bluuebunny/crossref_metadata_2025_split huggingface dataset:
EFFECTS OF SEVERAL INHALATION ANAESTHETICS ON THE KINETICS OF POSTSYNAPTIC CONDUCTANCE CHANGES IN MOUSE DIAPHRAGM
Authors: GAGE P.W. , HAMILL O.P. 
Published: July 2012

Miniature endplate currents were recorded with extracellular electrodes in mouse diaphragms in order to measure the kinetics of the conductance change produced by acetylcholine. Miniature endplate potentials (m.e.p.ps) were recorded intracellularly in the same fibres in which the currents were being recorded.
The general anaesthetics, ether, halothane, chloroform and enflurane at low (anaesthetic) concentrations increased the rate of decay of miniature endplate currents (m.e.p.cs) and reduced the amplitude of m.e.p.ps in this way.
At high concentrations the anaesthetics caused a reduction in the amplitude of both m.e.p.cs and m.e.p.ps, and a decrease in the rate of decay of the currents. With halothane and enflurane the decay of some currents became biphasic, with a prolonged tail.
It was proposed that the increased rate of decay of the conductance caused by the four agents at anaesthetic concentrations is due to an increase in the fluidity of the subsynaptic membrane. Prolongation of the currents at higher concentrations may be caused by an increase in membrane dielectric constant.
The effectiveness of the four anaesthetics in producing a 30% decrease in the time constant of decay of m.e.p.cs was shown to be related to their oil/water partition coefficients and followed closely the relationship between anaesthetic potency and oil/water partition coefficient. It is suggested therefore that the four anaesthetics may produce anaesthesia by changing the kinetics of postsynaptic conductance changes at synapses, perhaps by increasing membrane fluidity.
INHIBITION OF PERISTALSIS IN GUINEA‐PIG ISOLATED ILEUM AND COLON BY DRUGS THAT BLOCK PROSTAGLANDIN SYNTHESIS
Authors: BENNETT A. , ELEY K.G. , STOCKLEY HELEN L. 
Published: July 2012

Methods of analysing peristaltic activity have been evaluated by the use of recordings of longitudinal and circular muscle activity and of propulsion in whole segments of guinea‐pig ileum and colon.
Some prostaglandin synthesis inhibitors, and antagonists of prostaglandin action were tested for their suitability for studying the role of prostaglandins in peristalsis. Aspirin was suitable; at 10–200 μg/ml it had little effect on responses of longitudinal muscle strips of the guinea‐pig ileum to acetylcholine (ACh), histamine, nicotine or prostaglandin E2. Indomethacin (1–4 μg/ml) reduced responses to nicotine and prostaglandin E2. The prostaglandin antagonists polyphloretin phosphate and SC‐19220 reduced contractions of ileal longitudinal muscle caused by nerve excitation with either nicotine or transmural stimulation.
Aspirin (20–100 μg/ml) or indomethacin (1–4 μg/ml) applied serosally greatly inhibited all aspects of peristalsis in guinea‐pig ileum and colon. Inhibition of peristalsis of the ileum by aspirin was antagonized by prostaglandin E2 and that by indomethacin was removed by prostaglandin F2α or ACh. Inhibition of colonic peristalsis by aspirin was antagonized by prostaglandin E2 but rarely by ACh, and that by indomethacin by prostaglandin E1 or E2. Mucosal application of aspirin had little effect on either ileum or colon but indomethacin caused some inhibition.
These results support the supposition that prostaglandins contribute to peristaltic activity.
A COMPARATIVE STUDY OF THE ACTION OF γ‐AMINOBUTYRIC ACID AND PIPERAZINE ON THE LOBSTER MUSCLE FIBRE AND THE FROG SPINAL CORD
Authors: CONSTANTI A. , NISTRI A. 
Published: July 2012

The effects of γ‐aminobutyric acid (GABA) and piperazine were compared on two in vitro preparations, the lobster muscle fibre and the frog spinal cord.
Both GABA and piperazine increased the membrane conductance of single lobster muscle fibres without changing the membrane potential; sigmoidal log dose‐conductance curves for these agents were obtained and a similar model expressed the receptor interaction of both substances.
The actions of GABA and piperazine on lobster muscle were antagonized by picrotoxin and were Cl−‐dependent.
In the frog spinal cord GABA depolarized the dorsal roots presumably by mimicking the activity of the transmitter depolarizing the primary afferents; sigmoidal log dose‐response curves for GABA were obtained.
On the dorsal roots piperazine produced either depolarizations or biphasic responses; these were mainly indirect effects as was shown by experiments in the presence of tetrodotoxin (TTX).
The effects of GABA on the dorsal root (in TTX‐treated cords) were antagonized by picrotoxin whereas those of piperazine were more resistant to this alkaloid. The GABA‐induced responses appeared to be largely Na+‐dependent while both Na+ and Cl− seemed to mediate the effects of piperazine.
It is proposed that piperazine has GABA‐agonist activity on lobster muscle but little GABA‐like activity on the frog spinal cord.
A COMPARATIVE STUDY OF THE EFFECTS OF GLUTAMATE AND KAINATE ON THE LOBSTER MUSCLE FIBRE AND THE FROG SPINAL CORD
Authors: CONSTANTI A. , NISTRI A. 
Published: July 2012

The depolarizing actions of glutamate and its conformationally restricted analogue kainate were investigated on the lobster muscle fibre and the frog spinal cord using intracellular and extracellular recordings, respectively.
Bath‐applied kainate was less potent than glutamate on the lobster fibre but more potent on the frog cord. From the log‐log transformation of dose‐response curves it was proposed that more than one glutamate molecule was necessary to activate both the lobster and the frog receptor sites. In the frog, at least three kainate molecules were thought to be required for receptor activation.
The ionic dependence of glutamate and kainate responses appeared different for the two tissues.
Some possible explanations of the differential tissue sensitivity to kainate are discussed.
THE CHOLINERGIC COMPONENT IN THE REFLEX VASODILATATION ELICITED BY STIMULATION OF THE DEPRESSOR NERVES IN THE RABBIT
Authors: CHIARIELLO M. , CONDORELLI M. , DE CAPRIO L. , RENGO F. , SACCÀ L. , TRIMARCO B. 
Published: July 2012

The effects of the stimulation of the cephalic endings of the depressor nerve on the resistance in the perfused hindlimb were studied in the rabbit.
The vasodilatation thus elicited in the perfused hindlimb was reduced either by administration of guanethidine or by sympathectomy and abolished by subsequent treatment with atropine.
These data confirm the existence of two components in the genesis of the reflex vasodilatation: a passive component, due to the inhibition of sympathetic discharge, and an active component which in the rabbit is cholinergic in nature.
DECREASED PHENYLETHANOLAMINE‐N‐METHYLTRANSFERASE AND CATECHOL‐O‐METHYLTRANSFERASE ACTIVITY IN RABBIT ADRENAL GLANDS DURING PREGNANCY
Authors: PARVEZ H. , PARVEZ S. , RAZA‐BUKHARI A. , YOUDIM M.B.H. 
Published: July 2012

Phenylethanolamine‐N‐methyltransferase (PNMT) activity in adrenal gland was lower than the control values at day 24 of rabbit pregnancy and fell throughout the gestational period.
Catechol‐O‐methyltransferase (COMT) activity during pregnancy and parturition followed a similar pattern to PNMT.
Adrenaline content of the adrenal gland declined significantly during the last few days of pregnancy but at parturition showed a tendency to return towards normal.
The biochemical mechanisms which result in a decline in PNMT and COMT activities and adrenaline concentration appear to be the consequence of modifications in endocrine gland secretion during pregnancy.
A COMPARISON OF d AND l‐TRYPTOPHAN ON THE CEREBRAL METABOLISM OF 5‐HYDROXYTRYPTAMINE AND DOPAMINE IN THE DOG
Authors: BUDNY J. , DOW R.C. , ECCLESTON D. , HILL A.G. , RITCHIE ISOBEL M. 
Published: July 2012

After d and l‐tryptophan (50 mg/kg) were given intravenously in the dog, the concentration of the amino acid was increased in ventricular cerebrospinal fluid (CSF) during the subsequent 4 h of sampling, although the concentrations were significantly lower following the administration of the d‐isomer.
There was no evidence that d‐tryptophan increased the synthesis of 5‐hydroxytryptamine (5‐HT) in dog brain as judged by the failure to cause a change in 5‐hydroxyindoleacetic acid (5‐HIAA) concentrations in ventricular CSF different from that seen with controls.
There was no appreciable conversion of d‐tryptophan to l‐tryptophan in the dog.
d‐tryptophan was cleared more rapidly from plasma than l‐tryptophan.
No difference in plasma binding between d and l‐tryptophan was detected.
DETERMINATION OF HALOTHANE‐INDUCED SLEEPING TIME IN THE RAT: EFFECT OF PRIOR ADMINISTRATION OF CENTRALLY ACTIVE DRUGS
Authors: TURNBULL M.J. , WATKINS J.W. 
Published: July 2012

A method is described for the determination of halothane‐induced sleeping time in the rat.
The sleeping time exhibited a diurnal variation which was due, at least in part, to a change in the sensitivity of the central nervous system (CNS) to the anaesthetic.
Tolerance to halothane did not develop in rats repeatedly exposed to the anaesthetic over a period of over 48 hours.
Repeated sleeping time determinations have been used to follow changes in the sensitivity of the CNS to the anaesthetic occurring with time.
A tolerance to halothane was induced by pretreatment of rats with doses of amylobarbitone, pentobarbitone or meprobamate sufficient to keep animals anaesthetized for approximately 12 hours. This tolerance was followed by a period of halothane‐hypersensitivity.
Halothane‐tolerant animals awakened with higher brain halothane concentrations and were also tolerant to intracerebroventricularly administered pentobarbitone.
Halothane‐hypersensitive rats awakened with lower brain halothane concentrations and were also hypersentive to intracerebroventricularly administered pentobarbitone.
The possibility that the induction of cross‐tolerance to halothane may be indicative of a drug's potential to produce dependence is discussed.
ADRENOCEPTORS OF THE GUINEA‐PIG URINARY BLADDER
Authors: DAVE K.C. , DHATTIWALA A.S. 
Published: July 2012

Adrenaline, noradrenaline and isoprenaline (5 μg/ml) did not affect the resting tone of the isolated urinary bladder of the guinea‐pig.
The catecholamines (1–2 μg/ml) inhibited neuronally evoked contractions at various stimulation frequencies; the inhibition was maximum at 2 Hz and minimum at 50 Hz. Isoprenaline produced maximum inhibition.
Propranolol (0.5 μg/ml) completely blocked the catecholamine‐induced inhibition at all the frequencies employed. The concentration‐response curves of isoprenaline at 2, 10 and 50 Hz were characteristically shifted by propranolol (50 ng/ml). Phenoxybenzamine (0.2 μg/ml) was totally ineffective.
In some experiments adrenaline significantly raised the tone of the bladder exposed to propranolol; this effect could be blocked by phenoxybenzamine.
Acetylcholine‐induced bladder contractions were inhibited by adrenaline (2 μg/ml); the inhibition was completely blocked by propranolol (0.5 μg/ml).
The results indicate the presence of an inhibitory β‐adrenoceptor and suggest the possibility of an excitatory α‐adrenoceptor in guinea‐pig urinary bladder.
THE ACTION OF TETRAETHYL‐AMMONIUM CHLORIDE ON THE RESPONSE OF THE RAT ANOCOCCYGEUS MUSCLE TO MOTOR AND INHIBITORY NERVE STIMULATION AND TO SOME DRUGS
Authors: GILLESPIE J.S. , TILMISANY A.K. 
Published: July 2012

Tetraethylammonium chloride (TEA) 0.125 mm to 20 mm potentiates the response of the anococcygeus muscle to field stimulation of the motor adrenergic nerves without affecting the response to noradrenaline suggesting a pre‐synaptic origin of potentiation. The potentiation is greatest at low, submaximal, frequencies (2 Hz) of stimulation and only slight at the higher frequency of 20 Hz. This difference is due to the restraint imposed on the demonstration of potentiation by maximal or near maximal motor responses since reduction of the mechanical response at 20 Hz by either phentolamine (post‐synaptic block) or guanethidine (pre‐synaptic block) resulted in a great increase in potentiation of the response at this frequency.
TEA in concentrations up to 1 mm similarly potentites the response to inhibitory nerve stimulation and again the greatest effect is at low frequencies. Higher concentrations (5–20 mm) progressively depress the inhibitory response. It is suggested that TEA may specifically antagonize the post‐synaptic action of the inhibitory transmitter and that at higher concentrations of TEA this effect dominates the pre‐synaptic action in increasing transmitter release.
TEA has no effect on the motor response to tyramine.
TEA (5–20 mm) causes a maintained rise in muscle tone. Part of this is abolished by phentolamine but part is resistant. A similar muscle stimulant action of TEA is observed in muscles from rats previously treated with 6‐hydroxydopamine in which indirect sympathomimetic drugs and field stimulation could no longer produce a motor response. These results suggest that part of the motor effect of TEA is due to an increased spontaneous release of noradrenaline and part to a direct action on the muscle.
TEA 0.125 mm to 20 mm antagonize the stimulant action of carbachol. Dose‐response curves show a parallel shift to the right with no change in the maximum response suggesting a competitive atropine‐like action. Such an effect has previously been reported in amphibian tissue but not so far as we can determine in mammalian preparations.
The possible mode of action of TEA is discussed.
THE EFFECT OF HIGH RATES OF VASOPRESSIN ADMINISTRATION ON RENAL POTASSIUM AND SODIUM EXCRETION DURING POTASSIUM LOADING IN THE SHEEP
Authors: BEAL A.M. 
Published: July 2012

The influence of potassium loading on the renal excretion of sodium, potassium and solute during high rate vasopressin administration has been investigated in sheep.
Adrenalectomized sheep were infused with 0.43 m KCl at 2 ml/min for 2–2.5 hours. Coincident with the rise in plasma potassium concentration, the urinary excretion of sodium, potassium, solute and water was increased as was the reabsorption of solute‐free water. The rates of urinary excretion of sodium and potassium, osmolal clearance (COsm) and solute‐free water reabsorption (TcH2O) for the first 50 min of potassium infusion were each found to be linearly related to the plasma potassium concentration.
After 50 min an infusion of vasopressin at 1 or 4 mu/min was superimposed on the potassium infusion for a period of 30 minutes. The administration of vasopressin was consistently associated with further augmentation of potassium excretion and clearance, of osmolal clearance and of solute‐free water reabsorption to values above those anticipated from the pre‐vasopressin regression lines for these parameters. Urinary sodium showed a coincident depression in the rate of excretion and clearance during the same period.
Thirty to fifty minutes after the cessation of vasopressin infusion the potassium and sodium excretions had returned to values which approximated the pre‐vasopressin relations between plasma potassium and the urinary excretions of these ions.
Both rates of vasopressin infusion were equally effective in increasing the potassium clearance. Any differences in clearance between the two rates of vasopressin administration were not statistically significant.
The large increments in potassium excretion (averaging > 40%) were interpreted as indicating that, when vasopressin is present at high concentrations, the distal tubule is one site of action of the hormone in the nephron of sheep.
THE RELEASE OF A CORONARY VASODILATOR METABOLITE FROM THE GUINEA‐PIG ISOLATED PERFUSED HEART STIMULATED BY CATECHOLAMINES, HISTAMINE AND ELECTRICAL PACING AND BY EXPOSURE TO ANOXIA
Authors: BROADLEY K.J. 
Published: July 2012

A procedure involving two guinea‐pig isolated hearts perfused in series is described for detecting in the recipient heart the release of a possible coronary vasodilator metabolite from the donor heart.
Adrenaline and isoprenaline stimulated the rate and force of contraction and produced a multiphasic coronary vascular response, the predominant phase of which was vasodilatation. When the β‐adrenoceptors of the recipient heart were blocked, stimulation of the donor heart by the catecholamines was associated with a coronary vasodilatation of the recipient heart.
Histamine stimulated rate and force of contraction and was predominantly coronary vasodilator. After blockade of histamine H1‐and H2‐receptors in the recipient heart, coronary vasodilatation followed increases in activity of the donor heart in response to histamine.
These vasodilator responses of the recipient heart were attributed to the release from the donor heart of a vasodilator metabolite by the increased activity. This is the proposed mechanism for the predominant coronary vasodilator response to catecholamines and histamine.
Periods of electrically‐paced tachycardia and anoxia of the donor heart also led to the release of vasodilator activity.
The possible identity of the metabolite is discussed.
MORPHINE–NALOXONE INTERACTION IN THE CENTRAL CHOLINERGIC SYSTEM: THE INFLUENCE OF SUBCORTICAL LESIONING AND ELECTRICAL STIMULATION
Authors: JHAMANDAS K. , SUTAK M. 
Published: July 2012

The opiate antagonist naloxone, injected or topically applied to the cerebral cortex, had no significant effect on the spontaneous output of cortical acetylcholine (ACh) in rats.
Morphine (2.5 mg/kg) administered intravenously inhibited the release of cortical ACh. A subsequent injection of naloxone rapidly reversed morphine‐induced inhibition, and produced a sustained increase in the release of ACh. Topical application of naloxone solutions, after morphine, produced a slow and weak reversal of its inhibitory action.
Destruction of the medial thalamus abolished both the inhibitory effects of morphine on the cortical ACh release, and its antagonism by naloxone administered after the agonist.
Injection of naloxone in a low dose (0.1 mg/kg) increased the release of cortical ACh provoked by electrical stimulation of either the medial thalamus or the reticular formation in normal rats. In the morphine‐dependent rat, naloxone also facilitated the evoked release and its action was greater than in control animals. The facilitatory effect of naloxone on the cortical release evoked by stimulation of the medial thalamus was greater than its effect on the release evoked by stimulation of the reticular formation in both normal and morphine‐dependent rats.
Naltrexone, a narcotic antagonist, also facilitated the electrically stimulated release of cortical ACh.
It is suggested that (a) morphine and naloxone act at a subcortical site, probably the medial thalamus, to modify the cortical ACh release and that (b) naloxone may facilitate the electrically‐induced release of ACh in the CNS by antagonizing the effect of the endogenous morphine‐like factor, enkephalin.
EFFECTS OF l‐TRYPTOPHAN AND l‐METHIONINE ON ACTIVITY IN THE RAT
Authors: TAYLOR M. 
Published: July 2012

The effects of an intraperitoneal dose of 20 mg/kg L‐tryptophan and doses of 100 and 150 mg/kg of l‐methionine were investigated on activity in the rat.
Activity was measured by a time sampling behaviour categorization procedure, and began 15 min after compound administration, lasting for a total of one hour.
Total active behaviour in the first half hour was reduced after 20 mg/kg tryptophan, 100 or 150 mg/kg methionine. Only 20 mg/kg tryptophan led to a significant reduction in active behaviour during the second half hour.
Administration of 100 mg/kg methionine plus 20 mg/kg tryptophan, and 150 mg/kg methionine plus 20 mg/kg tryptophan had no discernible effect on activity.
The results draw attention to the role of another amino acid in the modification of the behavioural effects of tryptophan.
THE EFFECT OF METIAMIDE ON ACID SECRETION STIMULATED BY GASTRIN, ACETYLCHOLINE AND DIBUTYRYL CYCLIC ADENOSINE 3′, 5′‐MONOPHOSPHATE IN THE ISOLATED WHOLE STOMACH OF THE RAT
Authors: BUNCE K.T. , PARSONS M.E. , ROLLINGS NITA A. 
Published: July 2012

An isolated stomach preparation from immature rats is described. The lumen of the stomach was perfused and the hydrogen ion activity of the perfusate recorded continuously.
The preparation gave dose‐dependent responses to gastrin, acetylcholine and dibutyryl cyclic adenosine 3′,5′‐monophosphate and these responses were readily reversed on washing out the agonist.
The acid secretory response to gastrin was inhibited by metiamide at concentrations of 10−5 M and 3 × 10−5 m.
The acid secretory responses to acetylcholine and dibutyryl cyclic adenosine 3′,5′‐monophosphate were not inhibited by concentrations of metiamide up to 10−3 m.
These findings are discussed in relation to the role of histamine in the control of gastric acid secretion.
CARDIOVASCULAR EFFECTS OF DOPAMINE AFTER CENTRAL ADMINISTRATION INTO CONSCIOUS CATS
Authors: DAY M.D. , ROACH A.G. 
Published: July 2012

Dopamine (30 and 45 μg) administered intracerebroventricularly (i.c.v.) to a group of 10 conscious normotensive cats caused dose‐related increases in blood pressure and heart rate. In 4 of these animals the initial cardiovascular stimulant effects of i.c.v. dopamine were followed by hypotension and bradycardia.
α‐Methyldopamine (30 and 45 μg i.c.v.) produced qualitatively similar responses to dopamine except that the cardiovascular stimulant effects were smaller and the secondary depressant effects somewhat more prolonged.
Both stimulant and depressant effects of i.c.v. dopamine and α‐methyldopamine were greatly inhibited by autonomic ganglion blockade or by adrenergic neurone blockade.
The cardiovascular stimulant effects of both i.c.v. dopamine and i.c.v. α‐methyldopamine were selectively inhibited by β‐adrenoceptor blocking agents whilst the cardiovascular depressant effects of these substances were abolished by the α‐adrenoceptor blocker phentolamine or by the dopamine‐β‐hydroxylase inhibitor disulfiram.
Haloperidol by either i.c.v. or the intravenous route abolished both cardiovascular stimulant and depressant effects of i.c.v. dopamine, whilst pimozide by either route inhibited only the cardiovascular stimulant effects.
In 2 cats, injection of dopamine into the cisterna magna produced predominantly depressant effects on the cardiovascular system except with a higher dose which induced biphasic responses.
INHIBITION BY AMILORIDE OF SODIUM‐DEPENDENT FLUID REABSORPTION IN THE RAT ISOLATED CAUDAL EPIDIDYMIS
Authors: WONG P.Y.D. , YEUNG C.H. 
Published: July 2012

The rate of fluid reabsorption was studied in the rat isolated caudal epididymal sac in vitro.
Part of the fluid reabsorption was found to be dependent on intraluminal Na+. Amiloride (0.1 mm) completely inhibited this component of fluid reabsorption.
The log dose‐inhibition curve to amiloride was sigmoid and the IC50 value was found to be 1.6 μm.
THE EFFECT OF A NEW ANTI‐INFLAMMATORY DRUG, FLURBIPROFEN, ON THE RESPIRATORY, HAEMODYNAMIC AND METABOLIC RESPONSES TO E. coli ENDOTOXIN SHOCK IN THE CAT
Authors: PARRATT J.R. , STURGESS R.M. 
Published: July 2012

The intravenous administration of E. coli endotoxin (2.0 mg/kg) in cats anaesthetized with sodium pentobarbitone resulted in immediate pulmonary hypertension and reductions in lung compliance and systemic arterial Po2. These effects were abolished, or greatly reduced, by the prior intravenous administration of flurbiprofen in doses (100 and 250 μg/kg and 1.0 mg/kg) which were devoid of cardiovascular or metabolic effects. Flurbiprofen is thus the most active antipyretic‐analgesic drug so far examined in this experimental model.
Production of lactate, characteristic of the severe, secondary endotoxin shock phase, was delayed only by the highest dose of flurbiprofen; hypotension, hypoglycaemia and the reduction in cardiac output which occurs during this phase, were unaffected.
These findings are discussed with reference to the treatment of the ‘shocked lung’ syndrome of human septicaemia.