bluuebunny/crossref_metadata_2025_split huggingface dataset:
INHIBITORY EFFECT OF A PYRROLIDINE ALKALOID, CROTALABURNINE, ON RAT PAW OEDEMA AND COTTON PELLET GRANULOMA
Authors: GHOSH M.N. , SINGH H. 
Published: July 2012

The anti‐inflammatory activity of crotalaburnine (=anacrotine) was investigated against increased vascular permeability and oedema produced by formalin, carrageenin, hyaluronidase, 5‐hydroxytryptamine, dextran, bradykinin and prostaglandin, and against formation of granulation tissues by cotton‐pellet in rats. The effect was compared with the activity of hydrocortisone, phenylbutazone, sodium salicylate and cyproheptadine against different types of inflammation.
Crotalaburnine (40 mg/kg s.c. × 5 alternate days) had no significant inhibitory effect against formalin‐induced arthritis, while hydrocortisone (40 mg/kg s.c. × 10 days) was effective from the fifth day onwards.
Against carrageenin‐induced oedema both crotalaburnine (10 mg/kg s.c.) and phenylbutazone (100 mg/kg oral) produced a similar degree of inhibition. Hydrocortisone (10 mg/kg s.c.) produced slightly greater inhibition.
In normal rats crotalaburnine (10 mg/kg s.c), phenylbutazone (100 mg/kg oral) and sodium salicylate (500 mg/kg i.p.) inhibited hyaluronidase‐induced oedema. However, in adrenalectomized rats, there was a reduction of the inhibitory effect of sodium salicylate but not of phenylbutazone or crotalaburnine.
Crotalaburnine (40 mg/kg s.c. and 30 mg/kg i.p., respectively) was ineffective against 5‐hydroxytryptamine‐ and dextran‐induced oedema but against bradykinin‐ and prostaglandin‐induced oedema (in a dose of 20 mg/kg i.p.) it was quite effective. In a parallel series cyproheptadine (10 mg/kg oral and i.p., respectively) produced significant inhibition of 5‐hydroxytryptamine‐ and dextran‐induced oedema, while phenylbutazone (100 mg/kg i.p.) failed to produce any significant inhibition of prostaglandin‐induced oedema.
Against cotton‐pellet granuloma crotalaburnine, in half the dose of hydrocortisone, produced similar inhibition while phenylbutazone produced much greater inhibition in five times the dose of crotalaburnine given orally.
The possible mode of action of crotalaburnine as an anti‐oedema agent is discussed.
THE FACILITATORY ACTIONS OF 5‐HYDROXYTRYPTAMINE AND BRADYKININ IN THE SUPERIOR CERVICAL GANGLION OF THE RABBIT
Authors: WALLIS D.I. , WOODWARD B. 
Published: July 2012

The effects of 5‐hydroxytryptamine (5‐HT) on ganglionic transmission and on intrinsic modulation of transmission have been re‐examined and compared with the effects of bradykinin by means of electrophysiological techniques.
Early facilitation, which is maximal 40–75 ms after a conditioning stimulus, was considerably enhanced by 5‐HT. This enhancement was concentration‐dependent, the threshold concentration lying between 0.1 and 1 μm. With concentrations of 5‐HT 10 μm or greater, there was some depression of the Sa response to the conditioning stimulus.
5‐HT reduced or abolished the inhibition of a test response induced by a conditioning response 100–300 ms earlier. Facilitation was observed at these intervals at concentrations of 5‐HT of 25 μm or greater.
Late facilitation, which is maximal 700–2000 ms after a conditioning stimulus, was increased by 5‐HT, but the effect was not as great as on early facilitation and was not always seen with a concentration of 1 μm.
Bradykinin reduced early facilitation but increased the amplitude of the transmitted action potential in response to a single stimulus. The threshold concentration producing these effects was between 1 and 2 μm.
5‐HT produced a rapid depolarization of the ganglion cell membrane which was followed by an after‐hyperpolarization.
Bradykinin either produced no measurable change in ganglion cell resting potential or only very small, transient depolarizations.
The depression of transmission, enhancement of intrinsic facilitation and the depolarization of the ganglion cell membrane induced by 5‐HT may indicate more than one mode of action of this amine at the ganglionic synapse.
A MODULATING ROLE OF PROSTAGLANDINS IN CONTRACTIONS OF THE GUINEA‐PIG ILEUM
Authors: KADLEC O. , MAŠEK K. , ŠEFERNA I. 
Published: July 2012

The role of prostaglandins in contractions of the guinea‐pig ileum evoked either directly by acetylcholine or indirectly by angiotensin and by coaxial stimulation has been investigated.
Prostaglandin E2 in low concentration (6 Nm) slightly augmented both types of contraction. Indomethacin, an inhibitor of prostaglandin synthesis, markedly reduced the indirectly evoked contractions but did not affect contractions in response to acetylcholine. The addition of prostaglandin E2 to the preparation treated previously with indomethacin restored the effect of indirect stimulation.
The pretreatment of the preparation with guanethidine or α‐methyl‐p‐tyrosine prevented the inhibitory effect of indomethacin on indirectly evoked contractions. Prostaglandin E2 addition to such preparations considerably augmented both types of contraction.
The stimulation of non‐cholinergic, non‐adrenergic inhibitory nerves in the taenia coli and ileum preparations evoked hyperpolarization and relaxation of the preparations followed by action potentials and contraction. These responses were not changed by indomethacin pretreatment and prostaglandin E2, but rebound contraction was sometimes augmented by the prostaglandin.
Two mechanisms for the effects of prostaglandin E2 are suggested: a direct effect on smooth muscle, and an indirect action through the sympathetic nerves which by release of noradrenaline affect the acetylcholine release from parasympathetic nerve endings.
A VASODILATOR INNERVATION TO THE CENTRAL ARTERY OF THE RABBIT EAR
Authors: KALSNER S. 
Published: July 2012

The possibility of a vasodilator innervation to the isolated and perfused central artery of the rabbit ear was examined.
Stimulation of the periarterial nerves in the presence of noradrenaline or other agonist used to maintain a partial constriction of the ear artery, led to a decrease in intraluminal flow followed after the cessation of stimulation by an increase in flow beyond the pre‐stimulation level.
After blockade of adrenergic transmission with bretylium or guanethidine or of the α‐ and β‐adrenoceptors with phentolamine and propranolol, stimulation of the periarterial nerves in the presence of a background tone, led to a clearly detectable vasodilatation. This dilatation was not blocked by treatment with atropine or mepyramine; nor was it enhanced by physostigmine.
Pretreatment of rabbits with reserpine (2 mg/kg) to deplete catecholamine stores, eliminated both the vasoconstrictor and vasodilator responses to nerve stimulation. However, a lower dose of reserpine (0.2 to 0.5 mg/kg) selectively eliminated the vasoconstrictor component of periarterial nerve activation.
The ear artery dilated in response to low concentrations of prostaglandin E1, and E2, in the presence of noradrenaline, but treatment with inhibitors of prostaglandin synthesis, indomethacin, aspirin or eicosa‐5,8,11,14‐tetraynoic acid did not reduce the vasodilator response. Attempts to extract a prostaglandin in the bathing medium were unsuccessful.
The involvement of a purine nucleotide appeared unlikely since the ear artery dilated only in response to fairly high concentrations of adenosine 5′‐triphosphate (ATP), adenosine 5′‐diphosphate (ADP) and adenosine 5′‐monophosphate (AMP). Furthermore, dipyridamole, an inhibitor of adenosine uptake, enhanced dilatation due to exogenous ATP but not to periarterial nerve stimulation.
It is concluded that the central artery of the rabbit ear has a vasodilator innervation but the identity of the transmitter remains to be established.
EFFECTS OF DIPYRIDAMOLE ON NEUROGENIC AND NON‐NEUROGENIC DILATOR RESPONSES OF ARTERIAL SMOOTH MUSCLE
Authors: BELL C. 
Published: July 2012

In the isolated, perfused parametrial artery of the guinea‐pig dipyridamole (10–100 ng/ml) potentiated dilator responses to adenosine 5′‐triphosphate (ATP), glyceryl trinitrate and non‐cholinergic, non‐adrenergic inhibitory nerve stimulation to similar extents. In contrast dilator responses to acetylcholine were generally unaffected or reduced.
These results support previous electro‐physiological evidence that in this preparation cholinergic vasodilatation is mediated by a cellular mechanism different from that involved in the response to non‐cholinergic dilator nervous activation.
The results also suggest that potentiation of a neurally‐mediated inhibitory response of smooth muscle by dipyridamole does not necessarily implicate ATP as the transmitter involved in this response.
AN ANALYSIS OF THE PERIPHERAL EFFECTS OF l‐DOPA ON AUTONOMIC NERVE FUNCTION
Authors: ANTONACCIO M.J. , ROBSON R.D. 
Published: July 2012

The ability of intravenous l‐DOPA to block sympathetic and parsympathetic nerves has been studied in cats and dogs pretreated with a monoamine oxidase inhibitor.
l‐DOPA inhibited positive chronotropic and pressor responses to dimethylphenylpiperazinium (DMPP) and McN‐A‐343 in dogs, and contractions of the nictitating membrane produced by these ganglion stimulants in cats.
Responses of the cat nictitating membrane to preganglionic stimulation were inhibited by l‐DOPA to a greater extent than those to postganglionic stimulation of the cervical sympathetic chain.
In dogs, l‐DOPA had no vagolytic action, but depressed vasoconstrictor responses elicited in the perfused hind‐limb by electrical stimulation of the lumbar sympathetic chain.
The degree of lumbar sympathetic chain inhibition correlated with the pressor response following l‐DOPA, and both effects were prevented by prior decarboxylase inhibition.
These results suggest that the decarboxylation products of l‐DOPA do not impair parasympathetic nerve activity but depress sympathetic nerve function predominantly by inhibiting both muscarinic and nicotinic sites of sympathetic ganglia.
MUSCARINIC EXCITATION: A MICROELECTROPHORETIC STUDY ON CULTURED SMOOTH MUSCLE CELLS
Authors: PURVES R.D. 
Published: July 2012

Acetylcholine was applied iontophoretically to smooth muscle cells cultured from taeniae coli of new‐born guinea‐pigs. Responses were recorded with intracellular microelectrodes.
Acetylcholine induced depolarization, spike generation and contraction. Large conductance increases could be measured during the action of acetylcholine.
Injection of depolarizing currents through the recording electrode reversed the sign of potential responses. The reversal potential was −5 to −25 mV.
Minimum latencies of responses to acetylcholine were 120–500 ms. These values were not attributable to diffusion time.
Attention is drawn to the long latencies of a variety of muscarinic responses, and the suggestion made that muscarinic mechanisms as a class may be characterized by a long activation time.
THE SELECTION OF ARYLAMIDINOUREA ANTIMALARIALS BY THEIR PREDICTED PHYSICOCHEMICAL PROPERTIES
Authors: CRANFIELD R. , GOODFORD P.J. , NORRINGTON F.E. , RICHARDS W.H.G. , SHEPPEY G.C. , WILLIAMS S.G. 
Published: July 2012

A small group of arylamidinoureas for which the predicted physicochemical properties were widely spaced and uncorrelated was selected for study.
The antimalarial activity of each compound was measured against three species of plasmodium. Three corresponding regression equations were calculated relating the potency of each compound to its predicted physicochemical properties.
The potency of further test compounds was forecast for each species, by using the corresponding regression equation. These forecasts were compared with the measured activity of the test compounds, and were better than would be expected by chance.
It is suggested that only a few compounds in a series need be studied initially in order to derive regression equations with worthwhile predictive properties, if the compounds are selected according to appropriate criteria.
CENTRAL α‐ AND β‐ADRENOCEPTORS MODIFYING ARTERIAL BLOOD PRESSURE AND HEART RATE IN CONSCIOUS CATS
Authors: DAY M.D. , ROACH A.G. 
Published: July 2012

In conscious unrestrained cats noradrenaline, α‐methylnoradrenaline and clonidine, infused into the lateral cerebral ventricles (i.c.v.) caused dose‐related falls in blood pressure and heart rate; both effects were abolished after i.c.v. phentolamine.
In 12 out of 20 cats, i.c.v. isoprenaline and salbutamol when given caused dose‐related pressor responses and tachycardias. These effects were abolished after i.c.v. β‐adrenoceptor blocking drugs but were unaffected by α‐adrenoceptor blocking agents.
In 5 out of 20 cats, i.c.v. isoprenaline regularly produced dose‐related falls in blood pressure with associated tachycardias; both effects were abolished after i.c.v. β‐adrenoceptor blocking agents.
Intracerebroventricular dopamine produced cardiovascular responses which were qualitatively similar to those produced by i.c.v. isoprenaline.
Intracerebroventricular adrenaline produced complex responses in untreated animals but typical α‐effects were obtained after prior i.c.v. treatment with a β‐adrenoceptor blocking agent and typical β‐effects after i.c.v. pretreatment with an α‐adrenoceptor blocking agent.
The cardiovascular changes produced by i.c.v. β‐adrenoceptor agonists were abolished after systemic administration of hexamethonium or bethanidine.
The results are discussed in the light of the mode of action of β‐adrenoceptor stimulants and β‐adrenoceptor blocking agents in the treatment of hypertension.
EFFECTS OF NICOTINE GIVEN INTO THE BRAIN OF FOWLS
Authors: MARLEY E. , SELLER T.J. 
Published: July 2012

The effects of nicotine, given into the IIIrd ventricle of adult conscious fowls (Gallus domesticus) or infused into various brain regions of conscious young chicks, were tested on behaviour, electrocortical activity, respiratory rate and body temperature. Its effects given intraventricularly or applied externally to the brain‐stem of anaesthetized fowls were also examined.
After intraventricular nicotine, fowls squatted for 3 to 5 min with eyes closed, electrocortical activity resembling that during sleep but with superimposed spike activity. Following this, fowls reawakened and tachypnoea developed, together with partial abduction of the wings from the trunk, the back becoming horizontal and the tail flexed. These effects were prevented by pempidine.
Intraventricular nicotine suppressed or, less commonly, reduced operant key‐pecking, an effect unrelated linearly to dose.
Intraventricular nicotine given to fowls anaesthetized with chloralose produced brief apnoea, followed by increased amplitude of respiratory excursion for about 5 minutes. Respiratory rate accelerated slightly but tachypnoea did not develop. Nicotine applied directly to the ventral brain‐stem increased respiratory amplitude in three out of seven fowls.
In anaesthetized fowls, intraventricular nicotine raised blood pressure for 2 to 3 min, an effect prolonged up to 70 min by acute bilateral vagotomy, whereas pressor effects of intravenous nicotine were extended merely two to three fold. Dividing the spinal cord at C2 prevented pressor effects of intraventricular nicotine; those of intravenous nicotine were unaltered.
In young chicks, nicotine infused into the diencephalon, telencephalon and myelencephalon induced effects similar to those observed immediately after intraventricular nicotine, i.e. chicks squatted with closed eyes but recovered within 3 to 5 minutes. Simultaneously, electrocortical activity changed from an alert to the sleep pattern, usually with superimposed ‘spike’ activity. Tachypnoea and associated postural changes did not develop. Pempidine prevented the behavioural and electrocortical effects of nicotine.
EFFECTS OF CHOLINOMIMETIC AGENTS GIVEN INTO THE BRAIN OF FOWLS
Authors: MARLEY E. , SELLER T.J. 
Published: July 2012

Effects of cholinomimetic agents, given into the IIIrd ventricle of adult fowls (Gallus domesticus) or infused into the hypothalamus of young chicks, were tested on behaviour, respiratory rate and body temperature.
Carbachol evoked behavioural and electrocortical arousal but lacked postural and respiratory effects. Contrariwise, pilocarpine increased respiratory rate and induced postural changes, i.e. abduction of the wings, but lacked other behavioural effects and did not alter electrocortical activity. Benzoylcholine induced tachypnoea, postural changes and brief electrocortical arousal. Acetylcholine was ineffective unless given with physostigmine, when electrocortical arousal, postural changes and tachypnoea developed. Methacholine induced tachypnoea and postural changes.
Effects of carbachol and pilocarpine were prevented by hyoscine and those of benzoylcholine by pempidine; hyoscine and pempidine were required together to prevent the effects of methacholine and to attenuate those of acetylcholine with physostigmine.
THE EFFECTS OF BRETYLIUM AND GUANETHIDINE ON CATECHOLAMINERGIC TRANSMISSION IN AN INVERTEBRATE
Authors: SILINSKY E.M. 
Published: July 2012

Secretory potentials produced by stimulation of the salivary duct nerves were recorded intracellularly from cockroach isolated salivary glands. The secretory potential normally consisted of a 40–80 mV hyperpolarization of the gland cell.
Bretylium (0.1–1 Mm) reduced the amplitude of the secretory potential without affecting the response of the gland to dopamine (0.25–1 μm). In addition, bretylium caused an increase in the frequency of miniature secretory potentials and the appearance of nerve terminal action potentials.
Guanethidine (1 Mm) reduced the response to nerve stimulation without depressing the sensitivity of the salivary gland to dopamine (0.25–0.5 μm) and without causing an increase in the occurrence of miniature potentials. Higher concentrations (4–5 Mm) completely eliminated secretory potentials but also reduced the sensitivity of the gland cell to dopamine.
These results indicate a presynaptic depression of the secretory potential by both bretylium and guanethidine. It is suggested that, in this system, bretylium acts by depolarizing the nerve terminal while guanethidine does not.
VARIATION IN NORADRENALINE OUTPUT WITH CHANGES IN STIMULUS FREQUENCY AND TRAIN LENGTH: ROLE OF DIFFERENT NORADRENALINE POOLS
Authors: HUGHES J. , ROTH R.H. 
Published: July 2012

During adrenergic nerve stimulation the output/pulse of noradrenaline from the rabbit vas deferens and portal vein is not constant but increases as the stimulus frequency or train length is increased. Depending upon the stimulus frequency and train length the fractional release of noradrenaline may vary from less than 10−7 to greater than 10−4.
Endogenous tissue stores of noradrenaline were labelled by incubation with (–)‐[3H]‐noradrenaline and [14C]‐tyrosine. The output/pulse of newly synthesized [14C]‐noradrenaline remained constant as the train length was increased whilst the output/pulse of [3H]‐noradrenaline increased under the same conditions. This phenomenon was independent of the stimulus frequency. Newly synthesized noradrenaline also appeared in the superfusate following nerve stimulation more rapidly than exogenously loaded noradrenaline.
Both [3H]‐noradrenaline and [14C]‐tyrosine were found to label an easily releasable store of noradrenaline. Mobilization from this store was the same at low and high frequencies of nerve stimulation.
It is concluded that at least two functional stores of noradrenaline exist within the adrenergic nerve ending. Newly synthesized noradrenaline is probably only a minor constituent of transmitter output under normal conditions of adrenergic nerve activity.
At least two mechanisms control the amount of noradrenaline released per pulse during nerve stimulation. Facilitation of release with increasing train lengths appears to be due to the mobilization of transmitter from a secondary store. Facilitation of release with increasing stimulus frequency is not dependent on mobilization from any particular store and at present there is no satisfactory explanation for this phenomenon.
FORMATION OF A FACTOR INCREASING VASCULAR PERMEABILITY DURING ELECTRICAL STIMULATION OF THE SAPHENOUS NERVE IN RATS
Authors: LEME J. GARCIA , HAMAMURA L. 
Published: July 2012

Increased vascular permeability following electric antidromic stimulation of the rat saphenous nerve was observed in the skin area supplied by the nerve, confirming previous results by other authors.
The phenomenon was not affected by pretreatment of the rats with diphenhydramine, burimamide or their combination; atropine, methysergide, methysergide plus diphenhydramine, carboxypeptidase B, acetylsalicylic acid, indomethacin or methiazinic acid. It was partially reduced by previous injection of cellulose‐sulphate, a kininogen‐depleting agent.
Perfusates from the subcutaneous tissue of the paw area supplied by the saphenous nerve contained permeability increasing activity as shown by intradermal tests in other rats. This activity was present in perfusates collected during nerve stimulation but not in those collected before stimulation. It was not destroyed by heating to 100°C, or by α‐chymotrypsin or trypsin.
Bradykinin‐like activity may appear later in the perfusates, depending on the intensity of the stimuli.
It is concluded that following electrical antidromic stimulation of the saphenous nerve a permeability increasing factor is released, possibly from nerves. It is dialysable and can be distinguished from acetylcholine, histamine, 5‐hydroxytryptamine, plasma kinins, substance P, prostaglandins and high molecular weight proteins. The increased vascular permeability induced by this factor leads to plasma exudation and activation of the kinin system.