bluuebunny/crossref_metadata_2025_split huggingface dataset:
HAEMOGLOBINURIA CAUSED BY PROPYLENE GLYCOL IN SHEEP
Authors: POTTER B. J. 
Published: July 2012

Haemoglobinuria occurred in sheep anaesthetized by an intravenous injection of pentobarbitone sodium containing propylene glycol: an equivalent dose failed to cause haemoglobinuria in rabbits. Intravenous injection of an aqueous solution of 20% propylene glycol caused haemoglobinaemia and haemoglobinuria in sheep. Neither distilled water nor 20% glycerol in water administered under identical conditions produced these effects.Haemoglobinuria occurred on some occasions when an aqueous 20% solution of propylene glycol was administered to sheep after an injection of saline: it never occurred when a solution of 20% propylene glycol prepared with physiological saline was injected. It is suggested that saline may protect against the haemolytic action of propylene glycol in sheep and that propylene glycol should be avoided as a menstruum for pharmaceutical preparations to be used for injection into the blood stream of these animals.
THE EFFECT OF (+)‐LYSERGIC ACID DIETHYLAMIDE AND OTHER DRUGS ON THE CAROTID SINUS REFLEX
Authors: GINZEL K. H. 
Published: July 2012

In cats, lysergic acid diethylamide (LSD) selectively blocked the reflex blood pressure rise following carotid chemoreceptor stimulation. It also reduced or abolished the chemoreceptor component of the pressor response to occlusion of the common carotid arteries. It did not inhibit the respiratory reflexes arising from the carotid chemoreceptors, unless spontaneous respiration was interfered with as a whole. The site of action was central, probably below the intercollicular level, regardless of whether the drug was administered by the intravenous route or into the lateral ventricle of the brain.LSD did not block the baroreceptor depressor reflex elicited by stimulation of one carotid sinus nerve. LSD frequently caused the systemic pressure to fall, even after vagotomy and atropine, and this effect might account for the occasional reduction of the baroreceptor component of the carotid occlusion response. On the other hand, no relationship was found between the action of LSD on vasomotor tone and its blocking effect on the chemoreceptor pressor reflex.Some derivatives of LSD produced effects similar to those described for LSD, whether or not they possessed a psychotropic action in man, and independently of their efficiency as antagonists to 5‐hydroxytryptamine. Of a series of compounds chemically unrelated to LSD, chlorpromazine was found to block the chemoreceptor pressor rise after intracerebroventricular injection.
BIOLOGICAL ACTIVITY OF SYNTHETIC POLYPEPTIDES WITH BRADYKININ‐LIKE PROPERTIES
Authors: KONZETT H. , STÜRMER E. 
Published: July 2012

The biological activity of synthetic polypeptides containing the amino acids of natural pure trypsin‐bradykinin and snake‐venom‐bradykinin has been investigated. A series of tests for bradykinin‐like activity in stimulating plain muscle, depressing the blood pressure and increasing capillary permeability was used on various species. A nonapeptide with the following structure: H‐L‐Arg‐L‐Pro‐L‐Pro‐Gly‐L‐Phe‐L‐Ser‐L‐Pro‐L‐Phe‐L‐Arg‐OH elicited qualitatively and quantitatively the effects of the pure natural bradykinins. An octapeptide with the following structure: H‐L‐Arg‐L‐Pro‐Gly‐L‐Phe‐L‐Ser‐L‐Pro‐L‐Phe‐L‐Arg‐OH also exerted bradykinin‐like effects but was 50 to 100 times less active than the nonapeptide. Three other octapeptides and a heptapeptide were without any significant effect. Further work will demonstrate if the nonapeptide A is synthetic bradykinin or a peptide with bradykinin‐like activity.Note added since submission of this paper: The data from this investigation were personally precommunicated to Elliott, Lewis, and Horton, who have since found that the structure of pure trypsin‐bradykinin is identical with the structure of the nonapeptide A. Therefore, this synthetic nonapeptide is in fact synthetic bradykinin.
Action of various sympathomimetic amines on the isolated stripped vas deferens of the guinea‐pig
Authors: NEDERGAARD O. A. , WESTERMANN E. 
Published: July 2012

. The contractile potencies of some sympathomimetic amines and cholinergic drugs were studied in the isolated, stripped vas deferens of the guinea‐pig.
. α‐Methylnoradrenaline, adrenaline and metaraminol produced the same relative maximal responses as noradrenaline, which served as reference drug; on the other hand, octopamine, dopamine and α‐methyldopamine were much less active. Short term pretreatment of the animals with reserpine did not affect the maximal relative responses.
. Tyramine, α‐methyl‐m‐tyramine and hordenine methiodide had little effect on the untreated preparation. In the presence of just threshold concentrations of noradrenaline, the relative maximal responses to tyramine and hordenine methiodide were markedly increased.
. The relative maximal response to carbachol was the same as that to noradrenaline, while that to DMPP was smaller. In contrast to carbachol, the action of DMPP was potentiated by pretreatment of the preparation with noradrenaline.
The mobilization of free fatty acids from rabbit adipose tissue in situ
Authors: LEWIS G. P. , MATTHEWS J. 
Published: July 2012

. The epigastric adipose tissue of rabbits has been prepared so that the effects of close arterial injections and infusions on blood flow and release of free fatty acids (FFA) can be studied. The effects of pharmacologically active agents and hormone preparations have been investigated.
. Release of FFA was stimulated by synthetic adrenocorticotrophic hormone (ACTH), α and β melanophore stimulating hormone (MSH), porcine growth hormone, glucagon, thyrotropic hormone (TSH) and luteotropic hormone (LTH). Single injections of fat‐mobilizing agents produce a sustained rise in the release of FFA.
. Although pitressin caused release of FFA, synthetic vasopressin and oxytocin failed to do so. The FFA releasing activity of pitressin has therefore been attributed to a contaminant.
. Catecholamines were found not to stimulate release of FFA from this fat depot, but were found to increase plasma FFA when infused intravenously.
. Injections of acetylcholine, histamine, bradykinin, 5‐hydroxytryptamine, synthetic arginine vasopressin, and lysine vasopressin, oxytocin, angiotensin and FSH did not stimulate release of FFA although marked effects on blood flow were produced.
. Injections of prostaglandin E1 gave sustained increases in blood flow, and inhibited FFA release when stimulated by growth hormone.
. The mobilization of FFA is sometimes associated with an increased rate of blood flow.
Effect of rabbit antibodies against angiotensin‐II on the pressor response to angiotensin‐II and renal hypertension in the rat
Authors: HEDWALL P. R. 
Published: July 2012

. In the intact or nephrectomized rat, the pressor responses to synthetic angiotensin‐II‐amide, beta‐angiotensin‐II and native “rat angiotensin” could be inhibited by intravenous injection of rabbit serum containing antibodies against synthetic angiotensin‐II‐amide.
. The pressor responses to vasopressin or noradrenaline were not influenced by anti‐angiotensin serum.
. A single injection of anti‐angiotensin serum inhibited the pressor responses to angiotensin‐II‐amide for a period of 2.5 hr.
. Intravenous infusion or daily intraperitoneal injection of anti‐angiotensin serum did not influence blood pressure levels in renal hypertensive rats.
The inhibitory action of noradrenaline and adrenaline on acetylcholine output by guinea‐pig ileum longitudinal muscle strip
Authors: PATON W. D. M. , VIZI E. S. 
Published: July 2012

Noradrenaline and adrenaline reduce the output of acetylcholine by the guinea‐pig ileum longitudinal strip by up to 80%, both in resting conditions and after stimulation. The effect is graded with dose, and is detectable with noradrenaline 2 × 10−7 g/ml. Adrenaline is approximately 4 times as active as noradrenaline, and its action after being washed out is more persistent.
If resting output is high, both amines have a proportionately greater effect and their action, as dosage is increased, is to reduce resting output to a basal level, relatively constant from strip to strip, of about 10 ng/g/min.
With stimulation, the effect of the amine is greater at low frequencies, when the output per volley is high, than at high frequencies. The effect is reduced by increasing the number of shocks delivered. There thus appears to be a basal output per volley, of the order of 1–2 ng/g/volley, which can be reached either by relatively rapid stimulation, by prolonged stimulation, or by treatment with these amines.
If noradrenaline is applied during continued stimulation at 40/min, the depression of acetylcholine output during its presence is followed by an augmented output when the drug is withdrawn. The magnitude of this “overshoot” increases with the duration of noradrenaline exposure.
Phenylephrine 4 μg/ml. and amphetamine 20 μg/ml. reduced the acetylcholine output, but isoprenaline 1 μg/ml., dopamine 1 μg/ml. and methoxamine 10 μg/ml. were ineffective.
Phenoxybenzamine reduced the resting output and increased the stimulation output. Of the two other blocking agents examined, phentolamine had no effect on either resting or stimulation output and ergotamine transiently reduced stimulation output. The effect of phenoxybenzamine was not due to a reaction with either adrenoceptive or muscarinic receptors.
Phenoxybenzamine, phentolamine and ergotamine abolished the effect of adrenaline and noradrenaline on both resting output and on output in response to stimulation.
In strips obtained from animals treated with reserpine and guanethidine, a rise in resting acetylcholine output and in stimulation output at low frequencies was found. In these conditions, noradrenaline was still effective.
Reducing the hydroxytryptamine content of the strips by treatment with p‐chloro‐(±)‐phenylalanine did not significantly affect acetylcholine output.
It is concluded that acetylcholine output by the nervous networks of the longitudinal strip is under the normal control of the sympathetic by a species of presynaptic inhibition mediated by α receptors. This implies that for a tissue under dual autonomic control, withdrawal of sympathetic control will lead to a parasympathetic response which is not only unopposed but also itself enhanced.
Spontaneous and evoked release of neurotransmitter substances in the longitudinal muscle of the anterior mesenteric artery of the domestic fowl
Authors: BOLTON T. B. 
Published: July 2012

Changes in length of the longitudinal muscle of the anterior mesenteric artery of the domestic fowl (LMAMA) were recorded isotonically.
The actions of physostigmine and hyoscine suggest that the tone of the LMAMA is dependent on a resting release of acetylcholine within the tissue.
Catecholamines inhibited the contractions obtained in response to stimulation of cholinergic nerves; this was a β‐receptor effect. After β‐receptor blockade, noradrenaline, but not isoprenaline, weakly facilitated the effects of stimulating cholinergic nerves.
In the presence of hyoscine, nicotine relaxed preparations of the LMAMA in which the tone had been raised with barium chloride. These relaxations were considered to be due to a release of catecholamine probably from sympathetic nerves.
The cardio‐toxicity of isoprenaline during hypoxia
Authors: COLLINS J. M. , McDEVITT D. G. , SHANKS R. G. , SWANTON J. G. 
Published: July 2012

The effects of the intravenous injection of isoprenaline on heart rate and arterial pressure has been studied in dogs artificially respired with room air or with 12% oxygen—88% nitrogen.
In dogs breathing room air, isoprenaline in doses from 0.02 to 500 μg/kg increased heart rate and reduced arterial pressure. Ventricular fibrillation was produced in one out of three dogs given 250 μg/kg. This was the only dog breathing room air which was killed by isoprenaline.
In dogs breathing room air the repeated intravenous injection at 5‐min intervals of 2.5 μg/kg increased heart rate and reduced arterial pressure. No ill effects were produced by six doses.
In dogs respired with 12% oxygen—88% nitrogen the Pao2 was reduced from 84 to 38 mm Hg with no changes in Paco2. In these dogs death was produced by doses of isoprenaline which in dogs breathing room air produced normal responses.
The fatal dose of isoprenaline (10–50 μg/kg) reduced heart rate and arterial and pulse pressures; sinus rhythm persisted until arterial pressure was less than 50 mm Hg. Ventricular fibrillation did not occur; death occurred from cardiac asystole.
Death was produced in a similar way in dogs with hypoxaemia by giving four or five doses of isoprenaline (2.5 μg/kg) at 5‐min intervals or by two doses of 25 μg/kg.
The final reduction in arterial pressure during a fatal response resulted from a reduction in cardiac contractility.
These lethal effects of isoprenaline could be prevented by pretreatment with propranolol.
Effects of phenoxybenzamine on the uptake and metabolism of noradrenaline in the rat heart and vas deferens
Authors: IVERSEN L. L. , LANGER S. Z. 
Published: July 2012

. In the isolated rat heart perfused with various concentrations of (±)‐3H‐noradrenaline (3H‐NA) the addition of phenoxybenzamine, cocaine or desipramine to the perfusion medium resulted in an inhibition of 3H‐NA uptake which appeared on kinetic analysis to be of a competitive nature.
. Phenoxybenzamine also blocked the formation of labelled metabolites of 3H‐NA in the heart at all perfusion concentrations of 3H‐NA; this effect appeared to be unrelated to the inhibition of the neuronal uptake of NA produced by phenoxybenzamine, since no blockade of 3H‐NA metabolism was produced by cocaine in similar experiments.
. In slices of rat vas deferens incubated with various concentrations of 3H‐NA, cocaine and desipramine and phenoxybenzamine were also shown to act as competitive inhibitors of NA uptake. Cocaine and phenoxybenzamine were less potent inhibitors of uptake in the vas deferens than they were in the heart; desipramine was equally potent in both tissues.
. When vas deferens slices were incubated in a medium containing phenoxybenzamine for 30 min before the addition of 3H‐NA, the resulting inhibition of 3H‐NA uptake was increased and changed to a non‐competitive type of interaction.
. In hearts or vasa deferentia taken from animals pretreated in vivo with phenoxybenzamine (20 mg/kg), a significant inhibition of 3H‐NA uptake was found when the tissues were exposed to low concentrations of 3H‐NA but not when higher concentrations of 3H‐NA were used.
Sodium‐dependent accumulation of 5‐hydroxytryptamine by rat blood platelets
Authors: SNEDDON J. M. 
Published: July 2012

. The influence of sodium and potassium on the accumulation of 5‐hydroxytryptamine (5‐HT) by rat blood platelets was investigated.
. An absolute dependence of 5‐HT uptake on the sodium concentration in the medium was found.
. Removal of potassium reduced the uptake by about 60% High concentrations of potassium inhibited sodium‐dependent accumulation.
. The observations have been discussed in terms of a carrier‐mediated transport process for 5‐HT operating in the platelet membrane.
A hyoscine‐resistant contraction of isolated chicken oesophagus in response to stimulation of parasympathetic nerves
Authors: HASSAN T. 
Published: July 2012

. Contractions of the chicken isolated oesophagus or separated external muscle produced by stimulation of the vagus and descending oesophageal nerves were abolished by hyoscine (1–100 μg/ml.) if the duration of stimulation was less than 5 sec, but prolonged stimulation produced delayed contractions not antagonized by hyoscine.
. The contractions to nerve stimulation were abolished by nerve section but not by bretylium, hexamethonium or tubocurarine.
. In decerebrate chickens, intravenous hyoscine abolished the contractions of the oesophagus produced by nerve stimulation, but previous intravenous injection of hyoscine into chicks did not prevent subsequently isolated oesophageal preparations from contracting to nerve stimulation.
. Prolonged nerve stimulation of an isolated oesophageal preparation did not produce a contraction from a piece of isolated guinea‐pig ileum or post‐crop chick oesophagus suspended in the same organ‐bath.
. It seems possible that small amounts of a slow contracting substance were released from the stimulated nerves together with acetylcholine.
Aspects of the pharmacology of a new anthelmintic: pyrantel
Authors: AUBRY M. L. , COWELL PAULINE , DAVEY M. J. , SHEVDE S. 
Published: July 2012

Summary
. The pharmacological properties of an anthelmintic, pyrantel, and some of its analogues have been described and compared with piperazine in a variety of vertebrate and helminth preparations.
. Pyrantel and its analogues in common with nicotine and decamethonium cause spastic paralysis in chicks and contracture of the chick semispinalis and toad rectus abdominis muscles.
. In the soleus and anterior tibialis muscles of the cat, pyrantel in large amounts caused a short‐lived neuromuscular block that was preceded by initial depolarization.
. In preparations from cat and rat, pyrantel showed properties common to both competitive and depolarizing neuromuscular blocking drugs.
. Pyrantel blocked the contracture evoked by transmural stimulation and caused a marked contracture of the worm. Piperazine caused a gradually developing reduction in the responses to transmural stimulation and no contracture.
. Pyrantel and its analogues caused a slowly developing contracture of strip preparations of Ascaris, being more than 100 times more active than acetylcholine in this respect. Piperazine caused a relaxation of Ascaris strip preparations and in common with (+)‐tubocurarine blocked the responses to acetylcholine and pyrantel analogues on this preparation.
. Pyrantel caused depolarization and increased spike discharge frequency in single muscle cells of Ascaris, these changes being accompanied by increase in tension. Piperazine, on the other hand, caused hyperpolarization and reduction in spike discharge frequency and relaxation, and antagonized the effects of pyrantel.
Inhibition of rabbit intestine mediated by α‐ and β‐adrenoceptors
Authors: BOWMAN W. C. , HALL MOIRA T. 
Published: July 2012

Summary
. The effects of some α‐ and β‐adrenoceptor agonists and antagonists were studied on isolated segments of rabbit intestine in an attempt to characterize the two types of inhibitory response produced by sympathomimetic amines.
. Phenylephrine, an α‐adrenoceptor agonist, produced an inhibition of rapid onset, from which recovery occurred despite the continued presence of the drug. On washout there was an overshoot in contraction height. Isoprenaline, a β‐adrenoceptor agonist, produced an inhibition of slow onset which was maintained throughout the presence of the drug and there was no overshoot on washout.
. Adrenaline resembled phenylephrine more closely than it resembled isoprenaline, in that it showed more affinity for α‐adrenoceptors, whereas noradrenaline, and the transmitter released on periarterial nerve stimulation, behaved more like isoprenaline, although both types of receptor were affected.
. Adenosine‐5′‐triphosphate produced an inhibition resembling that produced by an α‐adrenoceptor agonist, whereas the dibutyryl analogue of cyclic adenosine 3′,5′‐monophosphate (cyclic 3′,5′‐AMP) produced an inhibition resembling that produced by a β‐adrenoceptor agonist.
. In critical concentrations theophylline augmented and imidazole inhibited β‐adrenoceptor mediated responses, as well as responses to dibutyryl cyclic AMP. However, additional actions of theophylline and imidazole were also demonstrated.
. Responses mediated by α‐adrenoceptors, but not those mediated by β‐adrenoceptors, were blocked by membrane stabilizers, quinidine being the most potent of those studied.
. The results are discussed in relation to the possible mechanisms of action of α‐ and β‐adrenoceptor agonists.
Some factors influencing the release of 5‐hydroxyindol‐3‐ylacetic acid in the forebrain
Authors: PADJEN A. , RANDIĆ MIRJANA 
Published: July 2012

Summary
. Electrical stimulation of the mid‐brain raphé in anaesthetized adrenalectomized rats produced a significant decrease in the forebrain content of 5‐hydroxytryptamine (5‐HT) and an increase in the concentration of 5‐hydroxyindol‐3‐ylacetic acid (5‐HIAA).
. Stimulation of peripheral sensory nerves did not influence either the forebrain content of 5‐HIAA or the efflux of 5‐HIAA from the cerebral cortex.
. Probenecid (200 mg/kg) caused a twofold increase in 5‐HIAA content of the rat's forebrain, while the efflux of 5‐HIAA from the cerebral cortex remained unchanged.
. Stimulation of the mid‐brain raphé in animals pretreated with probenecid does not produce the rise in the forebrain levels of 5‐HIAA seen in stimulated untreated controls and does not affect the efflux of 5‐HIAA from the cerebral cortex.
. In preliminary experiments, lysergic acid diethylamide (LSD 25) substantially reduced and/or prevented the increase in the release of 5‐HIAA in the forebrain observed in untreated animals with raphé stimulation.
The action of angiotensin on the human colon in vitro
Authors: FISHLOCK D. J. , GUNN A. 
Published: July 2012

Summary
. The action of angiotensin on the circular and longitudinal muscle of the human colon has been studied in vitro. The ED50 value (g/ml) of circular muscle was 8.7 × 10−8 and of longitudinal muscle 3.1 × 10−8, while the corresponding figures for acetylcholine were 1.6 × 10−6 and 1.1 × 10−6, respectively. Angiotensin caused a sustained contraction associated with prolonged tachyphylaxis.
. As the action of angiotensin was not antagonized by atropine, hexamethonium or procaine, angiotensin appeared to act directly on the smooth muscle of the human colon.
. Lidoflazine is not a specific antagonist of angiotensin.
Influence of thyroid hormones on the sensitivity of cardiac and smooth muscle to biogenic amines and other drugs
Authors: COVILLE P. F. , TELFORD J. M. 
Published: July 2012

Summary
. Rats and guinea‐pigs were injected with 1‐thyroxine or thyroidectomized. Sensitivity of isolated tissues and of the intact cardiovascular system to drugs was investigated.
. Thyroxine increased the sensitivity of the isolated perfused heart to noradrenaline, adrenaline, isoprenaline, acetylcholine and histamine.
. Thyroxine increased the sensitivity of the rat isolated uterus to noradrenaline, adrenaline, isoprenaline, acetylcholine, histamine and 5‐hydroxytryptamine.
. In contrast, thyroxine decreased the sensitivity of the isolated ileum to acetylcholine, histamine and 5‐hydroxytryptamine, but not to adrenaline.
. Thyroxine also decreased the sensitivity of the isolated aorta to noradrenaline, adrenaline, histamine and 5‐hydroxytryptamine.
. In pithed rats, thyroxine potentiated pressor responses to (+)‐amphetamine but not to noradrenaline or synephrine.
. In anaesthetized thyroxine‐treated rats, blood pressure responses to (+)‐amphetamine were potentiated while those to noradrenaline were unaltered. Responses to acetylcholine were increased, and the response to isoprenaline became purely pressor.
. Thyroxine‐induced changes in the sensitivity of the isolated uterus and ileum to modification of the concentration of calcium in the physiological salt solution paralleled the changes in drug sensitivity of these tissues.
. In general, thyroidectomy produced the opposite effects to those of thyroxine.
. It is concluded that there is no specific interaction between thyroxine and sympathomimetic amines, the effect of thyroxine on drug sensitivity being non‐specific.