bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nicotine washout rates from isolated rat ganglia in relation to recovery from nicotine depolarization
Authors: BROWN D. A. , SCHOLFIELD C. N. 
Published: July 2012

Summary
. Isolated rat superior cervical ganglia recovered more slowly from the depolarizing action of nicotine than from that of carbachol or acetylcholine. This was due to sustained high nicotine concentrations in the vicinity of the receptors, since recovery was hastened by adding hexamethonium to the washout fluid.
. Ganglia incubated for 4 min in 80 μm 3H‐nicotine accumulated nicotine to a level exceeding the extracellular space, as judged from the uptake of 3H‐mannitol.
. The subsequent efflux of 3H‐nicotine into non‐radioactive solution could. be largely resolved into two exponential components, with rate constants of 0·55 ± 0·04 and 0094 ± 0007 min−1. The former was similar to that for total mannitol efflux, and so might be largely ascribed to clearance of extracellular nicotine. The slower efflux might be due to clearance from intracellular compartments. Nicotine efflux rates were not affected by hexamethonium indicating that receptor‐activation did not modify the slow efflux.
. Efflux of choline compounds (3H‐acetylcholine, 3H‐choline and 3H‐carbachol) showed an additional, very slow component (rate constant 0·001 to 0·002 min−1).
. It was suggested that slow efflux of intracellular nicotine might sustain depolarization on washing by maintaining high perineuronal concentrations of nicotine. With choline compounds the efflux rate from such sources may be too slow to affect perineuronal concentrations.
Histochemical localization of adrenergic nerves in the guinea‐pig trachea
Authors: O'DONNELL STELLA R. , SAAR NILI 
Published: July 2012

Summary
Specific catecholamine fluorescence was demonstrated in guinea‐pig trachea in fine, varicose, nerve fibres running parallel to the tracheal smooth muscle fibres.
The density of nerves in tracheal smooth muscle was greater at the laryngeal end than at the bronchial end of the trachea.
The findings confirm pharmacological evidence for an adrenergic innervation of the guinea‐pig isolated tracheal chain preparation.
Role of pre‐ and postjunctional inhibition by prostaglandin E2 of lipolysis induced by sympathetic nerve stimulation in dog subcutaneous adipose tissue in situ
Authors: FREDHOLM B. B. , HEDQVIST P. 
Published: July 2012

Summary
Canine subcutaneous adipose tissue was isolated and autoperfused in situ after labelling of the noradrenaline stores by 3H‐(—)‐noradrenaline.
Prostaglandin E2 (10–200 ng/ml) increased blood flow and glucose uptake, and caused a dose‐dependent inhibition of lipolysis induced by sympathetic nerve stimulation (4 Hz). The actions of exogenous prostaglandin E2 are therefore similar to those of prostaglandin E1 in this tissue. There were no consistent effects of prostaglandin E2 on the vasoconstriction or on the 3H‐noradrenaline overflow induced by nerve stimulation.
Phenoxybenzamine (1·5–2 mg i.a.) caused a 5‐fold increase in 3H‐noradrenaline overflow and a 95% reduction of the vasoconstrictor response to nerve stimulation. The lipolytic response was similar to that of the control. Prostaglandin E2 (100–200 ng/ml) administered after phenoxybenzamine caused a 90% inhibition of lipolysis, while the vasoconstrictor response was enhanced to about 50% of control. Prostaglandin E2 inhibited 3H‐noradrenaline overflow by about 50% but it was still larger than that of the control.
It is suggested that exogenous prostaglandin E2 inhibits lipolysis induced by sympathetic nerve stimulation mainly by a postjunctional action in canine subcutaneous adipose tissue.
An assessment of sympathetic function in isolated tissues from mice given nerve‐growth‐factor antiserum and 6‐hydroxydopamine
Authors: HUGHES I. E. , KIRK JENNIFER A. , KNEEN BARBARA , LARGE B. J. 
Published: July 2012

Summary
Experiments were done on isolated tissues from mice injected with 0·9% w/v NaCl solution (saline), 6‐hydroxydopamine (6‐OHDA), nerve‐growth‐factor antiserum (NGF‐As) or a combination of these agents (NGF‐As 4–6‐OHDA).
Fluorescence histochemistry of vasa deferentia showed clear differences between each of the treatments but no such distinction was possible in cardiac ventricle or intestine.
Compared with controls, the chronotropic responses of atria to field stimulation were reduced by all three treatments in the order NGF‐As<6‐OHDA<NGF‐As + 6‐OHDA. Supersensitivity to noradrenaline occurred in atria from all treated groups.
In contrast, vasa deferentia from NGF‐As‐treated mice responded almost identically with controls to both field stimulation and to exogenous noradrenaline. Considerable functional impairment and noradrenaline supersensitivity were obvious in both the 6‐OHDA and the NGF‐As + 6‐OHDA groups but no distinction could be made between them.
The relaxation of superfused ileum following nerve stimulation was reduced in the NGF‐As group, whilst preparations from the two groups given 6‐OHDA usually gave a motor response which was blocked by atropine.
None of the treatments employed in these experiments caused complete sympathectomy although 6‐OHDA alone or in combination with NGF‐As produced a more pronounced effect than NGF‐As alone and the relative ineffectiveness of the latter is discussed. The implications of the motor response after 6‐OHDA in ileum when the nerves were stimulated is considered in the light of the cholinergic link hypothesis.
Effects of drugs and of electrical stimulation on the muscularis mucosae of rabbit large intestine
Authors: GALLACHER MAUREEN , MACKENNA B. R. , McKIRDY H. C. 
Published: July 2012

Summary
The muscularis mucosae of the rabbit large intestine shows spontaneous rhythmic contractions with an average frequency of about 11/minute.
The muscularis mucosae responds to acetylcholine, adrenaline and noradrenaline in a manner similar to that of whole segments of terminal large intestine.
The muscularis mucosae would seem to have a cholinergic motor innervation.
The effect of narcotic analgesics on the uptake of 5‐hydroxytryptamine and (—)‐metaraminol by blood platelets
Authors: AHTEE LIISA , SAARNIVAARA LAILA 
Published: July 2012

Summary
The effects of narcotic analgesic and related drugs were studied on the uptake of 5‐hydroxytryptamine (5‐HT) and (—)‐metaraminol by blood platelets.
The most potent drug in inhibiting the uptake of 5‐HT (10 μm) by human platelets was methadone, followed by pentazocine>piminodine ˜ pethidine ˜ anileridine ˜ cyclazocine ˜ thebaine > dextropropoxyphene. Alphaprodine, papaverine, apomorphine, nalorphine, codeine, and morphine were almost without effect. Methadone was slightly less active than desipramine, and had 10% of the activity of imipramine under similar conditions. Naloxone did not antagonize the effect of methadone on 5‐HT uptake.
The most potent inhibitor of metaraminol (3 μm) uptake by human platelets was piminodine, followed by pentazocine>anileridine>cyclazocine=methadone > dextropropoxyphene ˜ thebaine > papaverine ˜ alphaprodine >pethidine>morphine. The activity of morphine was 1% of that of piminodine. Piminodine was more potent than desipramine and protriptyline under similar conditions. The order of potency of drugs studied in inhibiting the uptake of metaraminol by rabbit platelets was similar to that obtained with human platelets.
The effects of the analgesics studied on inhibiting uptake of monoamines did not correlate with their pain‐relieving properties.
Pharmacological analysis of the acute inflammatory process induced in the rat's paw by local injection of carrageenin and by heating
Authors: LEME J. GARCIA , HAMAMURA L. , LEITE M. P. , SILVA M. ROCHA E 
Published: July 2012

Summary
Local injection of carrageenin in the rat's paw produced oedema and leakage of dye which had been administered previously by the intravenous route. A net dissociation between both parameters was observed: while oedema developed slowly, maximal intensity being attained after 4–5 h, dye‐leakage was maximum after 1 hour.
Anti‐inflammatory drugs such as acetylsalicylic acid and indomethacin were effective in reducing oedema and dye‐leakage when given before the injection of carrageenin, but much less effective when given 30 or 60 min after carrageenin. Hexadimethrine bromide was effective in reducing dye‐leakage also when given 1 h after the injection of carrageenin.
Combined administration of benadryl and methysergide, before the injection of carrageenin caused only a slight reduction in oedema and dye‐leakage.
When the paws were heated (55° C for 30 s) as a noxious stimulus the dissociation between maximal oedema and maximal dye‐leakage was not observed, both phenomena running parallel. Pre‐treatment of the animals with indomethacin did not afford any protection.
These results suggest that the inflammatory reaction to mild stimuli (carrageenin in our experiments) develops through different phases: initially the increased vascular permeability involves extravasation of plasma proteins and that phase is followed by an increased permeability mainly to water. Stronger stimuli (heating in our experiments) produce an overlapping of both phases, probably by inflicting severe damage to the vascular bed of the affected area.
The anti‐inflammatory drugs employed affected chiefly the initial phase of the response.
Some observations on the β‐adrenoceptor agonist properties of the isomers of salbutamol
Authors: BRITTAIN R. T. , FARMER J. B. , MARSHALL R. J. 
Published: July 2012

Summary
The pharmacological activities of the optical isomers of salbutamol have been examined. (–)‐Salbutamol was much more potent than (+)‐salbutamol on β‐adrenoceptors.
Both (–)‐ and (+)‐salbutamol showed high selectivity for β‐adrenoceptors in bronchial muscle compared to cardiac muscle, in this way resembling racemic salbutamol.
The use of isomeric activity ratio to detect differences between receptors was examined in the light of the results obtained with the isomers of salbutamol.
Microiontophoretic release of drugs from micropipettes: use of 24Na as a model
Authors: CLARKE G. , HILL R. G. , SIMMONDS M. A. 
Published: July 2012

Summary
The use of 24Na+ of high specific activity allowed its iontophoretic release from multibarrelled glass micropipettes to be followed over short periods with low currents.
When a negative retaining current was passed to reduce diffusional efflux between the periods of positive current expulsion of 24Na+, the rate of release of 24Na+ during the expulsion period progressively increased during the first minute before becoming constant.
The currents employed were similar to those normally used to regulate the microiontophoretic release of potent drugs such as γ‐aminobutyric acid. It is therefore concluded that, during the usual period of response to such drugs, the rate of release of drug is not constant but increasing.
The implications of these observations for the construction of microiontophoretic dose‐response relationships is discussed.
Sleep induced by small doses of tubocurarine injected into cerebral ventricles of dog
Authors: HARANATH P. S. R. K. , SHYAMALAKUMARI S. 
Published: July 2012

SummaryIn unanaesthetized dogs, sleep with the typical sleep pattern in the E.E.G. was produced with (+)‐tubocurarine when injected in a small dose (500 ng) into, or perfused in low concentration (100 ng/ml) through the cerebral ventricles.
Elongation of oestrous cycle in the guinea‐pig following subcutaneous or intra‐uterine administration of indomethacin
Authors: HORTON E. W. , POYSER N. L. 
Published: July 2012

Summary
Guinea‐pigs injected subcutaneously with 10 mg indomethacin twice daily, from day 7 of the oestrous cycle, had their oestrous cycles significantly lengthened (P < 0·001) by about 3 days.
When the indomethacin was incorporated into a slow‐release preparation and placed in the uterus (33 mg per horn), the oestrous cycle lengths of these guinea‐pigs were greatly prolonged and approached that produced by hysterectomy.
The measurement of corpora luteal size and progesterone levels in some of the guinea‐pigs autopsied on day 47 of the extended cycle showed functional corpora lutea to be present.
It was apparent that indomethacin had prolonged the life span of the corpus luteum. This would account for the increase in the length of the oestrous cycle.
Recent investigations suggest that normal corpora luteal regression, with the termination of the oestrous cycle, is induced by prostaglandin F2α released from the uterus on day 15. Since indomethacin prevents prostaglandin biosynthesis, it is probable in these experiments that this drug had prevented luteal regression by inhibiting the biosynthesis by, and release from, the uterus of prostaglandin F2α in luteolytic concentrations.
These results provide further evidence that the uterine luteolytic hormone in guinea‐pigs is prostaglandin F2α.
[3H]‐adenosine nucleotide and [3H]‐noradrenaline uptake by cold stored guinea‐pig taenia caecum; mechanical effects and release of [3H]‐adenosine nucleotide by noradrenaline, papaverine, and nitroglycerine
Authors: KUCHII M. , MIYAHARA J. T. , SHIBATA S. 
Published: July 2012

Summary
Cold storage (2° C) treatment progressively reduced noradrenaline uptake by the taenia caecum of the guinea‐pig. After 15 days of cold treatment, [3H]‐noradrenaline uptake by tissue was reduced to about 10% of control. On the other hand, prolonged cold storage failed to decrease [3H]‐adenosine uptake by the taenia caecum.
Cocaine (10 μm) inhibited noradrenaline uptake by about 82% but nucleoside uptake was inhibited by 20%. Cocaine treatment failed to decrease the residual noradrenaline uptake in the cold stored strips (more than 10 days). Phenoxybenzamine (1 μm) or oligomycin (1 μg/ml) treatment decreased the tissue adenosine uptake to about 34% and 28% of the respective controls.
Based on thin layer chromatography, it was estimated that approximately 68% of [3H]‐adenosine was converted into and retained as [3H]‐ATP in the fresh tissues, a small fraction was accountable as [3H]‐adenosine (18%) but virtually no [3H]‐AMP, [3H]‐cyclic AMP or [3H]‐ADP was detected. Similar distribution of radioactivity of nucleotides was observed in tissues cold stored for 8 days.
The inhibition of the mechanical activity of taenia by noradrenaline (10 μm), papaverine (100 μm) and nitroglycerine (100 μm) was accompanied by [3H]‐adenine nucleotide but not [3H]‐noradrenaline release. Treatment with phentolamine and propranolol (both 1 μm) had no effect on the adenine nucleotide release elicited by nicotine and electrical field stimulation, whereas such treatment reduced the inhibitory action of both stimuli.
These results suggest that the nucleotide release after application of electrical and chemical stimulation may be from an extraneurogenic source. Thus, we conclude that ATP or a related nucleotide is not the chemical transmitter of the non‐adrenergic inhibition in the taenia caecum of the guinea‐pig.
Tolerance pattern of the anorexigenic action of amphetamine in rats
Authors: GHOSH M. N. , PARVATHY S. 
Published: July 2012

Summary
When food intake in fasted male rats was recorded daily for two consecutive 2 h periods it revealed a characteristic pattern.
In the control rats the food intake was greater during the first than the second 2 h period. Following (±)‐amphetamine 5 mg/kg s.c. 30 min before food for 7 days there was a reversal of this normal food pattern. The rats consumed much less during the first 2 h period but progressively more during the second 2 h period.
The first 2 h food intake remained low throughout the treatment period and there was no evidence of development of tolerance despite continuation of treatment.
The second 2 h food intake steadily increased, contributing to the appearance of tolerance when only total 4 h food intake was recorded.
On withdrawal of amphetamine, there was immediate recovery of the first 2 h food intake. The second 2 h food intake, though decreased, remained high compared to the pretreatment level and may be responsible for the production of the ‘rebound’ phenomenon following withdrawal of amphetamine.
Effects of suramin on complement, blood clotting, fibrinolysis and kinin formation
Authors: EISEN V. , LOVEDAY C. 
Published: July 2012

Summary
The inhibition by suramin of complement components, and of blood clotting, fibrinolytic, and plasma kinin forming factors depended on the conditions of the assay and on the substrates used.
Haemolysis by complement was more effectively inhibited in red blood cell suspensions, than in agarose gel plates. In esterolytic tests, the activation of component 1 (C1) to C1 esterase was significantly inhibited by 0·1–0·3 mm suramin, and the activity of C1 esterase by 0·5 mm suramin.
Part of the anticoagulant effect of suramin is due to inhibition of the action of thrombin on fibrinogen.
Suramin did not inhibit fibrin degradation by the fibrinolytic system in plasma. In esterolytic tests, the activation of plasminogen was more potently inhibited than the activity of plasmin.
Activation of plasma kallikrein, measured either by kinin formation or by esterolysis, was inhibited by 0·1–0·3 mm suramin. Active plasma kallikrein was inhibited by 0·3–0·5 mm suramin. Pancreatic kallikrein was weakly inhibited, and urinary kallikrein not at all.
DEPOLARIZING ACTIONS OF γ‐AMINOBUTYRIC ACID AND RELATED COMPOUNDS ON RAT SUPERIOR CERVICAL GANGLIA IN VITRO
Authors: BOWERY N.G. , BROWN D.A. 
Published: July 2012

Potential changes in rat superior cervical ganglia were recorded in vitro with surface electrodes.
γ‐aminobutyric acid (GABA) produced a transient, low‐amplitude ganglion depolarization at rest, and a transient hyperpolarization in ganglia depolarized by carbachol. Depolarization was not prevented by preganglionic denervation. The log dose‐response curve for depolarization was sigmoid with a mean ED50 of 12.5 μm.
The ganglion was depolarized in similar manner by the following compounds (mean molar potencies relative to GABA (=1) in brackets): 3‐aminopropane sulphonic acid (3.4), γ‐amino‐β‐hydroxybutyric acid (0.27), β‐guanidino‐propionic acid (0.12), guanidinoacetic acid (0.057), δ‐aminovaleric acid (0.048), β‐alanine (0.01), 2,4‐diaminobutyric acid, γ‐guanidinobutyric acid, taurine and N‐methyl‐GABA (all <0.01). The following compounds did not depolarize the ganglion at 10 mm concentrations: α‐ and β‐amino‐n‐butyric acids, α‐amino‐iso‐butyric acid, glycine and glutamic acid.
Depolarization declined in the continued presence of GABA. Ganglia thus ‘desensitized’ to GABA showed a diminished response to other amino acids but not to carbachol.
The effect of GABA was not antagonized by hyoscine and hexamethonium in combination, in concentrations sufficient to block responses to carbachol.
Responses to GABA were blocked more readily than those to carbachol by bicuculline (IC50, 14 μm) and picrotoxin (IC50, 37 μm). Strychnine (IC50, 73 μm) was a relatively weak and less selective GABA‐antagonist.
It is concluded that sympathetic ganglion cells possess receptors for GABA and related amino acids which are (a) different from the acetylcholine receptors and (b) similar to GABA receptors in the central nervous system.
EFFECTS OF VINBLASTINE ON NORADRENERGIC AXONS
Authors: HANBAUER I. , JACOBOWITZ D.M. , KOPIN I.J. 
Published: July 2012

The effects of vinblastine and 6‐hydroxydopamine (6‐OHDA) on various parameters of adrenergic neurone functions in the rat were examined and compared.
During the first 12 h after injection of vinblastine, although the concentration of cardiac noradrenaline was unaltered, the turnover rate of the catecholamine in the heart was reduced to 40 ng g−1 h−1 compared to a rate of 66 ng g−1 h−1 in the hearts of animals treated with 0.9% w/v NaCl solution.
The uptake of noradrenaline by rat atria in vitro was inhibited by vinblastine (2.5 × 10−4 m) or 6‐OHDA (5 × 10−5 m), but only the inhibitory effect of vinblastine was readily reversible. The in vitro uptake of noradrenaline by atria of vinblastine‐ or 6‐OHDA‐treated rats was found to be impaired two days after injection of the drugs. After 14 days, however, the noradrenaline uptake was 71% of control values after vinblastine and 91% after 6‐OHDA.
In addition to intensely fluorescent nerve trunks in epicardial connective tissue septa, a decrease in the number of fluorescent adrenergic terminals in the atria and ventricles could be observed two days after vinblastine injection. It is suggested that intravenous vinblastine treatment, like 6‐OHDA, results in the destruction of adrenergic nerve terminals.
ABSORPTION, METABOLISM AND DISTRIBUTION OF [14C]‐O‐METHYLDOPA AND [14C]‐l‐DOPA AFTER ORAL ADMINISTRATION TO RATS
Authors: RIVERA‐CALIMLIM LEONOR 
Published: July 2012

The absorption, tissue distribution, and metabolism of [14C]‐O‐methyldopa were compared with those of [14C]‐l‐DOPA after oral administration to rats.
Total radioactivity in the plasma and brain of rats treated with [14C]‐O‐methyldopa was significantly higher (2 fold and 30–50 fold, respectively) than that of rats treated with [14C]‐l‐DOPA.
Total radioactivity in the gut washings and intestinal tissue 2 h after oral administration was significantly higher in rats treated with [14C]‐l‐DOPA than in rats treated with [14C]‐O‐methyldopa. The reverse was observed in the stomach tissues.
Peripheral metabolism of [14C]‐O‐methyldopa was much lower than that of [14C]‐l‐DOPA; the major metabolite of [14C]‐O‐methyldopa in the plasma is l‐DOPA, whereas l‐DOPA is mainly metabolized to phenylcarboxylic acids.
EFFECT OF ETHANOL ON THE OXIDATIVE METABOLISM OF TRYPTAMINE BY RAT LIVER HOMOGENATE
Authors: ASAAD M.M. , BARRY H. , CLARKE D.E. , DIXIT B.N. 
Published: July 2012

The effect of a wide range of ethanol concentrations (v/v) on indoleacetic acid (IAA) formation from the oxidative deamination of tryptamine was studied in vitro, in rat whole liver homogenate.
IAA production was inhibited progressively by ethanol in concentrations between 0.01% to 0.2%, but the inhibition declined when the ethanol concentration was increased further to 6%.
Ethanol‐induced inhibition of IAA formation was only partially reversed by excess aldehyde dehydrogenase, whereas reductions in IAA formation were completely prevented by pyrazole or ethanol (6% and 10%) itself.
Excess nicotinamide adenine dinucleotide failed to alter the inhibitory effect of ethanol and no evidence was obtained for inhibition of monoamine oxidase by ethanol or its metabolite, acetaldehyde.
We conclude that ethanol indirectly inhibits IAA production as a result of oxidation of ethanol by alcohol dehydrogenase, during which the oxidative metabolism of tryptamine is shifted towards the reductive pathway, thus favouring the formation of tryptophol in place of IAA.