bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE EFFECTS OF SOME PROSTAGLANDINS ON RESPIRATION IN ANAESTHETIZED CATS
Authors: McQUEEN D.S. 
Published: July 2012

Some prostaglandins have been found to be capable of affecting respiration in anaesthetized cats.
Prostaglandins E1, E2, F2α, A1 and A2 all elicited increases in respiratory frequency when administered to cats anaesthetized with either pentobarbitone or α‐chloralose. This effect was abolished by bilateral vagotomy.
Prostaglandins of the E and A series, but not prostaglandin F2α, elicited increases in tidal volume which were accompanied by falls in systemic blood pressure in cats anaesthetized with pentobarbitone. The changes in blood pressure were also obtained in cats anaesthetized with α‐chloralose, but not the tidal volume changes.
It is unlikely that the prostaglandins influenced respiration by direct actions on arterial chemoreceptors or baroreceptors.
Mechanisms by which the prostaglandins may be acting to affect respiration are discussed.
HYPOTENSIVE AND VASODILATOR ACTIONS OF SK&F 24260, A NEW DIHYDROPYRIDINE DERIVATIVE
Authors: FIELDEN R. , OWEN D.A.A. , TAYLOR E.M. 
Published: July 2012

The blood pressure of conscious normotensive, Goldblatt‐hypertensive and genetic‐hypertensive rats and normotensive dogs was lowered by SK&F 24260 (1,4‐dihydro‐2,6‐dimethyl‐4‐(2‐trifluormethylphenyl)‐3,5‐pyridinedicarboxylic acid diethyl ester).
Tachycardia always accompanied the hypotension. In rats propranolol abolished the tachycardia but in dogs there was only a small reduction in the heart rate response.
In conscious dogs there was an increase in left ventricular output and a marked fall in total peripheral resistance.
SK&F 24260 dilated resistance vessels in rat hindquarters. Dilatation was caused by doses of SK&F 24260 some 50 times smaller than those of hydrallazine.
In preparations of cat skeletal muscle and intestinal vascular beds SK&F 24260 selectively dilated resistance vessels in preference to capacitance vessels and resembled hydrallazine rather than papaverine which has no such selectivity.
Pre‐capillary sphincter vessels were also dilated by SK&F 24260. Changes in fluid equilibrium caused by SK&F 24260 were consistent with selective dilatation of resistance vessels.
FLOW AND COMPOSITION OF SKIN AND MUSCLE LYMPH OF THE HIND LIMB OF THE RABBIT AFTER INJURY
Authors: BACH CATHERINE S. , LEWIS G.P. 
Published: July 2012

Collection of skin lymph separately from muscle lymph has enabled us to repeat earlier experiments in which lymph was collected from the whole hind limb to determine whether the changes then observed were the result of changes occurring in the skin or the muscle or both.
After thermal and chemical injury, it appeared that most of the changes were due to leakage of enzymes from the muscle; after freezing, changes occurred in both skin and muscle lymph while ischaemia caused no significant changes in either skin or muscle lymph.
After mild thermal injury it took longer for the enzyme leakage to reach a maximum in muscle lymph than in skin lymph. It seems likely that the changes were buffered by the large tissue space of muscle.
Lactic dehydrogenase (LDH) activity appears to diffuse from muscle into skin since although intramuscular dimethyl sulphoxide (DMSO) causes the release of LDH into skin lymph, subcutaneous DMSO does not.
That proportion of muscle LDH released during injury might represent the unbound or ‘active’ portion since no matter how severe the injury only about 1% of the total muscle LDH was released into the lymph.
RELEASE OF PROSTAGLANDIN FROM THE RABBIT ISOLATED HEART FOLLOWING VAGAL NERVE STIMULATION OR ACETYLCHOLINE INFUSION
Authors: JUNSTAD M. , WENNMALM A. 
Published: July 2012

Rabbit hearts were perfused by the Langendorff technique. The lipid fraction in the perfusate from the heart was isolated and analysed for prostaglandins by thin layer chromatography and quantitative assay on the rat isolated stomach strip.
Infusion of acetylcholine at a rate of 8 μg/min significantly increased the outflow of prostaglandins from the heart, from 1.8 to 6.2 ng/minute.
Addition of atropine (1 μg/ml) to the perfusing medium completely abolished not only the mechanical response but also the increase in outflow of prostaglandins caused by infusion of acetylcholine.
Bilateral stimulation of the parasympathetic nerves to the heart at 5 Hz also significantly increased the outflow of prostaglandins from the organ from 5.2 to 8.3 ng/minute.
Both prostaglandin E1 and E2 were isolated from the lipid fraction of the perfusate.
The role of prostaglandins in relation to autonomic neurotransmission in the heart is discussed.
A COMPARISON OF THE EXPERIMENTAL ANTI‐ARRHYTHMIC PROPERTIES OF ACEBUTOLOL: (M & B 17,803), PROPRANOLOL AND PRACTOLOL
Authors: BASIL B. , JORDAN R. , LOVELESS A.H. , MAXWELL D.R. 
Published: July 2012

The β‐adrenoceptor blocking agent, acebutolol (M & B 17,803), has been compared with propranolol, practolol, lignocaine and quinidine for its ability to revert or prevent various types of experimental arrhythmias.
By intravenous infusion, acebutolol had one half the potency of propranolol in reverting an established ouabain‐induced ventricular arrhythmia in the anaesthetized dog. Practolol was ineffective in the conditions used.
High oral doses of acebutolol or propranolol significantly increased the arrhythmic dose of ouabain in the conscious rabbit. Similar doses of practolol produced a significant decrease (i.e. potentiation) in the dose of ouabain required to produce arrhythmia. Lignocaine and quinidine showed no or little activity in this test.
Propranolol, acebutolol and practolol were all effective in decreasing the frequency of ectopic beats induced by adrenaline and methylchloroform in the anaesthetized cat. Lignocaine and quinidine were only weakly effective.
Acebutolol and propranolol were equally effective either intravenously or orally in reducing the incidence of ventricular fibrillation produced by chloroform in mice.
It is suggested that the wide spectrum of experimental anti‐arrhythmic activity of acebutolol coupled with its cardioselectivity may make it an interesting compound in the treatment of cardiac arrhythmias in man.
LOWERING OF KININOGEN IN RAT BLOOD BY ADRENALINE AND ITS INHIBITION BY SYMPATHOLYTIC AGENTS, HEPARIN AND ASPIRIN
Authors: CASTANIA A. , ROTHSCHILD A.M. 
Published: July 2012

(–)‐Adrenaline lowered the kininogen content and transitorily elevated the fibrinolytic activity of plasma following intravenous injection into the rat. Its effect on kininogen increased when administered by intravenous infusion.
Although less effective, (–)‐noradrenaline had a similar action to adrenaline; (±)‐isoprenaline was inactive and failed to inhibit the effect of adrenaline.
The effect of adrenaline on kininogen could be reproduced in vitro by incubation of whole blood, but not cell‐free plasma, with the catecholamine for 5 min at 37° C.
Propranolol or phenoxybenzamine, as well as heparin or acetylsalicylic acid (aspirin), blocked the reduction of rat blood kininogen by adrenaline in vivo and in vitro.
DISTRIBUTION OF PENTAZOCINE IN BLOOD AND BRAIN OF THE BABOON FOLLOWING INTRAVENOUS INJECTION
Authors: CORONEOS N.J. , KEANEY N.P. , McDOWALL D.G. , PICKERODT V.W.A. , GLYNN J.P. , ROBERTSON A. 
Published: July 2012

In the baboon the blood levels of pentazocine between 1 and 60 min after intravenous injection of 0.5 mg/kg were measured by a gas chromatographic technique. From cerebral arteriovenous differences it was shown that the peak of the brain concentration occurred within 15 min and probably within 10 min of intravenous injection. At the time of peak concentration about 10% of the injected dose was in the brain, while the corresponding value at 60 min was 2%.
The concentration of pentazocine in the brain was an order of magnitude greater than the concentration in cerebral venous blood both at 5 min and 60 min after injection. No major brain interregional differences were demonstrated. Cerebrospinal fluid from the cisterna magna did not yield values from which the cerebral concentration of pentazocine could be predicted.
EFFECTS OF Gymnodinium breve TOXIN ON THE SMOOTH MUSCLE PREPARATION OF GUINEA‐PIG ILEUM
Authors: GRUNFELD Y. , SPIEGELSTEIN M.Y. 
Published: July 2012

The effects of Gymnodinium breve neurotoxin (GT) on smooth muscles were studied using the guinea‐pig isolated ileum.
The toxin caused strong spasmogenic effects at 1–4 μg/ml, characterized by prolonged tonic contraction with superimposed pronounced pendular movements. Tachyphylaxis was observed upon administration of successive doses.
Atropine blocked the contractile response elicited by GT, whereas mepyramine and hexamethonium failed to do so. These findings tentatively suggested a cholinergic involvement at a post‐ganglionic site of action.
In the presence of tetrodotoxin the effects of GT were abolished, excluding direct action of the toxin on the smooth muscle.
It is concluded that GT exerts its spasmogenic effects through stimulation of the post‐ganglionic cholinergic nerve fibres.
EFFECT OF ETHER ANAESTHESIA ON PHARMACOKINETICS OF N‐(2 HYDROXY ETHYL) 2‐PHENYL ETHYL CARBAMATE: INHIBITION OF ITS ENTEROHEPATIC CIRCULATION
Authors: OBIANWU HOPÉ O. 
Published: July 2012

The effect of the ether anaesthesia on the plasma half‐life of N‐(2 hydroxy ethyl) 2‐phenyl ethyl carbamate has been studied in rats.
The plasma half‐life of the carbamate was considerably shorter in animals anaesthetized with ether prior to drug administration than in control rats.
The longer plasma half‐life of the carbamate in control animals was shown to be due to enterohepatic circulation.
Inhibition of this phenomenon by ether was responsible for the shorter plasma half‐life of the carbamate in animals anaesthetized with this agent before drug administration.
The possible mechanisms by which the ether‐induced effect is brought about are discussed.
RELATIONSHIPS BETWEEN CHEMICAL STRUCTURE AND AFFINITY FOR POSTGANGLIONIC ACETYLCHOLINE RECEPTORS OF THE GUINEA‐PIG ILEUM
Authors: ABRAMSON F.B. , BARLOW R.B. , FRANKS FIONA M. , PEARSON J.D.M. 
Published: July 2012

Some phenylacetyl, diphenylacetyl, benziloyl and (±)‐cyclohexylphenylglycolloyl esters have been made with 2‐ and 3‐hydroxymethylpyrrolidines, 3‐hydroxymethyl‐N‐methylpiperidine, piperidin‐3‐ols, piperidin‐4‐ols, 2,2,6,6‐tetramethyl‐N‐methylpiperidin‐4‐ol, tropine, pseudotropine and quinuclidin‐3‐ol, and the affinity of these compounds and of their metho‐ and etho‐ derivatives has been measured for postganglionic acetylcholine receptors of the guinea‐pig isolated ileum.
Some of the compounds were very active indeed; the benziloyl esters of N‐methylpiperidin‐4‐ol methiodide, tropine methiodide, and quinculidin‐3‐ol, and the (±)‐cyclohexylphenylglycolloyl esters of N‐methylpiperidin‐4‐ol and its methiodide had affinity constants greater than 1010.
The effects of inserting an additional methylene group onto the nitrogen were extremely variable, ranging from a decrease in log K of 1.64 units to an increase of 0.97 units. The effects of replacing hydrogen by phenyl in the acid portion ranged from an increase of 1.04 units to an increase of 3.06 units and of replacing hydrogen by hydroxyl from a decrease of 0.09 units to an increase of 1.94 units.
The extent of the variation in the effects of a particular change in structure on affinity does not appear to be any different in these relatively rigid compounds from that observed with the same changes in open‐chain aminoalcohols.
Reasons for the variable effects of groups on affinity are discussed. If differences in effects on preferred conformations of these particular compounds in solution are of secondary importance, the effect of a group on affinity will be the net result of what it could contribute to binding, offset by the disturbance it causes to existing binding. The maximum effect observed in a large number of comparisons may indicate the contribution in the absence of disturbance and for groups containing only carbon and hydrogen it appears to be related to size, assessed from the increments in apparent molal volume at infinite dilution. The variation in the effects of these groups also appears to be related to size. Changes involving groups containing oxygen can produce bigger contributions to binding, and a bigger variation in contribution, than would be expected from their size.
It is difficult to predict the extent to which groups may fail to produce their maximum effects. Variation is greatest with groups which could produce the biggest changes and so are of the greatest interest.
The relevance of the results to the successful prediction of biological activity is discussed.
BLOCKADE OF PERIPHERAL VASCULAR RESPONSES TO ISOPRENALINE BY THREE β‐ADRENOCEPTOR ANTAGONISTS IN THE ANAESTHETIZED DOG
Authors: HAINSWORTH R. , KARIM F. , STOKER J.B. 
Published: July 2012

A dog's hind limb was vascularly isolated by strong nylon snares and its sympathetic nerve supply interrupted. Blood was perfused at constant flow into the femoral artery and drained from the femoral vein. In some dogs the cardiac nerves were cut.
Isoprenaline infused intravenously caused an increase in heart rate and a decrease in arterial resistance.
Practolol (2 mg/kg) effectively blocked heart rate responses to isoprenaline infused at up to 10 μg/min but was relatively ineffective in blocking arterial responses. ICI 66082 (2 mg/kg) reduced vasomotor responses and propranolol (0.5 mg/kg) abolished vasomotor responses.
Small cumulative doses of β‐adrenoceptor antagonists were given to some dogs. Practolol blocked heart rate responses in lower doses than were required to block vasomotor responses. Propranolol preferentially blocked vasomotor responses and ICI 66082 was intermediate between the other two in its effects.
COMPULSIVE GNAWING IN RATS AFTER IMPLANTATION OF DRUGS INTO THE VENTRAL THALAMUS. A CONTRIBUTION TO THE MECHANISM OF MORPHINE ACTION
Authors: BERGMANN F. , CHAIMOVITZ M. , PASTERNAK(NA'OR) V. , RAMU A. 
Published: July 2012

Implantation of morphine into various parts of the corpus striatum of rats evokes only weak gnawing responses.
Deposition of apomorphine, morphine or methadone in the region of the nucleus ventralis thalami produces a biphasic response, i.e. general excitation, followed by a period of intense gnawing.
The effect of both apomorphine and morphine is blocked by chlorpromazine, haloperidol and pimozide. However, pretreatment with α‐methyltyrosine methyl ester or α‐methyldopa prevents only the gnawing response to morphine, but not to apomorphine.
Systemic nalorphine, morphine or pethidine suppress the gnawing response, evoked by thalamic implants of apomorphine or morphine.
Systemic amphetamine potentiates the effect of thalamic deposits of morphine.
Compulsive gnawing, following implantation of morphine into the ventral region of the thalamus, probably results from enhanced production and release of catecholamines.
THE EFFECTS OF INTRAVENTRICULAR 6‐HYDROXYDOPAMINE ON BODY TEMPERATURE AND ARTERIAL BLOOD PRESSURE IN CATS AND RABBITS
Authors: LEWIS P.J. , RAWLINS M.D. , REID J.L. 
Published: July 2012

In unanaesthetized cats, the administration of 6‐hydroxydopamine (6‐OHDA), 750 μg, via the lateral cerebral ventricle produced a pronounced fall in rectal temperature but only a slight fall when repeated 7 days later. At this time hypothalamic noradrenaline concentration had diminished to 4% of control.
In these animals, the hypothermic response to exogenous noradrenaline, 100 μg, given via the same route was uninfluenced by pretreatment with 6‐OHDA.
In unanaesthetized rabbits, intraventricular noradrenaline, 100 μg, produced a rise in rectal temperature and a biphasic effect on arterial pressure, a rise lasting 30 min followed by a fall.
Intraventricular 6‐OHDA, 750 μg, in unanaesthetized rabbits produced a rise in body temperature and a rise in arterial pressure. The same dose given to rabbits depleted of central noradrenaline with central 6‐OHDA produced rises in body temperature and arterial pressure of similar magnitude, but of slower onset.
These results suggest that intraventricular 6‐OHDA releases noradrenaline from central neurones and that these neurones subserve thermoregulatory functions in both species. In the rabbit, central noradrenergic neurones can raise arterial pressure.
CAN THE ACTIONS OF ADRENOCEPTOR AGONISTS AND ANTAGONISTS ON PENTAGASTRIN‐INDUCED GASTRIC SECRETION BE DUE TO THEIR EFFECTS ON HISTAMINE FORMATION?
Authors: CURWAIN B.P. , HOLTON PAMELA , McISAAC R.L. , SPENCER JAN 
Published: July 2012

The effects of some adrenoceptor agonists and antagonists which have been reported to affect histamine formation in leucocytes (Assem & Feigenbaum, 1972) have been investigated on gastric secretion in conscious dogs with Heidenhain pouches.
Submaximal secretion in response to pentagastrin was enhanced by propranolol (0.1–1.0 mg/kg i.v.) and phenylephrine (1.0 μg kg−1 min−1 i.v. for 20 min), which increase histamine formation, and was decreased by phentolamine (2 mg/kg i.v.) and isoprenaline (0.05–0.2 μg kg−1 min−1 i.v. for 30 min), which decrease histamine formation. Practolol (2 mg/kg i.v.), which has no effect on histamine formation, had no effect on secretion.
Acid secretion in response to histamine was either unaffected or affected in the opposite direction by these drugs.
The effects of the drugs on pentagastrin‐induced secretion were not secondary to changes in mucosal blood flow (radioactive aniline clearance).
The results are consistent with the hypothesis that acid secretion in response to pentagastrin involves the formation of endogenous histamine.
DISSOCIATION OF CARDIAC INOTROPIC AND ADENYLATE CYCLASE ACTIVATING ADRENOCEPTORS
Authors: BENFEY B.G. , KUNOS G. , NICKERSON M. 
Published: July 2012

At higher temperatures, near the physiological range for mammals and nonhibernating frogs, the adrenoceptors for both inotropic responses to adrenaline and noradrenaline and for cyclic 3′,5′‐adenosine monophosphate (cyclic AMP) production in rat and frog isolated heart preparations, had typical β characteristics. Phenoxybenzamine potentiated the inotropic response and the accumulation of cyclic AMP; conversely, propranolol inhibited the two responses.
When the ambient temperature was reduced, the adrenoceptors mediating cyclic AMP production changed very little; they were blocked as effectively as at the higher temperature by propranolol and were not blocked by phenoxybenzamine. However, the adrenoceptors mediating the inotropic response were markedly changed by the decrease in temperature; phenoxybenzamine now inhibited this response and the inhibitory activity of propranolol was reduced about tenfold.
These results indicate that the adrenoceptors that mediate cardiac inotropic responses at physiological temperatures are distinct from those that mediate the production of cyclic AMP, and that the activation of adenylate cyclase and the accumulation of cyclic AMP are probably not intermediate steps in cardiac inotropic responses to catecholamines.
EVIDENCE FOR PARTICIPATION OF CATECHOLAMINES IN CARDIAC ACTION OF OUABAIN: POSITIVE CHRONOTROPIC EFFECT
Authors: SEIFEN E. 
Published: July 2012

The shortening of cycle length (=positive chronotropic effect) by ouabain produced in isolated spontaneously beating atria of the guinea‐pig was analyzed.
The action of ouabain was dose‐dependent; threshold response was seen at 1 × 10−7 m, and maximal response occurred at 4 × 10−7 M. The half‐time of the ouabain effect was about 20 minutes.
The positive chronotropic effect of ouabain was reduced to 40% by β‐adrenoceptor blockade (3.3 × 10−9 M propranolol) or by reserpine‐depletion of catecholamines. Incubation of reserpine‐treated atria with noradrenaline partially restored the action of ouabain.
The effect of ouabain was greatly dependent upon the calcium concentration. The optimal calcium level was 2.5 × 10−3 M. Calcium and ouabain acted synergistically.
Increasing calcium concentrations inhibited the positive chronotropic effect of noradrenaline in a manner similar to increasing ouabain concentrations.
A hypothesis is proposed which explains the chronotropic effect of ouabain on the basis of two mechanisms: (1) increase of the catecholamine concentration affecting the pacemaker; (2) mobilization of calcium, i.e. increase of the biologically effective intracellular calcium level.
CORTICAL POTENTIALS EVOKED BY NOCICEPTIVE STIMULI: THEIR DEPRESSION BY A FACTOR RELEASED DURING SAPHENOUS NERVE STIMULATION IN THE RAT
Authors: LEME J. GARCIA , LICO MARIA 
Published: July 2012

The amplitudes of the first positive and the first negative waves of cortical potentials evoked by electrical stimulation of the dental pulp in the rat were decreased following electrical stimulation of the peripheral cut end of the saphenous nerve.
This effect was greatly diminished when the stimulation of the saphenous nerve was performed with the saphenous or femoral veins ligated.
During stimulation of the saphenous nerve of a donor rat, the subcutaneous tissue in the area supplied by the nerve was perfused; when the perfusate (in which a permeability‐in creasing factor was detected) was injected intravenously into a recipient animal, a decrease in the amplitude of the evoked cortical potential of the recipient rat was also observed.
Intravenous injections of 5‐hydroxytryptamine, histamine, bradykinin, prostaglandins or adenosine‐triphosphate produced no effect on the evoked cortical potential, whereas large doses of acetylsalicylic acid caused a decrease.
It is suggested that a humoral factor, released during sensory nerve stimulation, may help to modulate the processing of afferent inputs from pain receptors.
EFFECTS OF CATECHOLAMINES ON THERMOREGULATION IN PIGEONS
Authors: CHAWLA NARESH , JOHRI M.B.L. , SAXENA P.N. , SINGHAL K.C. 
Published: July 2012

In unanaesthetized pigeons, kept at room temperature (20–23°C) the effects on cloacal temperature were examined of catecholamines, phenoxybenzamine and propranolol, injected into the cerebral ventricles.
Noradrenaline, adrenaline, dopamine and isoprenaline caused a fall in cloacal temperature.
Phenoxybenzamine produced a long‐lasting small rise in cloacal temperature. This rise is attributed to removal of the hypothermic effect of noradrenaline released continuously from adrenergic neurones ending in the anterior hypothalamus. Propranolol produced a slight fall in cloacal temperature.
The hypothermic effects of noradrenaline, adrenaline and dopamine were prevented by phenoxybenzamine but not by propranolol. They are therefore attributed to activation of α‐adrenoceptors.
The hypothermic effect of isoprenaline was not prevented by either phenoxybenzamine or propranolol. The effect can therefore not be attributed to activation of either α or β‐adrenoceptors. Propranolol actually accentuated the isoprenaline‐induced hypothermia.