Protection by physostigmine against the pressor effect of soman in the rat

McGee, John; Brezenoff, Henry E.

doi:10.1016/0024-3205(87)90557-1

Cited by 6 publications

(3 citation statements)

References 6 publications

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“…It is known that the action of an irreversible inhibitor on AChE can be prevented by a reversible inhibitor (Harris et al, 1978;Van Meter et al, 1978;Yamada et al, 1983;McGee & Brezenoff, 1987). The irreversible action of soman on bladder neurones was also prevented by pretreatment with pyridostigmine.…”

Section: Soman-induced Depression Ofmuscarinic Responsementioning

confidence: 99%

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Action of an irreversible acetylcholine esterase inhibitor, soman, on muscarinic hyperpolarization in cat bladder parasympathetic ganglia

Kumamoto

Shinnick‐Gallagher

1990

British J Pharmacology

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1 Intracellular recording techniques were used to examine the action of an irreversible acetylcholine esterase (AChE) inhibitor, soman, on the hyperpolarizations mediated through muscarinic cholinoceptors in cat bladder parasympathetic neurones. 2 Soman (0.1-10gM) depressed the amplitude and prolonged the duration of the muscarinic slow inhibitory postsynaptic potential (s-i.p.s.p.) elicited by a preganglionic tetanus (40 Hz for 1 s) in the presence of mecamylamine (20pum), phentolamine (1 pM) and caffeine (1 mM), in a dose-dependent manner. The effect of soman on the amplitude of the s-i.p.s.p. was partially reversible, while the effect on the duration was irreversible. 3 Soman hyperpolarized the membrane and decreased input resistance, but this effect could not account for soman-induced inhibition of the s-i.p.s.p. 4 Soman depressed the amplitude and prolonged the duration of a muscarinic hyperpolarization induced by pressure application of acetylcholine (ACh) in the presence of mecamylamine, phentolamine and caffeine. The time course of this effect paralleled that on the synaptically-evoked muscarinic s-i.p.s.p. S A reversible AChE inhibitor, pyridostigmine (10-100gM), also depressed the amplitude and prolonged the duration of a muscarinic hyperpolarization induced by either preganglionic stimulation or ACh pressure application. These actions were reversible, and not accompanied by a significant change in membrane potential or input resistance.6 The inhibitory action of soman (1 yM) on the muscarinic hyperpolarization was prevented by pyridostigmine (1OgM), but not by atropine (1 pM).7 These results demonstrate that soman prolongs not only the muscarinic hyperpolarization, but also inhibits its amplitude through a postsynaptic action, probably through AChE inhibition, in cat bladder parasympathetic neurones.

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Section: Soman-induced Depression Ofmuscarinic Responsementioning

confidence: 99%

“…It is known that the action of an irreversible inhibitor on AChE can be prevented by a reversible inhibitor (Harris et al, 1978;Van Meter et al, 1978;Yamada et al, 1983;McGee & Brezenoff, 1987 (Klein et al, 1979). Feigenbaum & El-Fakahany (1984) (Yamada et al, 1983) and soman (Churchill et al, 1984).…”

Section: Soman-induced Depression Ofmuscarinic Responsementioning

confidence: 99%

Action of an irreversible acetylcholine esterase inhibitor, soman, on muscarinic hyperpolarization in cat bladder parasympathetic ganglia

Kumamoto

Shinnick‐Gallagher

1990

British J Pharmacology

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“…The toxic effects of organophosphates, such as soman, are mediated through a hyperactivity of the cholinergic nervous system. Soman also has effects on the circulation (Stewart & McKay 1961;Kentera et a1 1982;Brezenoff et a1 1984;Maxwell et a1 1987;McGee & Brezenoff 1987;Scremin et a1 1991). A soman-induced pressor response was elicited at 60-70% inhibition of acetylcholinesterase activity (AChE) in brain stem and hypothalamus, and was suggested to be centrally mediated (Brezenoff et a1 1984;McGee & Brezenoff 1987).…”

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confidence: 99%

The Protective Effect of Nimodipine, a Calcium Antagonist, and Its Influence on Soman Clearance in the Anaesthetized Rabbit

Karlsson

Fredriksson

Sellström

et al. 1994

Journal of Pharmacy and Pharmacology

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The effect of pretreatment with a vasoactive compound, nimodipine, on soman intoxication in peripheral organs of rabbits was studied by measuring changes in the cholinesterase and acetylcholinesterase activity and by measuring clearance of soman in blood using gas chromatography/high resolution mass spectrometry. In animals receiving soman only, initial blood concentrations were approximately 100 ng mL-1 and were still detectable after 5 min. The clearance rate of soman in blood markedly increased following nimodipine pretreatment such that soman was below the detection limit (0.002-0.003 ng mL-1) in all samples. Soman injection caused a significant inhibition of the acetylcholinesterase activity in serum, and in brain. In rabbits pretreated with nimodipine, no significant inhibition of acetylcholinesterase activity occurred after soman injection. In view of the effects of nimodipine on soman clearance and on the acetylcholinesterase and cholinesterase inhibition during soman intoxication, we suggest that nimodipine has profound circulatory effects, which during soman intoxication, increase the vascular perfusion through the body and thereby increase the detoxifying capacity.

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Cerebral blood flow and metabolism in soman-induced convulsions

Shih

Scremin

1992

Brain Research Bulletin

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Protection by physostigmine against the pressor effect of soman in the rat

Cited by 6 publications

References 6 publications

Action of an irreversible acetylcholine esterase inhibitor, soman, on muscarinic hyperpolarization in cat bladder parasympathetic ganglia

Action of an irreversible acetylcholine esterase inhibitor, soman, on muscarinic hyperpolarization in cat bladder parasympathetic ganglia

The Protective Effect of Nimodipine, a Calcium Antagonist, and Its Influence on Soman Clearance in the Anaesthetized Rabbit

Cerebral blood flow and metabolism in soman-induced convulsions

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