bluuebunny/crossref_metadata_2025_split huggingface dataset:
Suppression of adrenocorticotrophic activity in the ascorbic acid deficient guinea‐pig
Authors: HODGES J. R. , HOTSTON R. T. 
Published: July 2012

Summary
Adrenocortical hyperactivity caused by a marked increase in circulating corticotrophin occurred in guinea‐pigs on a diet deficient in ascorbic acid.
Betamethasone prevented the rise in the blood ACTH concentration in scorbutic animals and also the increased steroid production per gramme adrenal tissue in vitro. It diminished the adrenal hypertrophy and partially suppressed the rise in plasma Cortisol.
Ninety minutes after the injection of ascorbic acid corticotrophin could no longer be detected in the plasma of scorbutic animals.
Neither the survival time nor the weight loss was affected by betamethasone treatment.
Comparison of the effects of isoprenaline, orciprenaline, salbutamol and isoetharine on the cardiovascular system of anaesthetized dogs
Authors: EKUE J. M. KOFI , SHANKS R. G. , ZAIDI S. A. 
Published: July 2012

Summary
The intravenous injection of isoprenaline, orciprenaline, salbutamol and isoetharine increased heart rate in anaesthetized dogs. Log dose‐response curves obtained with a series of doses of salbutamol and isoetharine were flatter than those for isoprenaline and orciprenaline. The order of activity of the drugs in increasing heart rate was isoprenaline, orciprenaline, and salbutamol=isoetharine.
The injection into the external iliac artery of isoprenaline, orciprenaline, salbutamol and isoetharine produced dose dependent increases in femoral blood flow. Log dose‐response curves for all drugs were parallel. The order of activity of the drugs was isoprenaline, salbutamol=isoetharine and orciprenaline.
Salbutamol and isoetharine were less active than orciprenaline in increasing heart rate but more active in increasing femoral blood flow.
These observations indicate that salbutamol and isoetharine have a greater effect on β2 than on β1‐adrenoceptors in the cardiovascular system.
Passage into the rat brain of dopa and dopamine injected into the lateral ventricle
Authors: CONSTANTINIDIS J. , GAILLARD J. M. , GEISSBUHLER F. , TISSOT R. 
Published: July 2012

Summary
The green fluorescence of catechols of the brain was studied in rats after intraventricular injection of l‐dopa or dopamine in untreated rats as well as in rats in which dopa decarboxylase (DC) was inhibited by Ro 4602, or the monoamine oxidase by nialamide.
From the patterns of fluorescence obtained in these conditions, it is concluded that in the areas close to the liquor space dopa is rapidly taken up by the endothelium of the brain capillaries and then converted into dopamine; when the DC is inhibited the dopa passes freely from the endothelium into the brain tissue.
On the other hand, dopamine passes from the liquor space via the ependyma directly into the brain tissue and from there into the capillary endothelium which is thus permeable to the amine in the direction from the brain tissue, in contrast to the impermeability in the direction from the capillary lumen.
Impulse transmission in the myenteric plexus‐longitudinal muscle preparation of the guinea‐pig ileum
Authors: KOSTERLITZ H. W. , LYDON R. J. 
Published: July 2012

Summary
In a preparation consisting of the myenteric plexus and the longitudinal muscle layer removed from a segment of guinea‐pig ileum, spontaneous action potentials occurred which were unaffected by tetrodotoxin but suppressed by Mn2+ and were therefore myogenic.
A single current pulse of 0·1 ms duration evoked a response consisting of an early action potential followed after a delay of about 200 ms by a complex of biphasic spikes. The first action potential was conducted for no more than 15 mm and the second complex for 30–70 mm.
Since the first action potential was unaffected by hyoscine or Mn2+ but abolished by tetrodotoxin, it was due to excitation of nerve fibres. The later complex of spikes was suppressed by hyoscine and Mn2+ and therefore due to excitation of smooth muscle. It was also inhibited by adrenaline or morphine, compounds which depress acetylcholine release. The evoked smooth muscle response was followed by absence of spontaneous electrical activity for 2–4 seconds.
The nerves travelling in a longitudinal direction had a mean maximum conduction velocity of 0·65 m/s, an absolute refractory period of 2·8 ms and a relative refractory period of about 20 ms.
The conduction velocity of the smooth muscle response evoked by stimulation of the nerve with a single pulse was 0·16 m/second. After a single pulse the muscle was inexcitable for 0·7–1·3 s; the delay of transmission from nerve to muscle was 210 ms. When instead of a single pulse a train of two—five pulses at 20 ms intervals was applied, the size, conduction distance and conduction velocity of the evoked smooth muscle response were increased.
Release of noradrenaline and dopamine by nerve stimulation in the cat spleen perfused with 3H‐dopamine
Authors: KIRPEKAR S. M. , YAMAMOTO H. 
Published: July 2012

Summary
Recovery of 3H‐dopamine and 3H‐l‐dopa infused intra‐arterially at a constant rate of 20 ng/min into the cat spleen perfused with Krebs bicarbonate solution was 52·6 ± 3·8% and 90·5 ± 3·1% respectively. Recovery of 3H‐dopamine in spleens treated with α‐methyl‐p‐tyrosine was 67·7 ± 6·7% and was not significantly different from untreated spleens.
Release of 3H‐dopamine by nerve stimulation after an infusion of 3H‐dopamine resembled release of endogenous noradrenaline. Release of 3H‐l‐dopa and 3H‐l‐tyrosine after their infusion did not occur in any consistent manner by nerve stimulation.
Preferential release of 3H‐noradrenaline formed from 3H‐dopamine was not observed during continuous nerve stimulation. Specific activity of released 3H‐noradrenaline remained constant during any single stimulation period with or without 3H‐dopamine infusion. Treating the cats with α‐methyl‐p‐tyrosine did not change the time course of 3H‐noradrenaline release.
Output of noradrenaline expressed as a percentage of the first minute output in both normal and α‐methyl‐p‐tyrosine treated spleens was not significantly different at various times during continuous nerve stimulation.
Specific activity of released noradrenaline formed from 3H‐dopamine was always greater than the specific activity of the spleen in normal spleens and spleens treated with α‐methyl‐p‐tyrosine.
It is concluded that newly synthesized or infused noradrenaline initially mixes with a more rapidly turning pool and only slowly with the entire tissue store. During continuous nerve stimulation there is no further preferential release of newly synthesized noradrenaline. Released noradrenaline truly represents the state of the releasable pool and will vary with the latter.
Excretion of nitrofurantoin in dog hepatic bile
Authors: CONKLIN J. D. , WAGNER D. L. 
Published: July 2012

Summary
After the intravenous administration of nitrofurantoin sodium to dogs at nitrofurantoin doses of 1·5–24·0 mg/kg, a substantial amount of nitrofurantoin is excreted in bile. The bile to blood drug ratios were about 200. A marked hydrocholeretic effect which correlated directly with the amount of nitrofurantoin administered was also observed.
The excretion of nitrofurantoin in bile and the hydrocholeretic effect were linear with the dose of drug over the range 1·5–12·0 mg/kg. Maximum increases in hepatic bile flows were usually from 5–10 ml/0·5 h, while average control bile flow was 1·6 ml ± s.d. 0·6/0·5 hours. The lowest dose at which the hydrocholeretic effect was still detectable was 0·09 mg/kg.
Apparent saturation of the biliary excretion system for nitrofurantoin and the hydrocholeretic mechanism occurred after a dose of 24·0 mg/kg. Saturation of the urinary system for nitrofurantoin excretion was noted after a dose of 6·0 mg/kg.
Biliary nitrofurantoin recoveries ranged from 16·5% ± s.d. 4·2 to 22·6% ± s.d. 4·7 for the 6 h period after doses of 1·5, 30, and 6·0 mg/kg. Urinary nitrofurantoin recoveries for the same interval ranged from 24·1% ± s.d. 6·6 to 36·2% ± s.d. 8·3.
In comparison to values obtained in normal dogs, only about one‐tenth of the drug excretion in bile and about one‐fifth of the hydrocholeretic effect were obtained after intravenous drug administration to dogs with hepatic impairment induced by CCl4.
Effects of non‐ionic surfactants that modify experimental tuberculosis on lipase activity of macrophages
Authors: D'ARCY HART P. , PAYNE SHEILA N. 
Published: July 2012

Summary
Six series of non‐ionic surface active polyethylene glycol ethers, whose effects on experimental tuberculosis have previously been correlated with their polyoxyethylene chain lengths, were examined for their influence on the activity of a lipase present in homogenates of normal mouse peritoneal macrophages. The surfactants are concentrated in the lysosomes of macrophages—a cell type in which the host‐parasite confrontation takes place. A preparation of soy bean oil was used as triglyceride substrate; and hydrolysis at pH 4·5 was compared in the presence and absence of surfactant, the products of hydrolysis being assayed by photodensitometry of thin‐layer chromatograms.
The compounds with short polyoxyethylene chains inhibited the release of fatty acid, compared with surfactant‐free standard, more than did those with long chains; and some of the latter showed actual enhancement of release. Accumulation of monoglyceride was observed in the presence of six of the seven long‐chained compounds, but with none of the seven short‐chained compounds.
The similarity between this correlation of chain length of the surfactants with their effect on macrophage lipase activity, and the known correlation of their chain length with their effect on experimental tuberculosis, suggests a possible connection. How this connection might relate to the mechanism of the varying effects on tuberculosis is briefly discussed.
Blockade by phenoxybenzamine of the contractor response produced by agonists in the isolated ileum of the guinea‐pig
Authors: COOK D. A. 
Published: July 2012

Summary
The effects of various concentrations of phenoxybenzamine (dibenzyline) on the contractor response of the isolated ileum of the guinea‐pig were investigated. The agonists tested were histamine, 5‐hydroxytryptamine (5‐HT), acetycholine and potassium chloride.
In addition, uptake of 14C‐phenoxybenzamine into the ileum was determined as a function of antagonist concentration. The uptake increases sharply at concentrations above 10−6 g/ml, (3×10−6m) and was not saturable at any concentration tested.
In the presence of low concentrations of phenoxybenzamine, the dose‐response curve for histamine undergoes a parallel shift of about 0·5 log units. At higher concentrations of phenoxybenzamine the maximum response is depressed. In the case of the other agonists, the maximum response is depressed as soon as any blockade becomes apparent.
The ease of blockade with phenoxybenzamine is 5‐HT ≥ histamine> acetylcholine ≥ potassium chloride.
These results do not lend support to the ‘spare‐receptor’ hypothesis and may be better explained by the ‘two‐site’ hypothesis of Moran & Triggle (1970).
It may further be concluded that the successful antagonism of potassium‐induced contractions in this preparation lies in the ability of phenoxybenzamine to prevent the action of released acetylcholine. In the case of the contraction induced by 5‐HT, phenoxybenzamine probably interferes with the 5‐HT receptor responsible for neuronal release of acetycholine.
Inhibitory effect of chlorpromazine on the syndrome of hyperactivity produced by l‐tryptophan or 5‐methoxy‐N,N‐dimethyltryptamine in rats treated with a monoamine oxidase inhibitor
Authors: GRAHAME‐SMITH D. G. 
Published: July 2012

Summary
The hyperactivity and hyperpyrexia produced by l‐tryptophan in rats treated with a monoamine oxidase inhibitor was inhibited by chlorpromazine.
Chlorpromazine did not inhibit the increased rate of synthesis of brain 5‐hydroxytryptamine (5‐HT) produced by tryptophan loading.
Hyperactivity and hyperpyrexia were also produced by 5‐methoxy‐N,N‐dimethyltryptamine (5‐MeODMT) in rats. Pretreatment with a monoamine oxidase inhibitor potentiated the hyperactivity response. Pretreatment of rats with p‐chlorophenylalanine did not inhibit hyperactivity produced by 5‐MeODMT.
Chlorpromazine inhibits hyperactivity caused by tryptophan or 5‐MeODMT after monoamine oxidase inhibition either by competition with 5‐HT or 5‐MeODMT, respectively, at receptor sites or by physiological antagonism.
Actions of prostaglandin F2α on the splenic vascular and capsular smooth muscle in the dog
Authors: DAVIES B. N. , WITHRINGTON P. G. 
Published: July 2012

Summary
The actions of prostaglandin F2α, which is known to be released by the spleen on sympathetic nerve stimulation, have been investigated in the isolated blood perfused spleen of the dog.
Low arterial concentrations of F2α (less than 10 μg/100 ml) caused marked reductions in splenic vascular resistance.
High arterial concentrations of F2α (above 10 μg/100 ml) caused increases in splenic vascular resistance.
Little action on splenic volume was observed by any arterial concentration of F2α.
The reductions in splenic vascular resistance caused by low arterial concentrations of F2α were reversed by blocking doses of phenoxybenzamine.
No appreciable interaction between F2α and the splenic responses to sympathetic nerve stimulation, adrenaline and noradrenaline was observed.
The role of the prostaglandins released by the spleen is discussed.
Investigation of the mechanism of action of oxotremorine on the guinea‐pig isolated ileum preparation
Authors: COX B. , HECKER SALLY E. 
Published: July 2012

Summary
The effects of oxotremorine on the guinea‐pig ileum have been investigated to determine whether any component of its action is due to acetylcholine release.
Log dose‐response curves to oxotremorine and acetylcholine were similar and both drugs were competitively antagonized by atropine.
Mipafox potentiated acetylcholine but not oxotremorine.
No evidence of an indirect component of the action of oxotremorine was obtained using various pharmacological procedures (tetrodotoxin, morphine, cooling, procaine and hemicholinium‐3).
Oxotremorine had no effect on acetylcholine release from mipafox treated ileum but decreased the release from physostigmine treated ileum.
It is concluded that oxotremorine acts directly on muscarinic receptors and not by releasing acetylcholine.
Influence of pH on aggregation and protein binding of barbituric acid and amylobarbitone
Authors: MIKIKITS W. , SKINNER A. , SPECTOR R. G. , WATTS D. C. 
Published: July 2012

Summary
Cryoscopic methods indicated that barbituric acid exists in aqueous solution as a monomer. Amylobarbitone is a monomer at pH 8, but appears to be polymerized at pH 2. The size of the oligomers increases with drug concentration.
Using a non‐equilibrium dialysis technique supportive evidence for the monomeric form of barbituric acid and the polymerization of amylobarbitone was obtained. The degree of polymerization appeared to increase with fall in pH. Binding constants for these barbiturates with bovine serum albumin were derived, but in acid media no binding was observed.
On the neuromuscular paralysis produced by procaine
Authors: HIRST G. D. S. , WOOD D. R. 
Published: July 2012

SummaryThe effects of procaine on neuromuscular transmission in the rat phrenic nerve diaphragm preparation have been examined using intracellular recording techniques.The paralysis produced by procaine resembled that produced by tubocurarine and it is concluded that this effect of procaine results from a change in post‐junctional sensitivity to transmitter; at low rates of stimulation procaine did not depress the transmitter release.During high frequency stimulation of the phrenic nerve a distinct form of prejunctional failure was observed. It is suggested that this depression results from a combination of local anaesthesia and anoxia and that it would explain reports of a reduction in the amount of transmitter released when assayed in a conventional manner.
Changes in the time course of transmitter action produced by procaine
Authors: HIRST G. D. S. , WOOD D. R. 
Published: July 2012

Summary
In addition to reducing the sensitivity of the end‐plate to transmitter, procaine produced changes in the time course of the end‐plate potential. The time to peak potential was reduced by procaine, whether recording from fibres paralysed by tubocurarine or from fibres paralysed by high magnesium concentration. The rate of decay of potential was also markedly reduced. Similar observations were made recording spontaneous miniature end‐plate potentials.
Procaine did not produce any marked change in the electrical constants of muscle fibres.
In the presence of procaine the accumulation of charge at the end‐plate was prolonged; the rate of decay of charge was reduced. It is suggested that the prolonged end‐plate potentials arise from a prolongation of the end‐plate current.
Factors influencing the inhibitory action of anti‐inflammatory drugs on carrageenin induced oedema
Authors: GREEN ANN Y. , GREEN D. , MURRAY PATRICIA A. , WILSON A. B. 
Published: July 2012

Summary
In a series of experiments carried out over 2½ years, the inflammatory response of the rat hind paw to injected carrageenin was relatively constant, but the anti‐inflammatory activity of phenylbutazone was subject to wide variation.
Phenylbutazone, aspirin and indomethacin were all well absorbed after oral administration, and the resultant plasma drug concentrations were closely similar to those produced when the drugs were administered intraperitoneally.
The anti‐inflammatory effect of the drugs on carrageenin oedema was variable and poorly correlated with log dose and plasma concentration.
There was a pronounced and linearly correlated increase in the anti‐inflammatory activity of phenylbutazone with increasing ambient temperature in the range 5–30° C.
Variations in relative humidity at constant temperature (20° C) did not influence the anti‐oedema potency of phenylbutazone.
For the precise evaluation of anti‐inflammatory activity in carrageenin oedema tests, it is concluded that accurate control of temperature is essential.
Effects of pethidine and nalorphine on the mechanical and electrical activities of mammalian isolated ventricular muscle
Authors: GRUNDY H. F. , TRITTHART H. 
Published: July 2012

Summary
. The strength of the isometric mechanical contraction of electrically‐driven ventricular muscle has been recorded simultaneously with the resting and action potentials; the effects of pethidine and of nalorphine on these parameters have been studied.
. When lower concentrations of pethidine (0·22–6·5 μg/ml) were perfused, isometric peak tension was decreased in parallel with the maximum upstroke velocity of the action potential; these actions are considered to result from membrane stabilization. At higher concentrations (11·8–109 μg/ml) pethidine usually produced, in addition, a progressive decrease in the resting and action potentials associated with marked irregularities in, or even abolition of, the mechanical response. It is suggested that these effects of the higher doses might be due to a depression of ATPase activity in the myocardial membrane.
. Compared with pethidine, nalorphine had similar, but weaker, actions.
Blockade of the reticulospinal inhibitory pathway by nitrous oxide and tetrodotoxin
Authors: FRANK G. B. , OHTA M. 
Published: July 2012

Summary
. The effects of nitrous oxide and tetrodotoxin were investigated on the reticulospinal inhibitory pathway in the acutely decerebrated cat.
. Both agents abolished the reticular inhibition of the segmental reflex potentials before they blocked either the segmental reflex potentials or the reticular facilitation of the reflex potentials.
. These results confirmed the hypothesis that preferential block of the reticulospinal inhibitory pathway might be an important neural mechanism of the excitement stage of anaesthesia.
On the role of central nervous system catecholamines and 5‐hydroxytryptamine in the nialamide‐induced behavioural syndrome
Authors: MODIGH K. , SVENSSON T. H. 
Published: July 2012

Summary
. Intraperitoneal administration of nialamide, 200 mg/kg, to mice elicited a pronounced increase in motor activity and rectal temperature concomitant with a gradual increase in the concentrations of 5‐hydroxytryptamine (5‐HT), noradrenaline (NA) and dopamine in the brain.
. In mice treated with l‐tryptophan, 300 mg/kg, 1 h before nialamide, the increase in motor activity appeared earlier than after nialamide alone, and the hyperthermia was more pronounced. The increase in 5‐HT concentrations in the brain was more pronounced in these animals, whereas the concentrations of NA and dopamine were of the same magnitude as after nialamide alone.
. Treatment with p‐chlorophenylalanine methylester‐HCl (PCPA), 400 mg/kg, 24 h before nialamide partially antagonized the increase in motor activity and the accumulation of NA and dopamine was not significantly different from that observed after nialamide alone.
. Treatment with PCPA, 800 mg/kg, 72, 48 and 24 h before nialamide, completely antagonized the increase in motor activity and rectal temperature. The accumulation of brain 5‐HT was greatly depressed in these animals. The concentrations of dopamine 1, 3 and 6 h and the concentration of NA 6 h after the nialamide injection were significantly lower in the mice given PCPA 800 mg/kg × 3, than in the mice given nialamide alone.
. Administration of dl‐5‐hydroxytryptophan, 30 mg/kg, 1 h after the nialamide injection, to mice pretreated with PCPA, 800 mg/kg × 3, restored the increase in motor activity and rectal temperature.
. l‐Tryptophan, 300 mg/kg, given 1 h before nialamide to mice pretreated with PCPA, 800 mg/kg × 3, elicited a moderate increase in motor activity and a slight increase in the accumulation of 5‐HT in the brain when compared to that after PCPA, 800 mg/kg × 3, and nialamide.
. Administration of α‐methyltyrosine methylester, 200 mg/kg, 2 h before nialamide partially antagonized the increase in motor activity and completely antagonized the increase in rectal temperature elicited by nialamide alone. The accumulation of brain NA and dopamine was inhibited in these animals.
. It is concluded that the excitation in mice, elicited by nialamide, is mediated largely via brain 5‐HT, but that also the brain catecholamines seem to contribute to this effect.
Influence of age and of testosterone on the response of male rats to parachlorophenylalanine
Authors: BOND VALERIE J. , SHILLITO ELIZABETH E. , VOGT MARTHE 
Published: July 2012

Summary
. Castrated male rats and male rats that had been castrated as well as adrenalectomized, showed hypersexual behaviour 24 h after treatment with parachlorophenylalanine (PCPA), as did intact rats.
. A dose of PCPA 100 mg/kg was sufficient to induce mounting behaviour; this dose lowered the cerebral 5‐hydroxytryptamine (5‐HT) to about 50% in 24 h and further to 40% in 72 hours.
. Groups of juvenile male rats treated chronically with PCPA 100 mg/kg or 50 mg/kg, or with testosterone propionate 1·25 mg, showed hair loss after three weeks of treatment (6 injections), because of increased social interaction.
. Groups of intact male rats 9–11 weeks old given testosterone propionate 1·25 mg subcutaneously, showed mounting behaviour 3–5 h after the injection which was indistinguishable from the behaviour seen 24 h after treatment with PCPA 100 mg/kg. The 5‐HT content of the brain was not altered by testosterone.
. The number of rats which showed mounting after PCPA treatment did not change with age, but the younger rats made more mounts in the observation time than rats more than three months old.
. The age of castration (3 weeks or 4 months) did not influence the results.