Effect of sweet almond oil on survival rate and plasma cholinesterase activity of aluminum phosphide-intoxicated rats

2011 ◽  
Vol 31 (5) ◽  
pp. 518-522 ◽  
Author(s):  
Hossein Saidi ◽  
Shayan Shojaie
Keyword(s):  
Survival Rate ◽  
Cholinesterase Activity ◽  
Plasma Cholinesterase ◽  
Control Group ◽  
Aluminum Phosphide ◽  
Time Intervals ◽  
Almond Oil ◽  
Plasma Cholinesterase Activity ◽  
Reduction Of Mortality ◽  
Sweet Almond

Introduction: Aluminum phosphide (ALP), as an effective pesticide and a substance used for protecting rice during storage, has become one of the commonest causes of poisoning and even suicide in developing countries including Iran and India. The authors aimed to study the efficacy of sweet almond oil as an antidote in ALP toxicity. Methods: The present experimental study was conducted over 35 rats. The animals were divided into four groups: one group as the control group and three other groups which received ALP alone or ALP and sweet almond oil with different time intervals. In addition to estimating the survival rate of the animals, plasma cholinesterase activity as a possible factor affected in ALP poisoning was evaluated. Results: Treatment by intragastric irrigation of sweet almond oil resulted in significant reduction of mortality. Moreover, mean plasma cholinesterase levels were inhibited in groups receiving ALP. Conclusion: Oral sweet almond oil, if especially used immediately after poisoning with ALP, improves the survival rate.

Potentiation of Mivacurium Blockade by Low Dose of Pancuronium

2003 ◽  
Vol 98 (5) ◽  
pp. 1057-1062 ◽  
Author(s):  
Cyrus Motamed ◽  
Riad Menad ◽  
Robert Farinotti ◽  
Krassen Kirov ◽  
Xavier Combes ◽  
...  
Keyword(s):  
Acetylcholine Receptors ◽  
Low Dose ◽  
Cholinesterase Activity ◽  
Plasma Concentrations ◽  
Orotracheal Intubation ◽  
Plasma Cholinesterase ◽  
Neuromuscular Blocking ◽  
Pharmacokinetic Analysis ◽  
Plasma Cholinesterase Activity ◽  
Before And After

Background Mivacurium is potentiated by pancuronium to a much greater extent than other relaxants. In a previous investigation we suggested that this potentiation could be due to the ability of pancuronium to inhibit plasma cholinesterase activity, but we did not measure plasma concentrations of mivacurium. In the current study we performed a pharmacokinetic analysis by measuring the plasma concentration of mivacurium when preceded by administration of a low dose of pancuronium. Methods After induction of general anesthesia with propofol and fentanyl and orotracheal intubation, 10 patients (pancuronium-mivacurium group) received 15 microg/kg pancuronium followed 3 min later by 0.1 mg/kg mivacurium, whereas 10 other patients (mivacurium group) received saline followed by 0.13 mg/kg mivacurium 3 min later. Plasma cholinesterase activity was measured before and 3 and 30 min after pancuronium dosing in the pancuronium-mivacurium group and was measured before and after administration of saline in the mivacurium group. Arterial plasma concentrations of mivacurium and its metabolites were measured at 0.5, 1, 1.5, 2, 4, 10, 20, and 30 min after injection. Neuromuscular blockade was assessed by mechanomyography. Results Plasma cholinesterase activity decreased by 26% in the pancuronium-mivacurium group 3 min after injection of pancuronium (P < 0.01) and returned to baseline values 30 min later; however, no significant variation was observed in the mivacurium group. The clearances of the two most active isomers (Cis-Trans and Trans-Trans) were lower in the pancuronium-mivacurium group (17.6 +/- 5.1, 14.7 +/- 5.3 ml. min-1. kg-1, respectively) than in the mivacurium group (32.4 +/- 20.2, 24.8 +/- 13.5 ml. min-1. kg-1; P < 0.05). Conclusions A subparalyzing dose of pancuronium decreased plasma cholinesterase activity and the clearance of the two most active isomers of mivacurium. Pancuronium potentiates mivacurium more than other neuromuscular blocking agents because, in addition to its occupancy of postsynaptic acetylcholine receptors, it slows down the hydrolysis of mivacurium.

Acceleration of Plasma Cholinesterase Activity by Quaternary Ammonium Salts

Science ◽  
1958 ◽  
Vol 128 (3315) ◽  
pp. 92-93 ◽  
Author(s):  
E. G. ERDOS ◽  
F. F. FOLDES ◽  
E. K. ZSIGMOND ◽  
N. BAART ◽  
J. A. ZWARTZ
Keyword(s):  
Quaternary Ammonium ◽  
Cholinesterase Activity ◽  
Plasma Cholinesterase ◽  
Quaternary Ammonium Salts ◽  
Ammonium Salts ◽  
Plasma Cholinesterase Activity

Management of Methomyl Poisoning

1990 ◽  
Vol 9 (4) ◽  
pp. 251-254 ◽  
Author(s):  
J. Martinez-Chuecos ◽  
F. Molinero-Somolinos ◽  
J. Solé-Violàn ◽  
R. Rubio-Sanz
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Total Dose ◽  
Activated Charcoal ◽  
Cholinesterase Activity ◽  
Gastric Lavage ◽  
Plasma Cholinesterase ◽  
Acute Stage ◽  
Plasma Cholinesterase Activity ◽  
Small Doses

Eleven patients who suffered methomyl poisoning were admitted to the intensive care unit. All of them showed cholinergic symptoms similar to that produced by organophosphate insecticides but of lesser intensity. Plasma cholinesterase activity was normal in four patients and moderately lower in the remainder (always above 32%). All of the patients showed miosis and none presented with bradycardia. No complications were detected in the acute stage or on further examination a month later. The treatment applied was: (1) gastric lavage or washing the skin; (2) the administration of activated charcoal; (3) small doses of atropine according to symptoms (average of total dose 4.3 mg). All of the patients recovered within 24-48 h. In conclusion, we can assume that methomyl poisoning does not produce serious complications if moderate surveillance is assumed. Only small doses of atropine are required to counteract symptoms.

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