bluuebunny/crossref_metadata_2025_split huggingface dataset:
DOPAMINE‐LIKE PROPERTIES OF EPHEDRINE IN RAT BRAIN
Authors: ZARRINDAST M.R. 
Published: July 2012

Ephedrine (3.1–50 mg/kg) was given intraperitoneally to rats and was found to cause a marked increase in spontaneous locomotor activity
In rats with a unilateral lesion in the substantia nigra made by stereotaxic injection of 6‐hydroxydopamine, ephedrine (12.5–150 mg/kg i.p.) caused a dose‐dependent turning towards the lesioned side
Turning behaviour and increase in locomotion produced by ephedrine were antagonized by pretreatment of the animals with pimozide, amino‐oxyacetic acid or reserpine plus α‐methyl‐ρ‐tyrosine, but not by pretreatment with phenoxybenzamine, propranolol or methergoline
In in vitro studies with synaptosomes prepared from rat brain, ephedrine blocked the uptake and caused the release of [3H]‐dopamine
Similar results with regard to locomotion and turning behaviour were obtained with (+)‐amphetamine
It is concluded that the increase in locomotion and turning behaviour produced by ephedrine is mediated through an indirect dopaminergic mechanism.
EFFECT OF ADENOSINE ON CAROTID CHEMORECEPTOR ACTIVITY IN THE CAT
Authors: McQueen D.S. , Ribeiro J.A. 
Published: July 2012

The effects of intracarotid (i.e.) injections or infusions of adenosine on chemoreceptor activity recorded from the peripheral end of a sectioned carotid sinus nerve have been studied in cats anaesthetized with pentobarbitone
Adenosine injections (0.1–100 μg) caused a rapid and marked increase of spontaneous chemoreceptor discharge, the intensity, duration and onset of which was dose‐dependent. Infusion of adenosine, 50 μg/min, also evoked an increase in discharge which persisted for the duration of the infusion
Both theophylline (1 mg i.e.) and aminophylline (1 mg i.e.) caused short‐lasting decreases in spontaneous discharge but did not prevent the excitatory effect of adenosine. Theophylline increased the excitatory action of adenosine
Naloxone (400 μg i.e.) antagonized the depressant effect of morphine on chemoreceptor discharge but not the excitatory action of adenosine
It is concluded that exogenous adenosine can excite the cat carotid chemoreceptors, an effect which is not prevented by theophylline in the doses studied. The physiological significance of the findings is discussed.
EFFECTS OF MIANSERIN, DESIPRAMINE AND MAPROTILINE ON BLOOD PRESSURE RESPONSES EVOKED BY ACETYLCHOLINE, HISTAMINE AND 5‐HYDROXYTRYPTAMINE IN RATS
Authors: CAVERO ICILIO , LEFÈVRE‐BORG FRANÇOISE , ROACH ALAN G. 
Published: July 2012

In rats anaesthetized with pentobarbitone, intravenous administration of desipramine (0.1 mg/kg), maprotiline (0.5 mg/kg) or mianserin (0.3‐3.0 mg/kg) did not modify the blood pressure lowering effects of acetylcholine (0.25‐1.0 μg/kg, i‐v.) which were significantly reduced by atropine (3.0 μg/kg, i.v.)
Maprotiline and mianserin, like promethazine (0.1 mg/kg, i.v.), inhibited the vasodepressor responses evoked by histamine (2.5‐ 10.0 μg/kg, i.v.). However, desipramine was inactive against histamine
In pithed rats, the pressor effects of intravenous 5‐hydroxytryptamine (5‐HT: 5.0–20.0 μg/kg) were antagonized by mianserin (0.01‐0.3 mg/kg, i.v.) and cyproheptadine (0.01 mg/kg) but were unaffected by maprotiline and desipramine
In syrosingopine pretreated rats given mianserin 0.1 mg/kg, intravenously, 5‐HT (20.0 μg/kg, i.v.) produced a significant fall in blood pressure which could be reduced by a large dose of mianserin (10.0 mg/kg, i.v.)
In conclusion, desipramine, maptrotiline and mianserin, in doses previously found to inhibit noradrenaline neuronal reuptake in the rat cardiovascular system, lack muscarinic receptor antagonist properties. Whilst maprotiline and mianserin blocked vascular histamine receptors, only mianserin, like cyproheptadine, was a potent antagonist of the 5‐HT receptors that mediate increases in blood pressure in rats. Finally, the vasodepressor effects of 5‐HT in syrosingopine pretreated rats given a small dose of mianserin were antagonized by a large dose of mianserin, suggesting that 5‐HT may activate two distinct types of receptors in the rat.
ADDITIVE AND NON‐ADDITIVE EFFECTS OF MIXTURES OF SHORT‐ACTING INTRAVENOUS ANAESTHETIC AGENTS AND THEIR SIGNIFICANCE FOR THEORIES OF ANAESTHESIA
Authors: RICHARDS C.D. , WHITE ANN E. 
Published: July 2012

The potency of a series of short‐acting anaesthetics was established by measuring the duration of the loss of righting reflex following a single bolus injection into the tail vein of male Wistar rats. The agents were, in order of potency, etomidate, alphaxalone, methohexitone, alphadalone acetate and propanidid
The potency of binary mixtures of these agents was also assessed to see whether the anaesthetic effects of different agents were additive as classical theories of anaesthesia suggest. Mixtures of alphaxalone and alphadalone acetate, alphaxalone and propanidid and methohexitone and propanidid all showed simple additive effects. Mixtures of alphaxalone and etomidate and of alphaxalone and methohexitone showed a greater potency than would be expected if their effects were simply additive. Mixtures of etomidate and methohexitone were not examined
Mixtures of alphaxalone and either methohexitone or pentobarbitone produced a greater depression of synaptic transmission in in vitro preparations of guinea‐pig olfactory cortex than would have been expected from the sum of the activities of the individual anaesthetics. Other combinations of anaesthetics did not show similar effects although the interaction between alphaxalone and etomidate was not examined
Neither alphaxalone nor pentobarbitone affected the membrane: buffer partition coefficient of the other for a model membrane system
These results are interpreted as evidence against the classical unitary hypotheses of anaesthetic action based on correlations of anaesthetic potency with lipid solubility and as supporting the view that different anaesthetics act on different structures in the neuronal membranes to produce anaesthesia.
ANTIFIBRILLATORY EFFICACY OF ENCAINIDE, LORCAINIDE AND ORG 6001 COMPARED WITH LIGNOCAINE IN ISOLATED HEARTS OF RABBITS AND GUINEA‐PIGS
Authors: ALMOTREFI A. A. , BAKER J. B.E. 
Published: July 2012

In Langendorff‐perfused rabbit hearts, electrical stimulation threshold and ventricular fibrillation threshold (VFT) were measured by applying rectangular impulses of 3 ms duration and increasing current at frequencies of 4 and 20 Hz respectively.
Perfusion with lignocaine or one of three new antiarrhythmic drugs, encainide, lorcainide and ORG 6001, produced significant, dose‐dependent increases in both thresholds.
On a dosage basis, encainide was seven times, lorcainide fourteen times and ORG 6001 twice as potent as lignocaine in raising VFT.
In Langendorff‐perfused guinea‐pig hearts, only lorcainide provided complete protection against ouabain‐induced ventricular fibrillation, while 6 of 6,3 of 6 and 2 of 6 hearts fibrillated in the presence of encainide, lignocaine and ORG 6001 respectively, but with infusion durations significantly higher than control.
These results indicate the potential antifibrillatory activity of these new antiarrhythmic agents.
FURTHER STUDIES ON 5‐HYDROXYTRYPTAMINE TRANSPORT IN PANCREATIC ISLETS AND ISOLATED β‐CELLS
Authors: LINDSTRÖM PER 
Published: July 2012

The transport mechanism for 3H‐labelled 5‐hydroxytryptamine (5‐HT) in isolated pancreatic islets of non‐inbred ob/obmice was further characterized.
Isolated β‐cells accumulated 5‐HT to the same degree and with the same Na+‐dependence as whole islets.
Imipramine inhibited the uptake in a concentration‐dependent way.
Reserpine did not affect the uptake or efflux rates.
Glucose stimulation of insulin secretion did not affect the uptake rate.
It is concluded that the observed islet uptake of [3H]‐5‐HT represents an intracellular accumulation by the β‐cells. Mechanisms at the level of the plasma membrane may be rate‐limiting for this process.
DIFFERENTIAL RESPONSES TO CARBACHOL, SODIUM NITRO‐PRUSSIDE AND 8‐BROMO‐GUANOSINE 3‘,5’‐MONOPHOSPHATE OF CANINE ATRIAL AND VENTRICULAR MUSCLE
Authors: ENDOH MASAO , YAMASHITA SHUJI 
Published: July 2012

The relation between force of contraction and cyclic nucleotide levels during muscarinic receptor stimulation, and after administration of sodium nitroprusside was assessed in canine isolated atrial and ventricular muscle.
The pD2 value (negative logarithm of ED50) for carbachol to decrease force of atrial contraction was similar to that required to inhibit adenosine 3′,5′‐monophosphate (cyclic AMP)‐mediated positive inotropic responses in ventricular muscle.
The cyclic AMP level of atrial muscle did not significantly change during carbachol‐induced negative inotropic action, whilst the guanosine 3′,5′‐monophosphate (cyclic GMP) level was elevated immediately after administration.
Sodium nitroprusside elevated cyclic GMP levels (without changing cyclic AMP levels) both in atrial and ventricular muscle. The force of atrial contraction was significantly reduced by the drug, whilst ventricular contractile force was unaffected.
8‐Bromo‐cyclic GMP markedly decreased contractile force in atrial muscle. In contrast, similar concentrations of 8‐bromo‐cyclic GMP had no effect on ventricular contractile force. 6 The positive inotropic action of phenylephrine on canine cardiac muscle, which is mediated through β‐adrenoceptors, was unaffected either by sodium nitroprusside or by 8‐bromo‐cyclic GMP.
The present results suggest that the effect of muscarinic receptor stimulation in canine atrial and ventricular muscle is related to different changes in intracellular cyclic nucleotide metabolism. The direct myocardial depressant action on atrial muscle seems to be related to an elevation of cyclic GMP level, whilst a reduction of cyclic AMP may be responsible for the indirect action (‘accentuated antagonism’) in both atrial and ventricular muscle.
INHIBITORY EFFECTS OF PROPRANOLOL ON THE CALCIUM CURRENT OF Helix NEURONES
Authors: AKAIKE N. , NISHI K. , OYAMA Y. 
Published: July 2012

Calcium current (ICa) and potassium current (IK) in isolated nerve cell bodies of Helix aspersa were independently separated after suppression of Na+ and K+ currents, and Na+ and Ca2+ currents, respectively. The suction pipette method was used. Under voltage clamp conditions, the effects of propranolol on both the ICa and IK were examined.
Propranolol inhibits the ICa at relatively low concentrations (10−6‐10−5m). The inhibitory action was dose‐dependent.
The IK was moderately suppressed by the drug at high concentrations (10−5‐5 × 10−4m).
Results provide evidence for a new aspect of the pharmacological action of propranolol on the excitable cell membrane.
A RE‐EVALUATION OF ACETYLCHOLINE RECEPTORS ON FELINE RENSHAW CELLS
Authors: KING K.T. , RYALL R.W. 
Published: July 2012

The effects of atropine, methylatropine and lachesine administered by ionophoresis were examined on responses of Renshaw cells to acetylcholine, acetyl‐β‐methylcholine, nicotine and DL‐muscarine in cats anaesthetized with pentobarbitone or chloralose.
The antagonists were as effective in antagonizing excitation by nicotine as they were in antagonizing excitation by acetylcholine and were only slightly more effective in antagonizing excitation by acetyl‐β‐methylcholine.
These results are discussed in relation to the characterization of acetylcholine receptors on Renshaw cells.
It is concluded that there are two distinct populations of receptors but that the nicotinic receptors are non‐selective in their activation by agonists and antagonists, whereas the muscarinic receptors display greater selectivity.
EFFECT OF HYPEROXIA ON UPTAKE AND METABOLISM OF 5‐HYDROXYTRYPTAMINE AND β‐PHENYLETHYLAMINE IN RAT LUNG: A SEX DIFFERENCE
Authors: BEN‐HARARI R.R. , LANIR A. , YOUDIM M.B.H. 
Published: July 2012

The uptake of 5‐hydroxytryptamine (5‐HT) and β‐phenylethylamine (PEA) and their deamination by monoamine oxidase (MAO) were studied in perfused lung from male and female rats exposed to 100% O2 at 1 ATA for up to 60 h.
The uptake and metabolism of 5‐HT in lungs from both male and female rats was not changed by exposure to O2.
The uptake and metabolism of PEA by lungs from male rats was unchanged. Uptake of PEA by lungs from female rats was inhibited 20% and 62% after 37 h and 50 h exposure respectively.
MAO activity, both in vitro and in perfused lung, was increased towards PEA after 35 h of hyperoxia.
Metabolism of PEA in perfused lung, measured over 30 min, was inhibited 52% after 50 h of O2 hyperoxia.
These results show that exposure to high concentrations of O2 damages lung, resulting in inhibition of uptake of PEA and consequently in inhibition of metabolism of PEA.
These results also indicate that, in lung from female rats, MAO‐type B is more susceptible to changes in O2 tension than MAO type A.
THE BENEFICIAL ACTIONS OF BEPRIDIL IN ACUTE MYOCARDIAL INFARCTION IN ANAESTHETIZED DOGS
Authors: MARSHALL R.J. , MUIR A.W. 
Published: July 2012

When administered intravenously shortly before acute coronary ligation in dogs anaesthetized with chloralose, bepridil (5 mg/kg) produced immediate and transient falls in coronary and systemic vascular resistance which were accompanied by marked decreases in myocardial oxygen extraction. These effects were followed by sustained decreases in heart rate and myocardial oxygen consumption.
This dose of bepridil reduced the number of premature ventricular beats and abolished fibrillation induced by coronary artery ligation without modifying the haemodynamic or metabolic consequences (lactate production) of myocardial ischaemia.
When administered 1.5‐2 h after ligation, bepridil did not compromise the critical perfusion of the acutely ischaemic zone but reduced the lactate production and ST‐segment elevation in the ischaemic zone.
These results suggest that bepridil may be a useful drug in the chronic treatment of angina pectoris and in this respect may possess advantages over β‐adrenoceptor antagonists.
In vivo PHARMACOLOGICAL STUDIES ON THE INTERACTIONS BETWEEN TRYPTAMINE AND 5‐HYDROXYTRYPTAMINE
Authors: JONES R.S.G. 
Published: July 2012

Three methods have been used in an attempt to study the interactions of tryptamine with central 5‐hydroxytryptamine (5‐HT) systems.
In groups of mice pretreated with tranylcypromine, tryptamine reduced the number of mice showing head twitches following the 5‐HT precursor, 5‐hydroxytryptophan. This effect was not seen in mice pretreated with saline and tryptamine itself did not induce head twitches in either group.
The swallowing reflex induced by 5‐hydroxytryptophan in rats anaesthetized with urethane was substantially reduced by tryptamine injected into the internal carotid artery. This effect was seen in rats pretreated with saline or tranylcypromine, in the latter case the effects being more profound and longer lasting. In addition, swallowing evoked by the 5‐HT uptake blocker, fluoxetine, and the 5‐HT releaser, p‐chloroamphetamine, was also reduced by tryptamine.
5‐HT or noradrenaline injected intravenously into 5 day‐old chicks caused a dose‐dependent behavioural depression resembling sleep. Tryptamine at high doses caused behavioural alerting effects. Tryptamine at low doses had no overt effects but enhanced depression induced by 5‐HT. At behaviourally excitatory doses tryptamine reduced the duration of the 5‐HT depression. Noradrenaline‐induced depression was not affected by high or low doses of tryptamine.
The results show that tryptamine can have complex actions on 5‐HT systems depending on the parameter studied and support the notion that tryptamine may be a controlling factor in 5‐HT‐mediated transmission.
EFFECT OF SULPHATED POLYSACCHARIDES ON THE α1‐ANTITRYPSIN INHIBITION OF AMIDOLYSIS CATALYSED BY COAGULATION CASCADE PROTEINASES
Authors: LONG W.F. , WILLIAMSON F.B. 
Published: July 2012

The ability of several sulphated polysaccharide anticoagulants to prevent α1‐antitrypsin inhibition of thrombin paralleled their ability to potentiate antithrombin III inhibition of thrombin. None of the compounds examined altered the ability of α1‐antitrypsin to inhibit activated coagulation factor X (Xa).
These results are consistent with the possibility that a direct polysaccharide‐proteinase interaction may be involved in the sulphated polysaccharide‐modulated inhibition of thrombin by antithrombin III.
A COMPARISON OF AN IMPROVED O‐PHTHALALDEHYDE FLUORO‐METRIC METHOD AND HIGH PRESSURE LIQUID CHROMATOGRAPHY IN THE DETERMINATION OF BRAIN 5‐HYDROXYINDOLES OF RATS TREATED WITH L‐TRYPTOPHAN AND p‐CHLOROPHENYL‐ALANINE
Authors: CURZON G. , KANTAMANENI B.D. , TRICKLEBANK M.D. 
Published: July 2012

The determination of 5‐hydroxytryptamine (5‐HT) and 5‐hydroxyindoleacetic acid (5‐HIA A) by reaction with o‐phthalaldehyde (OPT) in the presence of cysteine and subsequent fluorometry was compared with determination by a new high pressure liquid chromatography (h.p.l.c.) electrochemical method.
The methods were used to investigate a claim that the OPT method gives falsely high brain 5‐HT values for rats given tryptophan (> 25mg/kg i.p.) and as a consequence an inhibition of 5‐HT synthesis by tryptophan is obscured.
High concentrations of tryptophan caused some increase of fluorescence when added to 5‐HT solutions and carried through the OPT method, e.g. tryptophan (80 μg/ml) gave fluorescence = 5‐HT (0.13 mUg/ml). This interference was decreased by more than half and the sensitivity of the method increased if cysteine was added at more stages and fluorescence developed at 77°C instead of 100°C.
The h.p.l.c. and modified OPT methods did not give significantly different mean brain 5‐HT or 5‐HIAA values in rats given 0,25,100,250 mg/kg L‐tryptophan though values were somewhat higher by the OPT method with the highest dose. This method gave significantly higher residual brain 5‐HT values (12% of control) than did the h.p.l.c. method (8% of control) after inhibiting 5‐HT synthesis by p‐chlorophenylalanine (150 mg/kg× 3).
There was no indication that tryptophan inhibited 5‐HT synthesis even when brain tryptophan was increased about 30 fold (from 3.8 to 124 μg/g).
Results confirm the general reliability of the OPT method although h.p.l.c. has some advantages i.e. separation of 5‐hydroxyindoles from tryptophan, greater sensitivity, ease of automation.
PRE‐ AND POSTSYNAPTIC α‐ADRENOCEPTOR BLOCKING ACTIVITY OF RAUBASINE IN THE RAT VAS DEFERENS
Authors: DEMICHEL PATRICIA , GOMOND PATRICK , ROQUEBERT JACQUES 
Published: July 2012

The actions of raubasine, yohimbine and corynanthine at pre‐ and postsynaptic α‐adrenoceptors were studied in the rat vas deferens.
Low frequency electrical stimulation of the isolated vas deferens of the rat produced regular contractions that were inhibited by low concentrations of clonidine. This inhibition was presynaptic in origin and involved α‐adrenoceptors.
Presynaptic α‐adrenoceptor antagonist activity was assessed by studying the effect of increasing antagonist concentrations on cumulative clonidine dose‐response curves on the stimulated vas deferens.
Postsynaptic α‐adrenoceptor antagonist activity in the isolated vas deferens was assessed by comparing control cumulative noradrenaline dose‐response curves in the absence and in the presence of increasing concentrations of antagonists.
The results indicate that raubasine and corynanthine preferentially block postsynaptic α‐adrenoceptors. Yohimbine is more potent in blocking pre‐ than postsynaptic α‐adrenoceptors. The ratio of the pre/postsynaptic potency declines in the order yohimbine > raubasine > corynanthine.
EFFECT OF INTRACISTERNAL 5,7‐DIHYDROXYTRYPTAMINE ON THE ACUTE ANTIHYPERTENSIVE ACTION OF PROPRANOLOL IN THE SINO‐AORTIC DENERVATED ANAESTHETIZED DOG
Authors: MONTASTRUC JEAN‐LOUIS , MONTASTRUC PAUL 
Published: July 2012

The anti‐hypertensive effects of intravenously and intracisternally administered (±)‐propranolol were studied in anaesthetized dogs with acute neurogenic (sino‐aortic denervation) hypertension. The animals were pretreated 7 days earlier with intracisternally administered 5,7‐dihydroxytryptamine (5,7‐DHT 200 μg/kg plus desipramine 5 mg/kg i.v.).
5,7‐DHT (plus desipramine) failed to decrease both basic blood pressure and heart rate measured before sino‐aortic denervation. After 5,7‐DHT (plus desipramine) pretreatment, acute sino‐aortic denervation induced a rise in blood pressure and stimulated the heart rate, these effects being similar (in intensity and duration) to those observed in control (saline‐pretreated) debuffered dogs during the first hour following the deafferentation.
In debuffered dogs, (±)‐propranolol given by intracisternal (50 μg/kg) or intravenous (300 μg/kg) routes descreased both blood pressure and heart rate.
5,7‐DHT (plus desipramine) pretreatment abolished the antihypertensive effect of intracisternal propranolol whereas the action of intravenous propranolol was only delayed. In contrast, this pretreatment failed to reduce and even sometimes enhanced the negative chronotropic response induced by propranolol.
These results suggest that central 5‐hydroxytryptaminergic pathways play an important role in the acute hypotension elicited by intracisternal (±)‐propranolol in debuffered hypertensive anaesthetized dogs, but little, if any in propranolol‐induced bradycardia.
5′‐N‐ETHYLCARBOXAMIDOADENOSINE: A POTENT INHIBITOR OF HUMAN PLATELET AGGREGATION
Authors: CUSACK N.J. , HOURANI S.M.O. 
Published: July 2012

5′‐N‐ethylcarboxamidoadenosine (NECA) is an adenosine analogue which is 22,900 times more potent than adenosine as a vasodilator. Adenosine and some of its analogues are also inhibitors of human platelet aggregation. NECA was tested for its effects on human platelets.
NECA (1 μm) inhibited human platelet aggregation induced by adenosine 5′‐diphosphate (ADP), adrenaline, 5‐hydroxytryptamine (5‐HT) and thrombin more powerfully than adenosine. NECA was 5 to 10 times more potent than adenosine at inhibiting ADP‐ and adrenaline‐induced aggregation.
NECA, like adenosine, caused dose‐dependent increases in levels of platelet adenosine 3′,5′‐cyclic monophosphate (cyclic AMP), which were competitively inhibited by theophylline, an adenosine antagonist.
These effects of NECA, like those of adenosine, were completely stereospecific as the l‐enantiomer of NECA was inactive.
NECA did not interfere with the inhibition by ADP of prostaglandin E1 (PGE1)‐stimulated adenylate cyclase.
NECA is the most potent analogue of adenosine tested so far on human platelets, and is the first example of a 5′ modification to retain affinity for the platelet adenosine receptor.
STUDIES OF THE EFFECTS OF AGENTS WHICH ALTER CALCIUM METABOLISM ON ACETYLCHOLINE TURNOVER IN THE RAT DIAPHRAGM PREPARATION
Authors: GUNDERSEN CAMERON B. , JENDEN DONALD J. 
Published: July 2012

We measured the effects of agents, which are thought to alter the Ca2+ concentration in cells, on tissue and released acetylcholine and choline of rat diaphragm using a gas chromatographic mass spectrometric assay for acetylcholine and choline.
Lanthanum and ouabain increased the resting output of acetylcholine, while 4‐aminopyridine enhanced the evoked output of acetylcholine.
Guanidine first increased and then depressed acetylcholine release.
Theophylline, dinitrophenol and the ionophore, A‐23187, had no measurable effect on acetylcholine release and tetraethylammonium inhibited the release of acetylcholine.
Dinitrophenol caused a highly significant increase of the tissue and released choline.
None of these agents increased the tissue acetylcholine content. Tetraethylammonium caused a large decline of tissue acetylcholine while ouabain and guanidine caused smaller reductions of acetylcholine in diaphragm.
These results are discussed in relation to the hypothesis that intraterminal Ca2+ activity regulates the synthesis of acetylcholine in diaphragm nerve endings.