bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of β‐adrenoceptor blockade on human sweating
Authors: ALLEN JUDITH A. , JENKINSON D. J. , RODDIE I. C. 
Published: July 2012

Summary
Changes in cutaneous water loss were followed by continuously monitoring total body weight loss.
Sweating was induced in normal subjects by raising the environmental temperature or by subjecting them to the emotional stress of mental arithmetic.
Propranolol in a dosage of 0·15 mg/kg body weight intravenously had no significant effect on either thermal or emotional sweating, whereas thermal sweating was completely blocked temporarily by administration of atropine 2·4 mg intravenously.
It is concluded that β‐adrenoceptor blockade has no effect on physiological sweating in normal people.
The effects of hallucinogenic drugs on maze exploration in the rat over a 24 hour period
Authors: DAVIES J. A. , REDFERN P. H. 
Published: July 2012

Summary
The variation with clock‐hour in the behaviour of naive rats in a Y‐maze has been recorded.
The number of entries recorded was highest during the light period while the number of faecal boluses was highest during the dark period. Rearing showed a biphasic periodicity.
The responses to LSD, mescaline and amphetamine also showed significant variation with clock‐hour.
In general, amphetamine, 1·25 mg/kg, increased the number of entries and the number of rears, the effect being greatest at the end of the light period. LSD, 100 μg/kg, and mescaline, 12·5 mg/kg, decreased the number of entries and the number of rears.
All three drugs decreased the number of faecal boluses. The possible significance of these responses in terms of an effect on the emotional state of the animals is discussed.
THE EFFECT OF INDOMETHACIN ON THE RELEASE OF PROSTAGLANDIN E2 AND ACETYLCHOLINE FROM GUINEA‐PIG ISOLATED ILEUM AT REST AND DURING FIELD STIMULATION
Authors: BOTTING J.H. , SALZMANN R. 
Published: July 2012

Guinea‐pig ileum suspended in Krebs solution showed a continuous increase of tone which was lost by changing the bath fluid. Prostaglandin E2 was released from the ileum during incubation, and its concentration in the bath fluid appeared to correlate with the increase in tone.
Supramaximal field stimulation (10 Hz) resulted in increased release of prostaglandin E2 from the ileum. At lower rates of stimulation, the increase in the release of E2 compared with the resting output was not significant.
Indomethacin (1 and 10 μg/ml) produced a significant, dose‐related reduction of the amount of prostaglandin E2 measured in the bath fluid at rest and with field stimulation. Indomethacin inhibited the contraction of the ileum during incubation in Krebs solution.
Indomethacin (10 and 20 μg/ml) had no significant effect on the release of acetylcholine during field stimulation, but reduced the resting output of acetylcholine from guinea‐pig ileum in some experiments.
The results are discussed in the context of the role ascribed to prostaglandins as physiological modulators in transmitter release. No evidence for a prostaglandin‐mediated negative feedback mechanism on acetylcholine release was obtained.
GASTRIN RELEASE BY BOMBESIN IN THE DOG
Authors: BERTACCINI G. , ERSPAMER V. , MELCHIORRI P. , SOPRANZI N. 
Published: July 2012

The intravenous infusion of bombesin produced in intact dogs and, more strikingly in dogs provided with gastric fistulae a sharp increase in plasma levels of immunoreactive gastrin and at the same time a stimulation of gastric acid secretion. Gastrin response was correlated with the dose of bombesin from approximately 0.1 μg kg−1 h−1 (threshold) to 1 μg kg−1 h−1 (maximum gastrin release).
Atropine and metiamide reduced or inhibited gastric acid secretion stimulated by bombesin, but did not affect the rise in gastrin levels.
Acidification of the whole stomach or of a perfused antral pouch caused a reduced or delayed response to bombesin. However, the inhibitory effect of acidification could be surmounted by prolonging the duration of bombesin infusion.
Antrectomy greatly reduced the rise in gastrin levels and the increase in acid gastric secretion produced by bombesin, but left unaffected the gastric secretagogue effect of pentagastrin.
It is concluded that bombesin is a potent releaser of gastrin from the antral mucosa.
The possible influence of the renal effects evoked by bombesin in the dog on the gastrin response to the polypeptide is discussed.
ANTAGONISM OF TONE AND PROSTAGLANDIN‐MEDIATED RESPONSES IN A TRACHEAL PREPARATION BY INDOMETHACIN AND SC‐19220
Authors: FARMER J.B. , FARRAR D.G. , WILSON J. 
Published: July 2012

The effects of the prostaglandin synthetase inhibitor, indomethacin and the prostaglandin antagonist SC‐19220 (1‐acetyl‐2‐[8‐chloro‐10,11‐dihydrodibenz (b, f) (1,4)oxazepine‐10‐carbonyl] hydrazine), were examined on the tone of the guinea‐pig isolated tracheal preparation and on the responses of the preparation to prostaglandin F2α, arachidonic acid and methacholine.
Indomethacin (0.05–1.6 μg/ml) produced a long‐lasting inhibition of the intrinsic tone of the tracheal preparation and of the contractile responses to arachidonic acid. Much higher concentrations of indomethacin also reduced the responses of the preparation to methacholine. This effect was readily reversible and appeared to be unrelated to the action on tone.
The contractile responses of the preparation to prostaglandin F2α were enhanced by low concentrations of indomethacin (1–5 μg/ml) and inhibited by higher concentrations (2.5–80 μg/ml).
SC‐19220 was shown to inhibit responses of the preparation to prostaglandin F2α in concentrations (0.1–1 μg/ml) which had no effect on responses to methacholine. Similar concentrations also inhibited the intrinsic tone of the preparation and the responses to arachidonic acid.
The evidence suggests that prostaglandins may be involved in the maintenance of tone of the guinea‐pig isolated tracheal preparation.
THE SELECTIVITY OF β‐ADRENOCEPTOR ANTAGONISTS ON CARDIOVASCULAR AND BRONCHODILATOR RESPONSES TO ISOPRENALINE IN THE ANAESTHETIZED DOG
Authors: DALY M.J. , FLOOK JUDITH J. , LEVY G.P. 
Published: July 2012

The actions of five β‐adrenoceptor antagonists, chosen because of reported differences in their selectivities, were compared using the positive chronotropic, vasodepressor and bronchodilator responses to isoprenaline in anaesthetized dogs.
Propranolol was a potent antagonist of the isoprenaline responses in all three systems.
Practolol and acebutolol (M & B 17,803) blocked the positive chronotropic responses to isoprenaline to a greater extent than the vasodepressor or bronchodilator responses.
Butoxamine and α‐methyl dichloroisoprenaline showed the opposite selectivity, blocking the vasodepressor and bronchodilator responses to isoprenaline to a greater extent than positive chronotropic responses. However, both drugs were considerably less potent than the other antagonists studied and their selectivities were less clear‐cut than those of practolol or acebutolol.
All the antagonists lowered the resting heart rate and to a lesser extent the diastolic blood pressure. The effects of propranolol, practolol and acebutolol on heart rate probably result from cardiac β‐adrenoceptor blockade. With butoxamine and α‐methyl dichloroisoprenaline, however, the effects on heart rate probably result from a direct cardiodepressant action.
The relevance of the results to the problem of the sub‐classification of β‐adrenoceptors is discussed.
THE INHIBITORY ACTION OF OESTRADIOL‐17‐β AND PROGESTERONE ON VENOUS SMOOTH MUSCLE
Authors: McCALDEN T.A. 
Published: July 2012

The in vitro action of oestradiol‐17‐β (0.1, 1.0 and 10.0 μg/ml) and progesterone (0.1, 1.0 and 10.0 μg/ml) on the spontaneous activity of the portal veins in female rats at different stages of gestation was studied.
Progesterone caused the spontaneous mechanical activity in the rat portal vein to decrease in amplitude and increase in frequency. This action was dose‐dependent and the sensitivity of the tissue decreased throughout pregnancy.
Oestradiol‐17‐β had a biphasic effect on spontaneous mechanical activity in the rat portal vein. At 0.1 μg/ml the vessel was stimulated while a similar effect to progesterone occurred with higher concentrations. The tissue was more sensitive to oestradiol at 7 days of gestation than at either the 10‐14 or 17‐21 day periods of gestation.
These effects of oestradiol and progesterone were still seen after blockade of the β‐adrenoceptors.
Hydrocortisone (10 μg/ml) had no inhibitory effect on the spontaneous mechanical activity of the vein.
The veins from the 17‐21 days pregnant animals showed a smaller amplitude of contraction than comparable non‐pregnant females.
VARIATION IN ACTIVITY OF MONOAMINE METABOLIZING ENZYMES IN RAT LIVER DURING PREGNANCY
Authors: PARVEZ SIMONE , PARVEZ S.H. , YOUDIM M.B.H. 
Published: July 2012

Catechol‐O‐methyltransferase (COMT) and monoamine oxidase (MAO) activities in rat liver were measured during pregnancy, parturition and postpartum. Compared with activity in non‐pregnant controls, both enzymes showed a significant decrease in activity which was most pronounced at day 18.
The metabolism of intravenously infused [3 H]‐adrenaline to [3 H]‐metanephrine and to [3 H]‐acidic metabolites was also significantly depressed during pregnancy but had returned to control values by the 21st day.
The effects of reserpine and/or nialamide on hepatic COMT and MAO were studied in control and 20‐day‐pregnant rats. Their action on COMT activity differed in the two groups. MAO was inhibited to a similar extent in these groups whether the drugs were given separately or in combination.
It seems possible that the changes in endocrine function which occur during pregnancy are responsible for the observed alterations in enzyme activity.
CARDIOVASCULAR DEPRESSANT EFFECTS OF NEOMYCIN AND GENTAMICIN IN RHESUS MONKEYS
Authors: ADAMS H.R. 
Published: July 2012

The acute cardiovascular effects of neomycin and gentamicin, representative aminoglycoside antibiotics, were examined in surgically‐prepared anaesthetized rhesus monkeys.
Intravenous administration of 14, 28, and 56 mg/kg of neomycin consistently induced a dose‐dependent depression of systemic blood pressure, cardiac output, left ventricular contractile force, maximum dF/dt of left ventricular contraction, and heart rate. Neomycin produced similar cardiovascular depressant effects when heart rate was maintained constant by electrical pacing.
Maximum depression of haemodynamic values usually occurred within 2 to 5 min after injection of neomycin; values then gradually returned to control levels within 20 to 30 (14 mg/kg) or 60 to 80 (56 mg/kg) minutes.
Injection of CaCl2 (1.35 mEq Ca2+/kg, i.v.) during the peak depressant effect of neomycin produced a rapid and maintained restoration of cardiovascular function to control levels; conversely, noradrenaline (2 μg, i.v.) or isoprenaline (0.5 μg, i.v.) produced only transient reversal of the neomycin effects.
Similar evidence of cardiovascular dysfunction was observed with gentamicin.
These findings demonstrate the direct cardiovascular depressant effects of aminoglycoside antibiotics in a higher primate species, and suggest that this adverse response is related to an alteration of calcium ion function.
REFLEX BRADYCARDIA AND HYPOTENSION PRODUCED BY PROSTAGLANDIN F2α IN THE CAT
Authors: KOSS M.C. , NAKANO J. 
Published: July 2012

Intravenous administration of prostaglandin F2α results in a dose‐dependent increase in pulmonary arterial pressure, decrease in systemic arterial pressure and a delayed bradycardia. Pulmonary vasoconstriction was observed at doses as low as 0.1 and 0.3 μg/kg. The systemic depressor and heart rate lowering effects were observed at 1 μg/kg doses and above.
A moderate bradycardia was still observed after atropine blockade but was abolished following bilateral vagotomy. Neither of these procedures affected the pulmonary vascular response.
Injections of submaximal doses of prostaglandin F2α (1–4 μg/kg) produced a greater and longer lasting bradycardia when injected into the left atrium than was observed following intravenous administration. In addition the latency of onset was much shorter following left atrial injection. These doses resulted in no change in heart rate and a minimal hypotension when injected into the brachiocephalic artery or into the aortic arch.
Small doses of prostaglandin F2α administered at the level of the origin of the coronary arteries produced marked decreases in heart rate and blood pressure whereas no change occurred following injection of the same amount into the ascending aorta at more distal sites.
These results suggest that prostaglandin F2α produces bradycardia and hypotension in the cat by activating ‘receptors’ located in the left heart or by acting on structures perfused by means of the coronary arteries.
EFFECTS OF AZAPERONE ON CARDIOVASCULAR AND RESPIRATORY FUNCTIONS IN THE HORSE
Authors: LEES P. , SERRANO L. 
Published: July 2012

The butyrophenone tranquillizer, azaperone, was administered intramuscularly, at dose levels of 0.4 and 0.8 mg/kg, to ponies and its effects on cardiovascular and respiratory functions assessed.
Arterial blood pH, CO2 tension (PaCO2) and O2 tension (PaO2) remained relatively constant throughout the course of action of azaperone.
Azaperone did not modify plasma protein concentration but venous blood packed cell volume and haemoglobin concentration were reduced by 5 to 10% for at least 4 hours. These changes were probably caused by uptake of erythrocytes into the splenic reservoir.
Small increases in heart rate occurred for up to 60 min after administration of the drug, and this was followed by a slight bradycardia in some ponies.
Azaperone reduced mean arterial blood pressure (MAP) for at least 4 h, by which time its ataractic action was generally no longer apparent. The hypotension was caused, during the early phase of action at least, by a reduction in peripheral resistance, since cardiac output was increased slightly 20 min after its administration. Possible mechanisms underlying the cardiovascular changes are discussed.
In spite of reductions in arterial blood 02 content and MAP produced by azaperone, it is likely that tissue oxygenation was adequate, since arterial blood lactate concentrations were not increased.
BLOOD PRESSURE RESPONSES TO ADRENAL FIELD STIMULATION AS A MEASURE OF ADRENAL CATECHOLAMINE RELEASE
Authors: CLARKE D.E. , ROMANYSHYN W.M. 
Published: July 2012

A new method for studying adrenal medullary release is described in pithed rats using field stimulation of an entire adrenal gland.
The increases in blood pressure in response to field stimulation of the gland consisted of an initial short, variable component, due to stimulation of adrenergic vasomotor neurones and a secondary, longer lasting component, due to medullary catecholamine release.
Removal of the initial component by drugs or cardiac/coeliac ganglionectomy did not affect the magnitude of the secondary pressor component.
The secondary pressor component was frequency‐dependent, reproducible and stable with time. The extent of medullary catecholamine release could be assessed by comparing the blood pressure rise with those obtained after adrenaline injections.
The method appears to provide a reliable means by which adrenal medullary catecholamine release may be assessed without significant interference from vasomotor nerves.
BENZODIAZEPINES AND CENTRAL GLYCINE RECEPTORS
Authors: CURTIS D.R. , GAME C.J.A. , LODGE D. 
Published: July 2012

In cats, anaesthetized with pentobarbitone, intravenous diazepam (minimum dose 3.0 mg/kg) enhanced dorsal root potentials but did not significantly diminish the reduction by electrophoretic strychnine of the inhibitory action of electrophoretic glycine on dorsal horn interneurones.
In mice, intraperitoneal diazepam (2.5 mg/kg) had no appreciable effect on the potency of strychnine as a convulsant, although providing some protection against bicuculline.
These observations, together with the failure of chlordiazepoxide to either inhibit the firing of spinal interneurones or reduce antagonism between strychnine and glycine when administered locally, provide no support for the interaction between benzodiazepines and mammalian central glycine receptors which has been proposed on the basis of in vitro studies of strychnine binding.
A COMPARISON OF γ‐AMINOBUTYRIC ACID AND THE SEMI‐RIGID ANALOGUES 4‐AMINOTETROLIC ACID, 4‐AMINOCROTONIC ACID AND IMIDAZOLE‐4‐ACETIC ACID ON THE ISOLATED SUPERIOR CERVICAL GANGLION OF THE RAT
Authors: BOWERY N.G. , JONES G.P. 
Published: July 2012

The rat superior cervical ganglion possesses receptors for γ‐aminobutyric acid (GABA). This can be demonstrated in vitro by recording the changes in ganglionic surface potential which occur after the addition of GABA to the bathing solution.
The actions of three conformationally‐restricted analogues of GABA namely 4‐aminotetrolic acid (4‐ATA), trans 4‐aminocrotonic acid (4‐ACA) and imidazole‐4‐acetic acid (IAA) have been examined for activity at this peripheral receptor.
All three analogues depolarized the ganglion in a manner similar to GABA. Their actions were transient and were ‘occluded” by GABA; also the log dose‐response curve in each case was parallel to that of GABA. Molar potencies relative to GABA (=1) were 4‐ACA =1.48, IAA = 0.100, 4‐ATA = 0.0028.
The action of each analogue could be blocked by the GABA antagonists bicuculline and tetramethylenedisulphotetramine at doses which had relatively little effect on responses to the cholinomimetic carbachol.
4‐ACA and IAA (1 mM) significantly reduced the ganglionic accumulation of [3H]‐GABA (0.2 μM) by 88% and 58% respectively whereas 4‐ATA (1 mM), caused no significant reduction in [3H]‐GABA accumulation.
THE EFFECTS OF EDTA AND EGTA ON RENIN SECRETION
Authors: PEART W.S. , QUESADA T. , TENYI I. 
Published: July 2012

1The effects of the disodium salt of ethylenediamine tetra‐acetate (EDTA) and 1,2,bis,2 amino‐ethoxyethane‐NNN‘N’‐tetra‐acetic acid (EGTA) on renin secretion and vascular resistance were studied in the isolated perfused kidney of the rat.2Both substances produced a significant increase of renin release.3In the absence of calcium and magnesium, EDTA still increased renin release and there was now a considerable increase of perfusion pressure.4The rise of pressure but not the rise of renin was inhibited by the removal of potassium from the perfusate when EDTA was administered in the absence of calcium.5Propranolol and phenoxybenzamine had no effect on the vasoconstrictor action of EDTA.6EGTA was less effective as a renin releaser than EDTA until magnesium was removed from the perfusate. Further, it had only a small effect on perfusion pressure in contrast to EDTA.
THE EFFECT OF (—)‐ISOPRENALINE AND (±)‐SALBUTAMOL ON PEPSINOGEN AND ACID SECRETION IN THE DOG
Authors: DALY M.J. , STABLES R. 
Published: July 2012

1The β‐adrenoceptor agonists, (—)‐isoprenaline and (±)‐salbutamol, reduced pepsinogen secretion induced by pentagastrin in conscious dogs with Heidenhain pouches.2(—)‐Isoprenaline and (±)‐salbutamol also reduced gastric acid secretion while producing a moderate tachycardia.
INHIBITORY EFFECTS OF CLONIDINE ON RESPONSES TO SYMPATHETIC NERVE STIMULATION IN THE PITHED RAT
Authors: DOXEY J.C. , EVERITT J. 
Published: July 2012

The spinal sympathetic outflow to the eyelid, heart, splanchnic blood vessels, vas deferens and anococcygeus muscle was stimulated in pithed rats.
Clonidine inhibited sympathetic outflow to all of the tissues studied. The inhibitory effects of clonidine on cardiac nerves and hypogastric nerves were antagonized by phentolamine.
Clonidine produced a postsynaptic a‐adrenoceptor agonist action on the eyelid, splanchnic blood vessels and the anococcygeus muscle. These effects were also antagonized by phentolamine.
The effects of clonidine, naphazoline and oxymetazoline on pre‐ and postsynaptic α‐adrenoceptors were determined.
The presynaptic α‐adrenoceptors employed were situated in either the sympathetic cardiac or hypogastric nerve terminals. Increases in diastolic blood pressure were used to assess concurrent postsynaptic α‐adrenoceptor agonist activity.
The presynaptic α‐adrenoceptor agonist potencies of clonidine, naphazoline and oxymetazoline were very similar on cardiac nerve terminals whereas on the hypogastric nerve terminals oxymetazoline was about 6 times more potent than either naphazoline or clonidine.
The results support the view that presynaptic α‐adrenoceptors regulate transmitter release in sympathetic nerves. There appear to be subtle differences between the presynaptic α‐adrenoceptors of different sympathetic nerve endings.
ESTIMATION AND CHARACTERIZATION OF PROSTAGLANDINS IN THE HUMAN GASTROINTESTINAL TRACT
Authors: BENNETT A. , STAMFORD I.F. , STOCKLEY HELEN L. 
Published: July 2012

Prostaglandin‐like material was extracted from muscle and mucosa of surgically removed human stomach, ileum and colon and assayed against prostaglandin E2 on strips of rat gastric fundus. Superfused human isolated gastric mucosa released prostaglandin‐like material and release was increased by stretching or clamping the tissue.
The relative amounts of extracted biological activity were broadly as follows: gastric antral mucosa > colon muscle > gastric body mucosa ≅ ileal mucosa > colon mucosa ≅ gastric muscle ≅ ileal muscle.
Prostaglandin E and F were tentatively identified by chromatography and sensitivity to inactivation by alkali.
Prostaglandin E apparently contributed most to the biological activity, possibly because the assay tissue is more sensitive to prostaglandin E than to F. Chromatography of gastric body mucosal extracts located material running with prostaglandin E2 and a little with E1. Colonic muscle and mucosal extracts contained material with RF values of prostaglandins E1, E2, E3 and F1α, whereas F2α and F3α‐like substances were found only in the mucosa. The proportions of prostaglandin F varied between specimens.
The amount of extracted prostaglandin‐like activity was increased by adding cofactors and arachidonic acid, and lessened by homogenization with acid‐ethanol.
The type and amount of activity generated from arachidonic acid by partly purified colonic mucosal prostaglandin synthetase depended on the substrate concentration.
The possible relationships of prostaglandins to mucus secretion and other physiological and pathological gut functions are discussed.
AN INHIBITORY ROLE FOR NORADRENALINE IN THE MOUSE VAS DEFERENS
Authors: JENKINS D.A. , MARSHALL I. , NASMYTH P.A. 
Published: July 2012

Noradrenaline (0.1‐3.0 μM) inhibited the twitch responses to single pulse field stimulation of the isolated vas deferens of the mouse. The higher concentrations of noradrenaline (ca. 0.3‐3.0 μM) were required to make the tissue contract.
Phentolamine (10 μM) abolished the contractor response to higher concentrations of noradrenaline and antagonized the inhibitory effect of lower concentrations on the twitch response.
Propranolol (10 μM) potentiated both the contractor and the inhibitory effect of noradrenaline on the twitch response.
Isoprenaline (0.1‐3.0 μM) and salbutamol (1.0‐3.0 μM) both inhibited the twitch response. Their effects were antagonized by propranolol (10 μM), but not by practolol (10 μM).
The effects of uptake1 and uptake2 blocking agents were determined. Cocaine (10 μM) reduced the size of the twitch response in 2 out of 4 experiments. Imipramine (0.18 μM) also reduced the size of the twitch, as did oestradiol (3.7 μM) and a combination of cocaine and oestradiol.
Contractor responses to exogenous noradrenaline showed tachyphylaxis, but when this was not very marked, the response could be shown to be potentiated by uptake blocking agents.
The inhibitory effect of noradrenaline on the twitch response was greatly potentiated by cocaine (10 μM) and much less so by oestradiol (3.7 μM).
It is concluded that the transmitter responsible for the twitch response is either an unknown substance released from the sympathetic neurone, or noradrenaline acting upon a receptor with none of the characteristics of known α‐ or β‐adrenoceptors. In either case, noradrenaline can inhibit the output, probably by stimulation of presynaptic α‐adrenoceptors.