PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PRALIDOXIME COMPOUNDS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources
PubMed1975

Organophosphates--a pediatric hazard.

These agents act as anticholinesterases. Signs of toxicity are: overactivity of the parasympathetic nervous system, nausea, vomiting, diarrhea, sweating, abdominal cramps and copious secretions. Large doses may cause sustained depolarization of the motor end plate, leading to muscular paralysis. Death may ensue from respiratory failure. The extensive and often careless use of insecticides, fungicides and pesticides makes organophosphates a particular pediatric hazard. Atropine and pralidoxime chloride are effective for therapy.

Accidents↗
PubMed1975

Alteration in calcium metabolism as a mechanism for pyridine aldoxime methochloride (2-PAM) cardiac action in rabbit atria.

Pyridine aldoxime methochloride (2-PAM) increased the force of contraction of stimulated rabbit left atria in vitro. The threshold concentration was 2.3 times 10- minus 3 M whereas 9.2 times 10- minus 2 M produced the absolute maximum increase in tension of 83%. Pretreatment of rabbits with reserpine (2.5 mg/kg/day for 3 days) had no significant influence on the positive inotropic action of 2-PAM. In addition, propranolol (10- minus 8 and 10- minus 6 M) had no effect. Time to peak tension and the time to complete relaxation during each contraction cycle was significantly prolonged. 2-PAM increased the isometric tension developed by isolated aortic strips. The maximum tension developed by the control aortas to 2-PAM was 1.54 plus or minus 0.17 g and after 10- minus 6 M phentolamine, it remained 1.46 plus or minus 0.19 g. The rate of tension decline of stimulated atria was increased in the presence of 2-PAM from 49.7 plus or minus 2.40 to 28.50 plus or minus 1.32 seconds when the atria were placed in a low calcium (Ca)-containing Ringer's solution (0.24 mM CaCl2). When the bathing medium was changed from a low Ca (0.24 mM CaCl2) Ringer's back to normal Ca (2.4 mM CaCl2) Ringers solution, 2-PAM had no influence on the rate of recovery of the initial tension response of the atria. The 34-Ca uptake and efflux studies demonstrated that 2-PAM had no influence on the inward movement of Ca through the membrane but increased the rate of efflux during the phase II process. 2-PAM depressed the rate of uptake of 45-Ca by the isolated rabbit sarcoplasmic reticulum. The T1/2 for the control uptake was 1.80 plus or minus 0.07 minutes and in the presence of 2-PAM (2 times 10- minus 2, 5 times 10- minus 2, 1 times 10- minus 1 M) the T1/2 was increased to 4.50 plus or minus 0.22, 7.20 plus or minus 0.36 and 11.6 plus or minus 0.44 minutes, respectively. It is concluded from these studies that 2-PAM has a positive inotropic effect on isolated rabbit atria which is probably not related to the autonomic nervous system. The evidence obtained strongly suggests that the mechanism of the positive inotropic action is related to the effect of 2-PAM on the homeostasis of intracellular Ca storage sites.

Animals↗
PubMed1975

Presynaptic effects of neuromuscular cholinesterase inhibition.

Paraoxon, an irreversible organophosphorus inhibitor of cholinesterase, produces a myopathy beginning at the neuromuscular junction in rat diaphragm muscles. Thirty minutes after paraoxon was injected i.p. (0.5 mg/kg), neuromuscular cholinesterase activity was reduced to 36% of control. The frequency of miniature end-plate potentials (MEPPs) in diaphragms from paraoxon-treated rats was 109/sec compared with 2.9/sec in saline-injected controls. The faster frequency was seen after paraoxon gradually declined to control rates within 6 hours after injection. The quantum content of end-plate potentials was reduced to 66% of that seen in saline controls. Spontaneous and impulse-related antidromic activity was observed along the phrenic nerve after paraoxon which also gradually diminished with time. When the phosphorylated acetylcholinesterase was reactivated with 10(-3) pyridine-2-aldoxime methiodide, MEPP frequency was reduced significantly and antidromic activity was abolished. Block of axonal excitability with 10(-6) M tetrodotoxin reduces the effects of paraoxon on MEPP frequency and antidromic activity, while acetylcholinesterase remains inhibited. In vitro perfusion with 6 times 10(-8) M paraoxon increases MEPP frequency and initiates antidromic activity. It is concluded that inhibition of neuromuscular cholinesterase by paraoxon leads to an alteration of transmitter release, and this may be associated with ultrastructural abnormalities observed at the motor endplate.

Action Potentials↗
PubMed2002

[Experimental treatment of respiratory failure caused by omethoate poisoning in rats].

OBJECTIVE: To examine the therapeutic effect of combined use of pralidoxime-Cl and atropine with artificial ventilation on respiratory muscle paralysis caused by omethoate poisoning in rats. METHODS: Rats were administered with same doses of 2LD(50) omethoate and then treated with atropine (10 mg/kg) to resist effectively chlolinergic symptoms. When the rats had slow respiratory frequency and breathed with difficulty, the trachea was intubated and artificial ventilation was carried out (except for group A). The rats in group B were continuously treated with atropine. The doses of pralidoxime-Cl for group C, D and E were 15 mg/kg, 20 mg/kg and 40 mg/kg respectively, given at the same time as artificial ventilation and 1, 2 and 3 hours later. The dose of atropine was reduced to 1/3 to 2/3 of the first dose so as to maintain the rats atropinized. If the rat survived beyond 60 minutes after withdrawal of artificial ventilation, the combined treatment was considered successful. The function of isolated phrenic diaphragm of the rats was observed with MS-302 analyses instrument physiologically and pharmacologically. RESULTS: None of the rats in group B successfully withdraw from artificial ventilation. The rats in group C all successfully withdraw from artificial ventilation in 3 hours and the function of the isolated phrenic muscle remained good. The survival rats in group D and E were very low after withdrawal, even though the function of isolated phrenic muscle was good. CONCLUSIONS: The therapeutic effect of the combined use of suitable dose of pralidoxime-Cl and atropine with artificial ventilation on respiratory muscle paralysis caused by omethoate poisoning in rats was significant. This measure can facilitate reversal of the function of poisoned diaphragm and reduced the death rate in poisoned rats.

Animals↗
PubMed1992

Clinical, biochemical, electrophysiologic, and histologic assessment of chlorpyrifos induced delayed neuropathy in the cat.

The ability of a supralethal dose of chlorpyrifos to produce delayed neuropathy was examined using assessments of clinical signs, electromyography (EMG), motor nerve conduction velocity (MNCV), lymphocyte neuropathy target esterase activity (LNTE), and histologic changes in nervous system tissues. Cats were exposed to a single, im injection of corn oil (vehicle control), DFP (positive control) at 5.0 mg/kg, or chlorpyrifos at 300 mg/kg and observed for 60 days. Atropine and 2-PAM were administered to chlorpyrifos exposed cats one to two times a day for 14 to 24 days in response to the appearance of cholinergic signs. Anorectic cats during the acute toxicosis were force fed by hand and hydration was maintained by administering fluids sc. Onset of ataxia (mean +/- SD) for the positive control and chlorpyrifos exposed cats were 16.2 +/- 1.8 days (range of 14-19 days) and 19.0 +/- 1.4 days (range of 17-21 days), respectively. Functional deficits for both groups were confined to the hindlimbs and characterized by a crouched-waddling gait, hypermetria, and proprioceptive deficits. Maximal inhibition of LNTE activity was 96% at 24 hr postdosing in the positive control group and 46% at 7 days postdosing in the chlorpyrifos group. No EMG or MNCV abnormalities were detected in any of the treatment groups. Axonal degeneration was similar for the positive control and chlorpyrifos exposed cats. Ascending tracts of the cervical spinal cord and descending tracts of the thoracic and lumbar spinal cord were most severely affected and peripheral nerves were only mildly affected. The clinical and histologic effects produced indicate that chlorpyrifos can cause delayed neuropathy in the domestic cat. The moderate but prolonged inhibition of LNTE produced by chlorpyrifos is atypical of classic organophosphorus delayed neurotoxicants.

Animals↗