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Featured researches published by I. A. Chaudhry.


Naunyn-schmiedebergs Archives of Pharmacology | 1987

Modulation of stimulation-evoked release of newly formed acetylcholine from mouse hemidiaphragm preparation

G.T. Somogyi; E. S. Vizi; I. A. Chaudhry; H. Nagashima; Deryck Duncalf; Francis F. Foldes; Paul L. Goldiner

SummaryA radioisotope method has been developed for measuring the stimulation-evoked release of acetylcholine without the use of cholinesterase inhibitors from the mouse hemidiaphragm preparation which had been loaded with 3H-choline. Evidence has been obtained that 3H-choline was taken up by and released from both innervated and non-innervated mouse hemidiaphragm preparations. However, it was released in the form of 3H-acetylcholine in response to electrical field stimulation only from the innervated preparations. Long lasting (51 min) S1 stimulation of the preparations exhausted the radioactive acetylcholine stores to the extent that S2 did not evoke any release of 3H. These data suggest that when the labelled acetylcholine stores become exhausted, the labelled choline, still present in the tissue, cannot be released by electrical stimulation. Tetrodotoxin (1 μmol/1) administration and Ca withdrawal inhibited, 20–100 μmol/l 4-aminopyridine enhanced the release of 3H-acetylcholine in response to electrical stimulation. Activation of the presynaptic muscarinic receptors by the agonist oxotremorine (50 μmol/l) decreased the liberation of 3H-acetylcholine. The muscarinic antagonist atropine (1 μmol/l) abolished the inhibitory effect of oxotremorine and by itself increased the evoked release of the newly formed 3H-acetylcholine. Adenosine (50 μgmol/l) reduced the evoked release of radioactivity. Theophylline (30 μmol/l) prevented the inhibitory effect of adenosine and itself enhanced the release. Xylazine (1 μmol/l), an alpha2-adrenoceptor agonist did not affect the release. It is concluded that the stimulation-evoked release of 3H-acetylcholine from the mouse phrenic nerve hemidiaphragm preparation preloaded with 3H-choline is derived from the motor nerves. The release of acetylcholine is modulated by activation of presynaptic muscarinic and adenosine receptors.


Journal of The Autonomic Nervous System | 1987

Direct evidence that pancuronium and gallamine enhance the release of norepinephrine from the atrial sympathetic nerve by inhibiting prejunctional muscarinic receptors

Osamu Kobayashi; H. Nagashima; Deryck Duncalf; I. A. Chaudhry; Laszlo G. Harsing; Francis F. Foldes; Paul L. Goldiner; E.Sylvester Vizi

The effect of different non-depolarizing muscle relaxants (gallamine, pancuronium, vecuronium, D-tubocurarine) on [3H]norepinephrine release in response to electrical stimulation was studied in isolated guinea-pig atrium. High pressure liquid chromatography combined with electrochemical and radiochemical detection revealed that the released radioactivity was mainly in the form of [3H]norepinephrine release. Oxotremorine, a pure muscarinic agonist, reduced the release of tritium. Gallamine and pancuronium, like atropine, prevented the inhibitory effect of oxotremorine. D-Tubocurarine and vecuronium had no such effect. These findings indicate that gallamine and pancuronium exert a presynaptic antimuscarinic, atropine-like effect, by inhibiting muscarinic receptors located on the axon terminals of sympathetic neurons thereby enhancing norepinephrine release. It is suggested that this phenomenon might play some role in tachycardia observed during surgical anaesthesia when gallamine or pancuronium have been administered.


Acta Anaesthesiologica Scandinavica | 2003

A new short-acting non-depolarizing muscle relaxant (SZ1677) without cardiovascular side-effects

E. S. Vizi; Z. Tuba; S. Mahó; Francis F. Foldes; O. Nagano; M. Dóda; S. Takagi; I. A. Chaudhry; A. J. Saubermann; H. Nagashima

Background:  In order to facilitate rapid tracheal intubation, the development of a rapid onset, short duration, non‐depolarizing muscle relaxant without cardiovascular side‐effects would be a significant accomplishment in the field of anesthesiology. The aim of the present study was to test the action of a new non‐depolarizing muscle relaxant (SZ1677) on neuromuscular transmission, muscarinic (M2, M3) receptors and cardiovascular reactions and to compare it with clinically used muscle relaxants.


Neurochemistry International | 1989

Effects of LF-14, THA and physostigmine in rat hippocampus and cerebral cortex.

P.E. Potter; S. Nitta; I. A. Chaudhry; I. Lalezari; Paul L. Goldiner; Francis F. Foldes

The effects of physostigmine, tetrahydroaminoacridine (THA) and LF-14 [3,3-dimethyl-1(4- amino-3-pyridyl)urea], a 3,4-diaminopyridine derivative, were compared on inhibition of acetyl- cholinesterase (AChE) activity, and release of [(3)H]acetylcholine (ACh) from rat brain cortical and hippocampal slices. All three compounds caused a concentration dependent inhibition of AChE, with an order of potency physostigmine > THA >LF-14. The electrically stimulated release of ACh from hippocampal and cortical slices was decreased by 10(?5)M physostigmine, although the effect was significant only in cortex. THA (5 x 10(5)M) caused a slight, but not significant, decrease in ACh release from both tissues. In contrast, LF-14 (5 x 10(?5) M) caused an approx. 3-fold enhancement of stimulated release. When AChE was inhibited by prior addition of physostigmine, THA caused only a slight enhancement of ACh release, whereas LF-14 greatly increased release. ACh release was also reduced by stimulation of presynaptic muscarinic receptors with oxotremorine. In this case, THA had no effect on ACh release, while LF-14 was able to reverse the inhibition. This study suggests that LF-14 acts to promote ACh release through blocking K(+) channels, and has a less potent AChE inhibitory effect. It is possible that a compound like LF-14 could be useful in treating diseases of cholinergic dysfunction such as Alzheimers disease, by both promoting the release of ACh and inhibiting its breakdown.


Anesthesiology | 1989

Inhibition of Mobilization of Acetylcholine

Francis F. Foldes; I. A. Chaudhry; M. Kinjo; H. Nagashima

The authors have demonstrated earlier, by direct measurement of acetylcholine (ACh), that d-tubocurarine (d-Tc) and other nondepolarizing muscle relaxants decrease the release of ACh from the indirectly stimulated mouse hemidiaphragm preparation. It was the purpose of the present study to determine whether the decrease of the stimulated release of ACh and the increase in the intensity of the partial neuromuscular block observed at higher stimulation rates is caused by the inhibition of mobilization of ACh from reserve depots to release sites or by inhibition of the release process itself. To attain our objective, the authors have investigated the influence of the progressive increase of the rate of stimulation from 0.1 to 1, 2, 3, and 5 Hz on the force of contraction on the in vitro phrenic nerve-hemidiaphragm and in vivo sciatic nerve-tibialis anterior preparation in the absence of drugs and after about 20% neuromuscular block produced by d-Tc or by Mg2+. The latter is known to inhibit the Ca2+ dependent release of ACh. In the absence of drugs increasing the stimulation rate increased the force of contraction, in vivo and in vitro, during both indirect and direct stimulation. In the phrenic nerve-hemidiaphragm preparation the increase was significant at 1, 2, 3, and 5 Hz (P less than 0.001) with both types of stimulation. In the sciatic nerve-tibialis anterior preparation the force of contraction was only higher at 3 and 5 Hz (P less than 0.01). The similar magnitude of the increase of the force of contraction during direct and indirect stimulation indicates that it is caused by facilitation of the contraction of the muscle fibers.(ABSTRACT TRUNCATED AT 250 WORDS)


Acta Anaesthesiologica Scandinavica | 1995

Neurochemical evidence that [Ca2+]o antagonizes the effect of neomycin on acetylcholine release from mouse hemidiaphragm preparation: An attempt to assess the margin of safety

I. A. Chaudhry; K. Nitahara; H. Nagashima; E. S. Vizi

Although the neuromuscular junction is the most thoroughly studied synapse of any type and has become the model of our understanding of synaptic transmission, some questions remain unanswered; e.g. there has been no direct assessment of the size of margin of safety.


Neuropharmacology | 1987

Effect of mono- and diaminopyridines on release of [3H]norepinephrine from isolated guinea-pig atrium

T. Sugimori; H. Nagashima; E.S. Vizi; L.G. Harsing; I. A. Chaudhry; I. Lalezari; Deryck Duncalf; Paul L. Goldiner; Francis F. Foldes

Neurochemical evidence has been obtained that 4-aminopyridine, 3,4-diaminopyridine and 3,3-dimethyl-1-(4-amino-3-pyridyl)urea HBr (LF-14), concentration-dependently enhanced the stimulation-evoked release of [3H]norepinephrine ([3H]NE) from isolated guinea-pig atrium. The effects of aminopyridines, compounds known to inhibit potassium channels, were Ca0-dependent. High pressure liquid chromatography, combined with radiochemical detection, indicated that the increased stimulated release of radioactivity was due to [3H]NE. Since the aminopyridines studied also enhanced the release of [3H]NE from atrium treated with cocaine, a blocker of uptake1, it seems likely that the increased release of NE caused by the aminopyridines is due to the enhanced release of NE from sympathetic axon terminals and not to the inhibition of reuptake. It is probable that the sympathomimetic cardiac effects (positive inotropic and chronotropic effect) of aminopyridines observed in animal experiments is due to the increased release of NE, caused by these compounds.


Anesthesia & Analgesia | 1989

Species variation in the site and mechanism of the neuromuscular effects of diadonium in rodents.

Francis F. Foldes; I. A. Chaudhry; Tamador Barakat; Carlos Flores; M. Kinjo; George B. Bikhazi; H. Nagashima

The unusually wide, 80-fold species variation observed by others (1,2) in the neuromuscular (NM) potency of diadonium, a nondepolarizing muscle relaxant (MR), between cat and man suggested that the site and mechanism of its NM effect may vary in different species. To obtain information on this question, the NM potency of diadonium and the reversibility of its NM effect by neostigmine and/or 4-aminopyridine (4AP) was investigated on the in vitro phrenic nerve--hemidiaphragm preparations of rats, mice and guinea pigs. The concentration of diadonium that caused 90% NM block (IC90) was much greater in guinea pigs, 2.74 ± 0.02 and 1.28 ± 0.01 μ, when the preparations were stimulated with single stimuli at 0.1 Hz or with 0.1 s trains of 50 Hz tetani every 10 s, respectively, than in rats (IC90 = 62.4 ± 0.89 and 52.1 ± 1.00 μM) or mice (IC90 = 51.9 ± 0.98 and 44.4 ± 0.22 μM). In guinea pigs, the NM blocking effect of diadonium could be antagonized by neostigmine. This indicates that in this species the NM blocking effect of diadonium is primarily caused by inhibition of the interaction of acetylcholine (ACh), released by the nerve impulse, with the cholinergic receptors (cholinoceptors) of the postjunctional membrane (p.j.m.). By contrast, in rats and mice diadonium was not antagonized by neostigmine but was reversed by 4-aminopyridine. This suggests that in these species, in contrast to other nondepolarizing MR, diadonium does not inhibit NM transmission postsynaptically, but by inhibiting the positive nicotinic feedback mechanism of mobilization of ACh from reserve depots to release sites, causes a presynaptic NM block. The different sites and mechanisms of the diadonium block in guinea pigs on one hand, and in rats and mice on the other, are probably caused by differences in the interaction of diadonium and the ACh recognition sites of the cholinoceptors of the p.j.m. in the 3 species. No similar species variation could be demonstrated in the sites and mechanisms of any of the nondepolarizing MR in clinical use.


Aminopyridines and Similarly Acting Drugs: Effects on Nerves, Muscles and Synapses#R##N#Proceedings of a IUPHAR Satellite Symposium in Conjunction with the 8th International Congress of Pharmacology, Paris, France, July 27–29, 1981 | 1982

4-Aminopyridine Analogs of Novel Chemical Structure

Y. Ohta; I. A. Chaudhry; I. Lalezari; Francis F. Foldes

Publisher Summary This chapter discusses a study to investigate 4-aminopyridine (4-APYR) analogs of novel chemical structure. In this study, several analogs of 4-APYR were synthesized and tested in the rat in vitro phrenic nerve–diaphragm and the in vivo sciatic–tibialis anterior preparation. The ability of the compounds to influence the course of pentobarbital anesthesia in rats was also investigated. Of the compounds synthesized so far, 4,p-acetyl-aminobenzenesulfonyl-4-aminopyridine (LF-1), 4-pyridylcarbonic acid ethyl ester (LF-5), l-(4-pyridyl)-2, 2-diethylurea (LF-10), and l(4-pyridyl)-2,2-diethylurea (LF-II) had similar antagonistic effect as 4-APYR on the pancuronium and d-tubocurarine (d-Tc) induced NM block in vitro and in vivo. In vitro except for LF-5 the new analogs were more potent antagonists of NM block than 4-APYR. In vivo LF-1 and LF-5 were less potent and LF-10 and LF-II were about as potent as 4-APYR. In contrast to 4-APYR, none of the new compounds increased the intra-arterial blood pressure in anesthetized rats. However, LF-1 and LF-10 similarly to 4-APYR delayed the onset and prolonged the duration of pentobarbital anesthesia in rats.


Archive | 1995

The Protein Binding of SZ1676, SZ1677 and Rocuronium and Their Inhibitory Effect on Human Cholinesterases

I. A. Chaudhry; Francis F. Foldes; H. Nagashima

SZ1676,1-[3α,17β-bis(acetyloxy)-2β-(1,4-dioxa-8-azaspiro[4.5]dec-8-yl)-5α-androstan-16β-yl]-1-(2-propenyl)pyrrolidinium.Br, and its 3-OH derivative, SZ1677, are steroid type, nondepolarizing muscle relaxants(MR) under investigation. Rocuronium,1 another steroid type nondepolarizing MR, has been recently introduced into clinical practice. The present study has been undertaken as a part the characterization of the pharmacological profile of these MR.

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Paul L. Goldiner

Albert Einstein College of Medicine

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I. Lalezari

Albert Einstein College of Medicine

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E. S. Vizi

Hungarian Academy of Sciences

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George B. Bikhazi

Children's Memorial Hospital

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