride or unithiol. The activity of ChE in blood was detected before and 1/2, 1, 2, 4 and 24 h after poisoning in dimehypo and intervention groups. RESULT: The ChE activity of four dose subgroups at 1 h after poisoning were (1.04 +/- 0.21), (0.84 +/- 0.12), (0.71 +/- 0.12), (0.66 +/- 0.07) U/ml respectively; the ChE activity of pralidoxime methylchloride intervention groups were (1.01 +/- 0.18), (1.17 +/- 0.11), (1.01 +/- 0.04), (1.03 +/- 0.12) U/ml respectively; and the ChE activity of unithiol intervention groups were (1.15 +/- 0.15), (1.26 +/- 0.27), (1.08 +/- 0.08), (1.04 +/- 0.12) U/ml respectively. The inhibited ChE in blood was recovered by either treatment with pyraldoxime methylchloride or unithiol. These two drugs had similar effects of recovering the activity of ChE(P > 0.05), but at higher doses(1/4 and 1/2 of LD50) the effects of both were not so good. CONCLUSION: Pralidoxime methylchloride and unithiol could partly recover the activity of ChE inhibited by dimehypo.

Animals↗
PubMed2002

[The neuromuscular transmission effects induced by pralidoxine chloride on rats with acute isocarbophos poisoning].

OBJECTIVE: To study the effects of improving the neuromuscular transmission (NMT), "non-AChE-reactivating effects", by oximes in treating acute isocarbophos poisoning. METHODS: The effect of pralidoxime chloride(PAM-Cl) on the neuromuscular transmission(NMT) in rats exposed to isocarbophos was studied by using the stimulation single fiber electromyography (SSFEMG) to determine the single fiber action potential. RESULTS: After the rats exposed to isocarbophos were treated by PAM-Cl, the mean consecutive difference(MCD) value [(25.99 +/- 5.84) microsecond] of single fiber action potential was significantly lower than that before PAM-Cl treatment [(33.21 +/- 4.09) microsecond, (P < 0.01)], but no AChE reactivation in blood and gastrocnemius was observed. CONCLUSION: PAM-Cl has "non-AChE-reactivating effects", it could markedly improve isocarbophos-induced NMT block of gastrocnemius.

Acute Disease↗
PubMed1992

Inhibition of human brain and RBC acetylcholinesterase (AChE) by heptylphysostigmine (HPTL).

Heptylphysostigmine (HPTL), a derivative of the AChE inhibitor physostigmine (PHY), is under investigation as a therapeutic agent in Alzheimer's disease. HPTL is active against human RBC AChE both in vitro and in vivo. Activity of HPTL against human brain has not been documented. We have developed an in vitro assay system using particulate membrane fractions which permits comparison of inhibition and recovery kinetics of human RBC (primarily globular dimer) and brain (primarily globular tetramer) membrane-bound forms. Under these conditions the HPTLIC50 is similar for the two forms. RBC AChE inhibition spontaneously reverses in 24 h, as occurs in vivo. In striking contrast, activity of inhibited brain enzyme does not recover on overnight incubation. DDVP-induced inhibition, but not HPTL inhibition, can be reversed by the oxime 2-PAM. Some recovery of HPTL inhibition, but not to the level seen with RBC AChE, occurs on addition of heat-stable fractions from serum or CSF. Brain enzyme recovers rapidly from PHY in this system. Responses of brain and RBC AChE to HPTL indicate that these forms are functionally as well as structurally distinct. Since brain inhibition apparently does not spontaneously reverse like RBC inhibition, peripheral measurements of patient responses should be assessed with caution during treatment with HPTL.

Acetylcholinesterase↗
PubMed2004

[In vitro reactivation of acetylcholinesterase inhibition by O-isopropylmethylfluorophosphonate using the bisquarternary oxime, HS-6].

The ability of the oxime HS-6 [1-(4-hydroxyiminomethylpyridinium)-3-(4-carbamoylpyridinium)-2-oxa-propane dichloride] to reactive in vitro the enzyme acetylcholinesterase inhibited by the nerve agent sarin [O-isopropylmethylfluorophosphonate] was evaluated. The reactivators 2-PAM [2-hydroxyiminomethyl-1-methylpyridinium chloride], toxogonin [1,3-bis(4-hydroxyiminomethylpyridinium)-2-oxa-propane dichloride] and H-oxime HI-6 [1-(2-hydroxyiminomethylpyridinium)-3-(4-carbamoylpyridinium)-2-oxa-propane dichloride] were chosen for comparison. The oxime HS-6 was an effective reactivator of sarin-inhibited AChE. It is not as effective as the H-oxime HI-6, but it is better than 2-PAM and obidoxime.

Acetylcholinesterase↗
PubMed1992

High-pressure injection injury involving a 2-PAM chloride autoinjector.

High-pressure injection injuries to the hand are often associated with severe morbidity and should be considered surgical emergencies. The severity of these injuries is usually due to vascular compromise and the inflammatory nature of the material injected, such as paint, grease, and solvents. We present a case of a high-pressure injection of 2-PAM chloride into the finger of a 3-year-old boy. In this case, operative treatment was not necessary and all symptoms resolved.

Accidents, Home↗
PubMed1992

[Experimental studies on the efficacy of PAM against sumithion poisoning].

The efficacy of 2-Pyridine aldoximide methiodide (PAM) for lethal acute poisoning by fenitrothion (FNT) was investigated in mice and dogs. Sumithion (FNT 51.7%, emulsifiers 12.5% and xylol 35.8%) was used as fenitrothion. 1. FNT at 1500 mg/kg was administered orally to mice. After ten minutes 50 mg/kg of PAM was injected once iv, and plasma, erythrocyte, brain, liver and kidney ChE activities were investigated 30 and 60 min later. Recovery in ChE activity was found in every organ but the brain at 30 min, but no efficacy of PAM was observed at 60 min. 2. After administering 1500 mg/kg of FNT orally to mice, the life-saving effect was studied from the changes in mortality due to variation of PAM route, dosage and number of administrations. With oral administration of 1500 mg/kg of FNT, 75 to 85% of the animals died. The mortality ranged from 80 to 95% when the animals received a single intravenous injection of 50 mg/kg of PAM between zero and 60 min following the FNT administration. Thus, a single intravenous administration of PAM at 50 mg/kg showed no life-saving effect on the animals given FNT. However, the mortality was reduced to 45% when the animals received repeated subcutaneous injections of 20 mg/kg of PAM at a 3-hr interval from just after administration of FNT over 24-hr. In other repeated subcutaneous injection experiments, the mortality ranged from about 55 to 65%. In any PAM-treated group, the survival time was prolonged. This life-prolonging effect was more marked in the case of repeated subcutaneous injections of PAM by 12-hr and even more by 24-hr, than in the case of a single intravenous injection. FNT treatment caused marked salivation and watery diarrhea, and PAM clearly inhibited these signs of the muscarinic action of FNT. There was a high relationship between this inhibitory effect of PAM on the muscarinic action and its life-prolonging or life-saving effect. 3. PAM (150 mg/animal/shot, iv) was given 12 or 13 times during 7 hr from 10 min (4 animals), 3 hr (1 animal) and 6 hr (2 animals) after administration of FNT at 150 mg/kg. The effects of PAM on survival, plasma ChE activity, plasma protein (TP) and hematocrit (Ht) values were examined. The 3 dogs given FNT alone all died within 53 hr of administration, whereas 6 out of 7 animals treated with PAM survived.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

[Therapeutic efficacy of pralidoxime chloride on acute dichlorvos poisoning].

OBJECTIVE: To study the therapeutic efficacy and mechanism of oxime drug, pralidoxime chloride (PAM-Cl), on acute dichlorvos (DDV) poisoning. METHODS: The toxic signs and survival rate were recorded and ChE activity in blood was determined in treatment group with PAM-Cl and non-treatment group after DDV was given to rats and mice by gastrogavage; the therapeutic efficacy and reactivation of DDV-inhibited ChE by PAM-Cl were observed on the patients with acute DDV poisoning. RESULTS: (1) The alleviated and delayed toxic signs as well as higher survival rate were found in PAM-Cl treatment group compared with non-treatment group. (2) After the rats were exposed to DDV, the ChE activities of whole blood in different time within 24 h were statistically significantly higher in PAM-Cl treatment group than in non-treatment group (P < 0.05). (3) After PAM-Cl treatment, muscular fasciculation and other nicotinic signs in poisoned patients were disappeared and the inhibited blood ChE activities were gradually reactivated to normal level. CONCLUSION: PAM-Cl has therapeutic efficacy against acute toxicity of DDV through its reactivation of inhibited ChE.

Acute Disease↗