bluuebunny/crossref_metadata_2025_split huggingface dataset:
FURAZOLIDONE‐PETHIDINE INTERACTION IN RABBITS
Authors: ELTAYEB I.B. , OSMAN O.H. 
Published: July 2012

The intravenous injection of pethidine in rabbits pretreated with furazolidone administered orally but not systemically resulted in severe interaction and fatal hyperpyrexia.
Treatment with p‐chlorophenylalanine, chloropromazine or cyproheptadine protected the rabbits against the furazolidone‐pethidine interaction, while α‐methyl‐p‐tyrosine was ineffective.
5‐Hydroxytryptophan produced a fatal hyperpyrexia in furazolidone pretreated rabbits.
Pretreatment of rabbits with 1,1,1‐trichloro‐2, 2‐bis(p‐chlorophenyl)ethane (DDT) accelerated and enhanced the furazolidone‐pethidine interaction, while oxytetracycline pretreatment completely prevented the interaction.
It is concluded that furazolidone‐pethidine interaction might depend mainly on potentiation of the effects of 5‐hydroxytryptamine in the CNS and that the transformation of furazolidone into an active monoamine oxidase inhibitor metabolite might occur mainly in the gut microflora in the gut lumen.
THE DEVELOPMENT OF ANTISERA TO PROSTAGLANDINS B2 AND F2α AND THEIR ANALYSIS USING SOLID‐PHASE AND DOUBLE ANTIBODY RADIOIMMUNOASSAY METHODS
Authors: DIGHE K.K. , EMSLIE H.A. , HENDERSON L.K. , SIMON L. , RUTHERFORD F. 
Published: July 2012

A method for the production of highly substituted prostaglandin‐bovine serum albumin conjugates has been developed.
Antisera to prostaglandins B2 and F2α were raised in rabbits immunized with prostaglandin‐bovine serum albumin conjugates.
The antisera were assessed for specificity and sensitivity by the double antibody radioimmunoassay method and after they were covalently linked to powdered cellulose to form a ‘solid‐phase’ system.
Solid phase radioimmunoassays were developed using conventional shaking and in the presence of sucrose which obviates the need for continuous mixing of the incubates.
AN INHIBITORY EFFECT OF ATROPINE ON RESPONSES OF THE VAS DEFERENS OF THE MOUSE TO FIELD STIMULATION
Authors: JONES MARGARET E.L. , SPRIGGS T.L.B. 
Published: July 2012

Atropine is shown to impair responses of the vas deferens of the mouse to field stimulation by acting at a site proximal to the smooth muscle cells.
The inhibitory effect of atropine is prevented by desmethylimipramine and reversed by dexamphetamine, and appears similar to the adrenergic‐neurone blockade of guanethidine.
Electronmicroscopical studies show the presence in vas of presumptive noradrenergic axons which have acetylcholinesterase reaction product associated with their axolemmae.
These results are discussed in relation to the controversial hypothesis of a ‘cholinergic link’ in noradrenergic transmission.
SOME CHARACTERISTICS OF PRE‐ AND POST‐SYNAPTIC INHIBITORY RECEPTORS AT THE HERMIT CRAB NEUROMUSCULAR JUNCTION
Authors: BALASHOV N. , EARL JANET , LARGE W.A. 
Published: July 2012

The effects of γ‐aminobutyric acid (GABA), β‐guanidinopropionic acid (βGP) and picrotoxin on the pre‐ and post‐synaptic receptors of the hermit crab neuromuscular junction were studied quantitatively using electrophysiological techniques. Reductions in excitatory junction potential (e.j.p.) amplitude and membrane resistance were measured simultaneously from the same cells.
The pre‐ and post‐synaptic receptors were activated by the same order of concentration of GABA, whereas βGP stimulated the pre‐synaptic receptors at a concentration ten times lower than was required to affect the post‐synaptic membrane.
Picrotoxin appeared to antagonize the pre‐synaptic action of βGP in a competitive manner. The affinity constants (± s.e. mean) for picrotoxin 5 × 10−6 M and 2 × 10−4 M were 6.80 (± 0.46) × 105 M−1 and 6.42 (± 1.8) × 105 M−1 respectively.
The effect of GABA on e.j.p. amplitude also appeared to be antagonized competitively by picrotoxin whereas the post‐synaptic effect was antagonized in a non‐competitive manner.
Possible differences in the nature of the pre‐ and post‐synaptic receptors are discussed.
RAPID EFFECTS OF ENVIRONMENTAL DISTURBANCE ON RAT PLASMA UNESTERIFIED FATTY ACID AND TRYPTOPHAN CONCENTRATIONS AND THEIR PREVENTION BY ANTILIPOLYTIC DRUGS
Authors: CURZON G. , KNOTT P.J. 
Published: July 2012

Changes of plasma unesterified fatty acid (UFA) and tryptophan concentration in group‐housed rats following removal of their cage‐mates and the effects of antilipolytic drugs on these changes were investigated.
Removal of group‐housed 24 h fasted rats but not fed rats from cages resulted in increased plasma UFA concentration in the remaining rats which was associated with significant increases of the proportion of free tryptophan but significant falls of total tryptophan concentration. These rapid changes were not associated with brain tryptophan changes. Plasma tyrosine concentration was unaffected.
The fall of plasma tryptophan did not appear to be due to passage into red cells as erythrocyte tryptophan concentration remained unchanged.
Plasma UFA concentrations correlated positively and significantly with corticosterone concentrations which were also increased following removal of cage‐mates.
Plasma UFA increases and tryptophan changes in the fasting rats were both prevented by nicotinic acid or propranolol. Corticosterone concentration was increased by nicotinic acid but unaffected by propranolol.
The possible importance of these rapid changes of plasma tryptophan and of their prevention by antilipolytic drugs is discussed.
AN ELECTROPHYSIOLOGICAL ANALYSIS OF THE EFFECT OF Ca IONS ON NEUROMUSCULAR TRANSMISSION IN THE MOUSE VAS DEFERENS
Authors: BENNETT M.R. , FLORIN T. 
Published: July 2012

A study has been made of the effects of changing the external calcium concentration [Ca] 0 and the external magnesium concentration [Mg] 0 on the synaptic potential due to noradrenaline release.
When [Ca] 0 was varied in the range 0.7 to 1.8 mM, the synaptic potential increased as about the second power of [Ca] 0.
Increasing [Mg] 0 depressed the synaptic potential; however, variation of [Ca] 0 in the presence of high [Mg] 0 did not significantly change the power relationship between the synaptic potential and [Ca] 0.
The facilitated increase in the synaptic potential during short trains of impulses at different frequencies was quantitatively predicted on the assumption that each impulse leaves residual Ca ions bound to release receptors in the nerve terminal.
INTERACTION OF MONO‐ AND DIVALENT METALLIC CATIONS AND OF INDOMETHACIN ON THE MEMBRANE POTENTIAL OF VASCULAR ENDOTHELIAL CELLS in vitro
Authors: NORTHOVER B.J. 
Published: July 2012

Endothelial cells depolarized progressively when heated for 5 h at 45° C in the presence of calcium (1 mM), cupric (0.08 mM) or ferrous (0.04 mM) ions. In the absence of these ions, heating caused only slight depolarization. Higher concentrations of these ions caused depolarization even at normal body temperature (37° C).
Cuprous and potassium ions, although producing depolarization at 37° C, failed to augment the depolarization due to heating to 45° C.
Hydrogen peroxide caused depolarization which was potentiated by the presence of calcium, cupric or ferrous ions, but not by the presence of cuprous or potassium ions.
Indomethacin (0.25 mM) reduced the depolarization caused by calcium, cupric or ferrous ions at 37° C and also reduced the potentiation of heat‐induced and hydrogen peroxide‐induced depolarization which these divalent metallic cations produced. However, indomethacin failed to modify the depolarization caused by cuprous or potassium ions.
FORECASTING THE ANTIMALARIAL ACTIVITIES OF ARYLAMIDINOUREAS FROM THEIR MEASURED PHYSICOCHEMICAL PROPERTIES
Authors: GILBERT D. , GOODFORD P.J. , NORRINGTON F.E. , WEATHERLEY B.C. , WILLIAMS S.G. 
Published: July 2012

The octanol: water partition coefficient (PC), protein binding coefficients to albumin (Ba) and haemoglobin (Bh), proton magnetic resonance (PMR) chemical shifts and pKa of 8 arylamidinoureas have been measured.
There were statistically significant correlations for 7 of the 8 compounds between the predicted lipophilicity parameter π and log PC, Ba and Bh, and also between Hammett's electronic parameter π and the PMR and pKa observations.
3‐Chloro, 4‐nitrophenylamidinourea showed a larger deviation from these correlations than any other compound. Geometric calculations based on the covalent radii and bond angles of the molecule suggested that the neighbouring chloro and nitro substituents were interacting sterically.
Molecular orbital calculations and the observed ultra‐violet spectrum provided further evidence for such an interaction, and suggested that the nitro group is twisted out of the plane of the benzene ring in this molecule.
Such steric interactions can introduce an additional source of error when attempts are made to correlate the biological and predicted physicochemical properties of compounds.
Generalized parameters such as π and π cannot be used with confidence to predict the properties of compounds in which such steric interactions occur.
STUDIES UPON THE MECHANISM BY WHICH ACETYLCHOLINE RELEASES SURPLUS ACETYLCHOLINE IN A SYMPATHETIC GANGLION
Authors: COLLIER B. , KATZ H.S. 
Published: July 2012

Acetylcholine (ACh) releases surplus ACh from the superior cervical ganglion of the cat and the experiments described in this paper tested whether this results from exchange of endogenous ACh with exogenous ACh; the experiments also attempted to characterize pharmacologically the mechanism of this action of ACh.
The surplus ACh in the ganglion was radioactively labelled by perfusion of the ganglion with [3H]‐choline‐Krebs solution containing diisopropylphosphofluoridate, and the release of surplus [3H)‐ACh by [14C]‐ACh injected close arterially to the ganglion measured. The amount of [3H]‐ACh released by [14C]‐ACh was 33 ± 5 times greater than was the amount of [14C]‐ACh accumulated by ganglia. The amount of exogenous ACh accumulated by ganglia that had first formed surplus ACh was not different from exogenous ACh accumulation by ganglia that had not formed surplus ACh. Thus, it is concluded that surplus ACh release by ACh is not the result of ACh exchange.
In other experiments, surplus [3H]‐ACh was accumulated in ganglia exposed to physostigmine. Nicotine, pilocarpine or ACh released surplus ACh; the effect of both nicotine and ACh was blocked by hexamethonium; atropine blocked the effect of ACh but not that of nicotine. It is concluded that both nicotinic and muscarinic receptors can be involved in the release of surplus ACh by cholinomimetic agonists.
EFFECTS OF DRUGS ACTING ON CEREBRAL 5‐HYDROXYTRYPTAMINE MECHANISMS ON DOPAMINE‐DEPENDENT TURNING BEHAVIOUR IN MICE
Authors: MILSON J.A. , PYCOCK C.J. 
Published: July 2012

The effects of drugs acting on cerebral 5‐hydroxytryptaminergic mechanisms on drug‐induced turning behaviour in mice with unilateral destruction of nigro‐striatal dopaminergic nerve terminals have been studied.
Administration of l‐tryptophan (400 mg/kg) or 5‐hydroxytryptophan (200 mg/kg) increased brain 5‐hydroxytryptamine and decreased the turning induced by both apomorphine (2 mg/kg) and amphetamine (5 mg/kg).
Parachlorophenylalanine (3 × 500 mg/kg) decreased brain 5‐hydroxytryptamine and increased both apomorphine and amphetamine‐induced circling behaviour.
Varying the protein content of dietary intake significantly altered brain 5‐hydroxytryptamine and tryptophan levels, spontaneous locomotor activity and amphetamine‐induced circling behaviour in these mice.
Systemic administration of methysergide (0.5–4 mg/kg), lysergic acid diethylamide (0.025‐0.2 mg/kg), cyproheptadine (2.5–20 mg/kg) or clomipramine (0.6–20 mg/kg) produced no consistent effect on drug‐induced turning behaviour.
The results suggest that circling behaviour due to striatal dopamine receptor stimulation is depressed by an elevation of brain 5‐hydroxytryptamine and enhanced by a reduction in brain 5‐hydroxytryptamine.
The possible physiological relationship between dopamine and 5‐hydroxytryptamine neurones in the basal ganglia is discussed.
THE EFFECT OF LITHIUM CHLORIDE ON ONE‐TRIAL PASSIVE AVOIDANCE LEARNING IN RATS
Authors: JOHNSON F.N. 
Published: July 2012

Expression of a one‐trial passive avoidance learning response in rats was examined following injections of lithium chloride or sodium chloride before and after initial training and before the first day of testing. Five tests were given at daily intervals, 24 h after training being the time of the first test.
Lithium given before the first day of testing impaired response expression on the first and all subsequent days of testing; the rate of extinction was unaffected.
Given both before and immediately after initial training, lithium impaired response expression on the first day of testing but slowed down the subsequent rate of extinction, leading eventually to improved performance on the fifth day, as compared with placebo‐treated control subjects.
The results are interpreted in the light of the hypothesis that lithium impaired the central processing of sensory information.
THE EFFECT OF EDROPHONIUM ON ERYTHROCYTE ACETYLCHOLINESTERASE AND NEUROMUSCULAR FUNCTION IN THE RAT
Authors: BARBER H.E. , CALVEY T.N. , MUIR K.T. , TAYLOR K. 
Published: July 2012

The relation between the concentration of edrophonium in plasma, inhibition of red cell acetylcholinesterase, and neuromuscular transmission was studied in the rat.
In both in vivo and in vitro conditions, red cell acetylcholinesterase activity was predictably related to the concentration of the quaternary amine.
After low doses of edrophonium (1.0 μmol/kg) there was a significant correlation between the monophasic potentiation of twitch tension and the plasma concentration of the drug. In contrast, with higher doses of edrophonium (4.0 or 10.0 μmol/kg) a biphasic potentiation of twitch tension was observed; this was only correlated with the plasma concentration of the drug during the secondary decline in neuromuscular facilitation. Subsequent recovery of normal neuromuscular transmission invariably occurred at a constant plasma concentration of edrophonium.
EFFECT OF ATROPINE ON THE DECAY OF MINIATURE END‐PLATE CURRENTS AT THE FROG NEUROMUSCULAR JUNCTION
Authors: FELTZ ANNE , LARGE W.A. 
Published: July 2012

The effect of atropine on the time constant of decay (τ) of miniature end‐plate currents was investigated.
The atropine‐induced shortening of τ was accompanied by a reduction in the voltage‐sensitivity of τ.
This effect of atropine was reversible and dose‐dependent, the voltage sensitivity being abolished with high concentrations of atropine (2.5 × 10−5 m).
LITHIUM OROTATE, CARBONATE AND CHLORIDE: PHARMACOKINETICS, POLYDIPSIA AND POLYURIA IN RATS
Authors: SMITH D.F. 
Published: July 2012

The pharmacokinetics of the lithium ion administered as lithium orotate were studied in rats. Parallel studies were carried out with lithium carbonate and lithium chloride.
No differences in the uptake, distribution and excretion of the lithium ion were observed between lithium orotate, lithium carbonate and lithium chloride after single intraperitoneal, subcutaneous or intragastric injections (0.5‐1.0 mEq lithium/kg) or after administration of the lithium salts for 20 days in the food.
The findings oppose the notion that the pharmacokinetics of the lithium ion given as lithium orotate differ from lithium chloride or lithium carbonate.
Polyuria and polydipsia developed more slowly in rats given lithium orotate than in those given lithium carbonate or lithium chloride, perhaps due to an effect of the orotate anion.
ISOTONIC AND ISOMETRIC RESPONSES OF DIFFERENTTONIC MUSCLES TO AGONISTS AND ANTAGONISTS
Authors: MICHELSON M.J. , SHELKOVNIKOV S.A. 
Published: July 2012

With isotonic recording the percentage of muscle shortening as compared with the maximal possible shortening, and with isometric recording the percentage of developed tension were determined. In relatively ‘thick’ muscles, such as dorsal leech muscle, frog rectus abdominis or protractor pharynx of holothuria (0.3‐0.8 mm thick), the concentrations of a full agonist (carbachol) producing a given percentage of tension, (e.g. 50%) are about 5 times greater than the concentrations, producing the same percentage of shortening. In ‘thin’ muscles the difference between the percentage of shortening and tension is either small (retractor dentis of the sea urchin, 0.1 mm thick, response to carbachol) or absent (guinea‐pig ileum, 0.06 mm thick, responses to methylfurmethide). The possible mechanism underlying this difference is discussed.
With partial agonists (dodecamethonium and heptamethonium) the fractional tension of the frog rectus abdominis is always less than the fractional shortening and the correlation between shortening and tension is the same as in the case of full agonists.
The blocking activity of (+)‐tubocurarine on the frog rectus abdominis is the same in isotonic and in isometric conditions.
On the frog rectus abdominis the alkylating agent, decamethonium mustard, does not produce any ‘parallel shift’ of the dose‐response curve for carbachol, the only result of alkylation being a decrease in maximal response, which is more pronounced in isometric than in isotonic conditions. The degree of decrease is in accordance with the correlation between percentage of shortening and percentage of tension in the absence of alkylating agent. Probably this muscle does not possess any ‘spare receptors’.
On the frog muscle the dose‐isometric response curve for acetylcholine (ACh) is shifted toward greater concentration about 33‐fold as compared with the dose‐isotonic response curve but after the inhibition of cholinesterases the shift is only about 6‐fold. The same shift (5‐fold) is observed for carbachol, which is not hydrolysed by cholinesterases. The results with ACh are due to the fact, that after cholinesterase inhibition the sensitivity to ACh increases in isotonic conditions only 13‐fold, but in isometric conditions it increases 71‐fold. Probably under isometric conditions, when the muscle remains in the extended state, the rate of hydrolysis of ACh is much greater than under isotonic conditions when the muscle is shortened during contraction.
PROSTAGLANDIN PRODUCTION BY RABBIT ISOLATED JEJUNUM AND ITS RELATIONSHIP TO THE INHERENT TONE OF THE PREPARATION
Authors: FERREIRA S.H. , HERMAN A.G. , VANE J.R. 
Published: July 2012

Pieces of rabbit jejunum were bathed in Krebs solution at 37°C in an isolated organ bath bubbled with O2 and 5% CO2. The bathing fluid was collected regularly and assayed for prostaglandins.
The preparations maintained a continuous sub‐maximal muscle contraction, referred to as inherent ‘tone’. Prostaglandins E2 and F2α were continuously generated by the intestine and released into the bathing fluid. The amounts released first declined over 2 h and then steadily increased. The release was also greater after 48 h storage in the refrigerator and after mechanical damage.
There was no change in prostaglandin release when the rabbit jejunum was contracted by acetylcholine or physostigmine or relaxed by adrenaline, hyoscine, papaverine, dinitrophenol, or calcium‐free Krebs solution.
Addition to the bathing fluid of the prostaglandin precursor, arachidonic acid, did not increase the release of prostaglandins although it contracted the tissue. Thus, output of prostaglandins from the tissue was not limited by substrate concentration but more probably by the capacity of the prostaglandin synthetase.
Prostaglandin output was decreased by bubbling the bathing fluid with N2 rather than O2; at the same time the preparation relaxed.
Aspirin‐like drugs such as indomethacin also decreased or abolished prostaglandin formation and this, too, was accompanied by loss of tone of the isolated preparation.
Pieces of rabbit jejunum stored in Krebs solution containing indomethacin initially released little or no prostaglandin into the bathing fluid. However, prostaglandin release increased with repeated washing of the preparation.
The results suggest that intra‐mural prostaglandin production contributes to the inherent tone of the rabbit jejunum, that trauma increases prostaglandin production and that the inhibitory effects of anoxia are linked with the lack of prostaglandin production and activity. The relevance of these findings to intestinal activity in vivo is discussed.
THE EFFECT OF QUINIDINE ON MEMBRANE ELECTRICAL ACTIVITY IN FROG AURICULAR FIBRES STUDIED BY CURRENT AND VOLTAGE CLAMP
Authors: DUCOURET P. 
Published: July 2012

The action of quinidine sulphate 50 μm has been investigated on frog auricular trabeculae transmembrane currents recorded with a double sucrose gap apparatus. Results were obtained either in current or in voltage clamp conditions.
Quinidine modified the time course of repetitive activity elicited by long lasting depolarizing currents and reduced the range of current over which repetitive activity could be triggered, eventually abolishing repetitive responses altogether.
Several authors have emphasized the limitations of the voltage clamp method. Taking into account these limitations, the numerical values of the parameters obtained in the present work must not be considered as exact values but may be interpreted as indicators of the variations of the parameters.
The results are in agreement with previous findings that the main features of the action of quinidine are to produce (a) a reduced maximum rate of depolarization (MRD), (b) a reduced total amplitude of action potential, (c) a flattening of the plateau of the action potential, (d) a slight prolongation of the tail of the action potential, (e) an increased effective refractory period without greatly prolonging action potential duration, (f) no change of resting potential and of 50% repolarization time.
The analysis of ionic conductances has provided explanations for the above effects.
Quinidine reduced the reactivation kinetics of the sodium inward current, and decreased sodium conductance and the steady state of activation. These effects account for (a) and (b).
Quinidine increased the activation and inactivation time constants of sodium conductances, which account in part for (e).
Quinidine delayed reactivation of slow inward current, reduced calcium conductance, and decreased the steady state of activation of calcium conductance. These effects could account for (c).
The amplitudes of the two components of the delayed conductances responsible for repolarization were decreased by quinidine, and the time constant of activation for the faster of the two was slowed. These effects could account for (d) and in part for (e).
ANALYSIS OF THE EFFECTS OF p‐METHOXY‐PHENYLETHYLAMINE ON SPINAL CORD NEURONES
Authors: JORDAN L.M. , McCREA D.A. 
Published: July 2012

Para‐methoxyphenylethylamine (PMPEA) was applied microiontophoretically onto interneurones and motoneurones in the spinal cords of acute spinal cats anaesthetized with α‐chloralose. Its effects were compared with those of noradrenaline (NA) and 5‐hydroxytryptamine (5‐HT).
PMPEA had effects on interneurones which were similar to those of NA and/or 5‐HT; its action was predominantly depressant, and it rarely affected interneurones which could not be influenced by NA or 5‐HT.
The actions of PMPEA on interneurones excited by electrical stimulation of leg nerves showed that the population of interneurones influenced by the drug coincides with the population affected by NA and 5‐HT and by intravenously administered PMPEA.
Renshaw cells, which are excited by intravenous PMPEA, were either not affected or depressed by microiontophoretically applied PMPEA.
Alpha motoneurones, which are depolarized by intravenous PMPEA, were hyperpolarized by microiontophoretically applied PMPEA. Antidromic firing of the cells could be blocked by PMPEA.
The differences between the effects of intravenous infusion and the iontophoretic application of PMPEA upon motoneurones is most easily explained by inhibition of interneurones and a concomitant disinhibition of motoneurones. A similar mechanism may also account for the different effects seen with intravenous and iontophoretic application of PMPEA on Renshaw cells.