bluuebunny/crossref_metadata_2025_split huggingface dataset:
DRUG‐INDUCED CHANGES IN CAPILLARY FILTRATION COEFFICIENT AND BLOOD FLOW IN THE INNERVATED SMALL INTESTINE OF THE ANAESTHETIZED CAT
Authors: RICHARDSON P.D.I. 
Published: July 2012

A modification of the Folkow Technique for simultaneous measurement of blood flow and capillary filtration coefficient (CFC) in the cat jejunum is described. The modification retained the sympathetic innervation of the preparation, and in the present experiments, drugs were administered intravenously.
There is evidence that CFC is a cardiovascular quantity independent of blood flow or regional vascular resistance in these preparations. Low doses of drugs may affect CFC without altering the blood pressure, blood flow, or heart rate.
Under control conditions the CFC, a measure of functional exchange vessel area, was lower than previously reported for similar, but denervated preparations.
α‐Adrenoceptor stimulation with phenylephrine (1.0 μg kg−1 min−1, i.v.) caused a fall of 75–85% from control values of CFC with concomitant rises in blood pressure of 0–15% and falls in blood flow of 10–40%. The heart rate rose by 0–15%. Phentolamine (0.5–2.0 mg/kg, i.v.) caused a rise in CFC and a slight fall in vascular resistance, and blocked the effects of phenylephrine on this tissue.
β‐Adrenoceptor stimulation with isoprenaline (0.2 μg kg−1 min−1, i.v.) caused a rise in CFC of 75–110%, a fall in blood pressure of 0–10%, a rise in blood flow of 10–60% and a rise in heart rate of up to 35%. Propranolol caused a transient rise in CFC when injected i.v. in a dose of 0.1 mg/kg, which was adequate to block the effects of isoprenaline.
Angiotensin (25–100 ng kg−1 min−1, i.v.) caused falls in CFC of up to 100% and rises in vascular resistance. Aminophylline (0.2–0.4 mg kg−1 min−1, i.v.) caused rises in CFC of up to 200% with falls in vascular resistance.
Histamine (0.01 to 1.0 μg kg−1 min−1, i.v.) had little effect on vascular resistance, but 10 and 40 μg kg−1 min−1 caused falls in vascular resistance. Doses up to and including 10 μg kg−1 min−1 caused falls in CFC, but the higher doses, or smaller doses after histaminase inhibition caused rises in CFC. α‐Adrenoceptor blockade reversed the fall in CFC caused by small doses of histamine, to a rise. Mepyramine completely blocked the effects of histamine on these preparations.
5‐Hydroxytryptamine (33–100 μg kg−1 min−1, i.v.) caused a rise in vascular resistance and a fall in CFC of up to 85%. These effects were blocked by methysergide (250 μg/kg, i.v.).
Rises in CFC indicate an increase in functional exchange vessel area in the tissue, and falls in CFC a decrease in the area available for vascular exchange. These changes are examined against the possibility of the drugs causing reflex adjustments in sympathetic tone, of systemic deactivation of intravenously administered drugs, and of drug effects on vascular permeability.
THE RELEASE OF LABELLED ACETYLCHOLINE AND CHOLINE FROM CEREBRAL CORTICAL SLICES STIMULATED ELECTRICALLY
Authors: RICHARDSON I.W. , SZERB J.C. 
Published: July 2012

In order to establish the origin of the increased efflux of radioactivity caused by electrical stimulation of cerebral cortical slices which had been incubated with [3H]‐choline, labelled choline and acetylcholine (ACh) collected by superfusion were separated by gold precipitation.
In the presence of physostigmine electrical stimulation (1 Hz, 10 min) increased the release of only [3H]‐ACh which was greatly enhanced by the addition of atropine.
Continuous stimulation in the presence of physostigmine resulted in an evoked release of [3H]‐ACh which declined asymptotically. This evoked release appeared to follow first‐order kinetics with a rate constant which remained stable over the course of prolonged stimulation.
The rate constant for the evoked release of [3H]‐ACh with 1 Hz stimulation was three times greater in the presence of physostigmine and atropine than in the presence of physostigmine alone, while the size of the store from which [3H]‐ACh was released was nearly identical under these two conditions.
In the absence of physostigmine and atropine, stimulation caused the appearance of only [3H]‐choline in the samples.
Reduction of [3H]‐ACh stores before the application of physostigmine resulted in a reduced evoked release of total radioactivity, both in the absence or presence of physostigmine and atropine, and decreased the evoked release of [3H]‐ACh without affecting the release of [3H]‐choline.
Results suggest that electrical stimulation of cortical slices which had been incubated with [3H]‐choline causes the release of only [3H]‐ACh, both in the presence or absence of an anticholinesterase. The evoked increase in the efflux of total radioactivity is therefore a good measure of the release of [3H]‐ACh.
THE EFFECT OF NERVE STIMULATION ON THE AXONAL TRANSPORT OF NORADRENALINE AND DOPAMINE‐β‐HYDROXYLASE
Authors: KEEN P. , McLEAN W.G. 
Published: July 2012

A method for stimulating the lumbar sympathetic outflow from the spinal cord of the rat is described which does not require artificial respiration of the animal.
In some, but not all experiments continuous stimulation at 2 Hz or intermittently at 10 Hz accelerated the rate at which noradrenaline and dopamine‐β‐hydroxylase accumulated central to a ligature on the sciatic nerve by approximately 40%.
It is concluded that, although nervous activity is not necessary for axonal transport of transmitter granules in sympathetic neurones, intense nervous activity may accelerate the rate of granule transport.
THE INNERVATION OF THE RATCERVIX AND ITS PHARMACOLOGY In vitro AND In vivo
Authors: HOLLINGSWORTH M. 
Published: July 2012

Contractions of the rat cervix and uterine horns were measured both in vitro and in vivo as changes in luminal perfusion pressure during perfusion at constant flow.
Spontaneous cervical and uterine horn contractions in vitro were reduced from rats pre‐treated with 17β‐oestradiol compared to those ovariectomized only or those pre‐treated with 17β‐oestradiol plus progesterone.
The rat cervix exhibited similar in vitro sensitivities to methacholine, oxytocin, isoprenaline and phenylephrine as did the uterine horns.
Transmural stimulation produced cervical and uterine horn contractions, which were blocked by hyoscine or tetrodotoxin, suggesting a cholinergic motor innervation. This was supported by histological findings.
In vivo, the injections of propranolol (1.9 × 10−7 mol/kg) or pempidine (3.2 or 6.4 × 10−6 mol/kg) were followed by large cervical and smaller uterine horn contractions, suggesting an adrenergic inhibitory tone mediated by β‐adrenoceptors.
The evidence for a cervical sphincter is discussed.
EFFECTS OF ADRENALINE, NORADRENALINE, ISOPRENALINE AND SALBUTAMOL ON THE PRODUCTION AND RELEASE OF RENIN BY ISOLATED RENAL CORTICAL CELLS OF THE CAT
Authors: JOHNS E.J. , RICHARDS H.K. , SINGER BERTHA 
Published: July 2012

Isolated renal cortical cells of the cat have been demonstrated to produce renin on incubation in vitro. After 2 h of incubation, without added agonist, the total amount of renin in the flask increased by a mean of 27.2%. The increase in renin content of the incubation flask was found to be present in the medium.
Noradrenaline (1.18 × 10−4 M) and adrenaline (1.09 ×; 10‐4 M) added to the incubation medium stimulated renin production by 45 and 34% respectively, compared with the incubated controls. Most of the increase in renin production was present in the incubation medium.
Isoprenaline did not stimulate renin production. However, when added to the incubation medium at a concentration of 0.72 × 10‐4 M there was a significant decrease in the cellular content and a significant increase in the medium content of renin. This increase was at least as great as that observed with adrenaline and noradrenaline.
Salbutamol had an effect similar to isoprenaline, i.e. it induced the release of renin into the medium without affecting production. In this respect it was about a third as potent as isoprenaline.
STIMULATION OF THE HYPOTHALAMO‐PITUITARY‐ADRENAL AXIS BY COMPOUNDS FORMED IN INFLAMED TISSUE
Authors: LEME J. GARCIA , SCHAPOVAL ELFRIDES E.S. 
Published: July 2012

Rat paws were injected with carrageenin, and their subcutaneous tissue perfused 135 min later. These perfusates were injected intravenously into receptor rats in which they caused an attenuation of inflammatory responses.
The effect was not observed in adrenalectomized receptor rats nor in receptors with electrolytic lesions in the median eminence of the hypothalamus but persisted in adrenal‐demedullated animals.
The active perfusates also induced eosinopenia in normal or adrenal‐demedullated animals, but not in adrenalectomized rats, and produced an increase in blood corticosterone with a concomitant decrease in the amounts of adrenal ascorbic acid.
The active perfusates did not affect the responses of isolated preparations to histamine, bradykinin, prostaglandins and 5‐hydroxytryptamine neither did they elicit changes of the arterial blood pressure in receptor animals.
The anti‐inflammatory activity present in perfusates from inflamed paws seems to be formed slowly at the site of the developing inflammatory reaction, since perfusates collected 30‐65 min after the injection of carrageenin were ineffective, as was plasma taken from donor rats at various time intervals after carrageenin injections.
It is suggested that the anti‐inflammatory factor present in the active perfusates exerts its action by stimulation of the hypothalamo‐pituitary‐adrenal axis.
THE POSSIBLE OCCURRENCE OF ENDOGENOUS ANTI‐INFLAMMATORY SUBSTANCES IN THE BLOOD OF INJURED RATS
Authors: ATKINSON D.C. , HICKS R. 
Published: July 2012

Using the carrageenin rat paw oedema test as an assay, an attempt has been made to confirm the presence of anti‐inflammatory activity in the blood of rats with a chronic inflammatory lesion induced by a polyester sponge, and to relate such activity to the systemic anti‐inflammatory effect exerted in situ by the lesion. In addition, plasma from rats given acetic acid intraperitoneally has been examined for anti‐inflammatory properties.
The activity of serum obtained from sponge‐bearing adrenalectomized Wistar rats did not differ significantly from that obtained from animals without implants. Furthermore, implanted sponges exerted no systemic anti‐inflammatory effect.
Similar experiments were performed in sponge‐bearing adrenalectomized Sprague‐Dawley rats, plasma instead of serum being examined for anti‐inflammatory activity. The plasma removed from such animals possessed no anti‐inflammatory activity, whilst implanted sponges exerted a small, yet significant, systemic inhibitory effect.
When the irritancy of sponge implants was augmented with croton oil, more marked systemic anti‐inflammatory effects were observed. However, the plasma obtained from rats injured in this manner exerted no anti‐inflammatory effect.
No anti‐inflammatory activity could be detected in plasma samples obtained from rats treated with doses of acetic acid capable of producing pronounced systemic anti‐inflammatory effects.
It was concluded that the induction of these inflammatory lesions in rats does not appear to lead to a detectable release of endogenous anti‐inflammatory substances into the circulation.
USE OF THE LOGISTIC FUNCTION FOR THE CALCULATION OF DOSE‐RATIOS AND POTENCY RATIOS
Authors: BARLOW R.B. 
Published: July 2012

Dose‐ratios and potency ratios, obtained with the guinea‐pig isolated ileum by calculating matching concentrations from a least‐squares fit using a logistic relationship between response and dose, differ from those obtained with the more usual assumption that response is a linear function of log dose over a limited range.
The differences are not due to the mathematical treatment of the results but arise from changes in sensitivity associated with the production of very high or very low responses.
With this preparation there is no advantage in avoiding the linear transformation and fitting the results to the complete dose‐response curve though this might not apply to results obtained from other tissues with less variable sensitivity.
THE ESTIMATION OF 3,4‐DIHYDROXYPHENYLACETIC ACID, HOMOVANILLIC ACID AND HOMO‐lSOVANILLIC ACID IN NERVOUS TISSUE BY GAS‐LIQUID CHROMATOGRAPHY AND ELECTRON CAPTURE DETECTION
Authors: PEARSON J.D.M. , SHARMAN D.F. 
Published: July 2012

A gas chromatographic method using electron capture detection is described for the estimation of three acidic metabolites of dopamine, 4‐hydroxy‐3‐methoxyphenylacetic acid (homovanillic acid, HVA), 3,4‐dihydroxyphenylacetic acid (DOPAC) and 3‐hydroxy‐4‐methoxyphenylacetic acid (homo‐isovanillic acid, iso‐HVA). The method is based on the formation of the trifluoroacetyl‐hexafluoroisopropyl derivatives of the three acids.
The method has been applied to the estimation of DOPAC, HVA and iso‐HVA in tissues from the central and peripheral nervous systems.
VASOPRESSIN RELEASE BY NICOTINE: THE SITE OF ACTION
Authors: BISSET G.W. , FELDBERG W. , GUERTZENSTEIN P.G. , SILVA M. ROCHA E. 
Published: July 2012

In cats anaesthetized with chloralose the release of neurohypophysial hormones was examined after injection of nicotine into the cerebral ventricles or cisterna magna or its topical application through perspex rings to the ventral surface of the brain stem. The release was measured by assaying the hormones in samples of venous blood
Injected into a lateral or the third cerebral ventricle, nicotine (0.5 to 1 mg) produced release of vasopressin without oxytocin. When the aqueduct was cannulated, preventing access to the fourth ventricle and to the subarachnoid space, this release did not occur.
Vasopressin was also released without oxytocin when nicotine (0.25 to 2 mg) was injected into the subarachnoid space through the cisterna magna. With this route of administration the nicotine did not enter any part of the ventricular system.
Applied through paired perspex rings placed across the ventral surface of the brain stem, nicotine again produced release of vasopressin without oxytocin. The amount of nicotine placed in each ring was usually 80 μg, but a release was obtained with 10 μg and in one experiment with as little as 5 μg.
The bilateral region on the ventral surface of the brain stem where nicotine acts when producing release of vasopressin lies lateral to the pyramids and in a longitudinal direction, 6 to 9 mm caudal to the trapezoid bodies.
The vasopressin release by nicotine injected intraventricularly or intracisternally, or applied topically to the ventral surface of the brain stem was not due to absorption of nicotine into the blood stream, nor to blood pressure effects.
It is concluded that nicotine acts on the ventral surface of the brain stem probably by activating the central projection to the supra‐optic and possibly also the paraventricular nuclei of afferent pathways in the sinus and vagus nerves which control the release of vasopressin in response to changes in blood volume or distribution.
THE EFFECTS OF LYSERGIC ACID DIETHYLAMIDE ON THE RESPONSE TO FIELD STIMULATION OF THE RAT VAS DEFERENS AND THE RAT AND CAT ANOCOCCYGEUS MUSCLES
Authors: GILLESPIE J.S. , McGRATH J.C. 
Published: July 2012

The effect of lysergic acid diethylamide (LSD) on the response to field stimulation in vitro of the rat vas deferens and anococcygeus muscle was examined.
LSD in concentrations from 10−9 to 10−6 M caused an increase in tone or rhythmic activity in both tissues, effects identical to those produced by guanethidine or tyramine. The motor effects of all three drugs were abolished by phentolamine 2 × 10−6 M. Methysergide 2 × 10−7 M given before LSD reduced the motor effect but was ineffective once the LSD contraction had developed.
LSD 10−9 to 10−6 M reduced and eventually abolished the response to motor adrenergic nerve stimulation in the anococcygeus muscle with no effect on the response to noradrenaline (NA) and no evidence of differential sensitivity according to the number of stimulating pulses. In the vas deferens LSD abolished the initial twitch component with no effect on the secondary slow contraction. LSD had no effect on the response to inhibitory nerve stimulation in the anococcygeus.
These results suggest that in the anococcygeus LSD closely resembles guanethidine in its effects as an adrenergic neurone blocking drug with indirect sympathomimetic actions. In the vas deferens these properties would explain the block of the initial twitch component in the motor response to field stimulation and the increase in rhythmic activity but do not explain the resistance of the secondary slow component of the motor response.
REDUCTION OF ANTIGEN‐INDUCED CONTRACTION OF SENSITIZED HUMAN BRONCHUS in vitro BY INDOMETHACIN
Authors: DUNLOP LYN S. , SMITH A.P. 
Published: July 2012

Contraction of passively sensitized human bronchus induced by antigen challenge in vitro, was reduced by the prostaglandin F2α synthetase inhibitor, indomethacin.
Prostaglandin F2α was released during challenge and this release was inhibited by indomethacin.
There was a significant correlation between prostaglandin F2α release and antigen challenge‐induced contraction, suggesting that this substance may contribute to the bronchoconstrictor response of sensitized human bronchus to antigen.
THE ROLE OF H1 AND H2‐RECEPTORS IN THE CORONARY VASCULAR RESPONSE TO HISTAMINE OF ISOLATED PERFUSED HEARTS OF GUINEA‐PIGS AND RABBITS
Authors: BROADLEY K.J. 
Published: July 2012

The effects of histamine on the isolated perfused hearts of guinea‐pigs and rabbits were examined. Records of contractile force, heart rate and coronary perfusion pressure were obtained.
Histamine exerted positive inotropic and chronotropic effects which were antagonized by burimamide and attributed to stimulation of H2‐receptors.
The coronary vascular response to histamine differed between guinea‐pigs and rabbits. In guinea‐pig hearts, three phases were apparent: (a) An initial vasodilatation preceding any effects on heart force and rate was antagonized by mepyramine and therefore mediated by histamine H1‐receptors in the coronary circulation. (b) A secondary vasoconstriction was attributed to the increased myocardial compression during the positive inotropic and chronotropic responses. (c) The final, more predominant, component was a prolonged vasodilatation probably associated with the increased metabolic activity of the heart.
The latter two components were abolished together with the myocardial responses by burimamide. The remaining coronary vascular response was biphasic, consisting of a vasodilatation immediately followed by vasoconstriction. Both were antagonized by mepyramine and therefore mediated by H1‐receptors.
The coronary vascular response of rabbit hearts was similar but no direct vasodilatation was observed and it was concluded that histamine receptors in the coronary vasculature involve only vasoconstriction.
DOPAMINE‐INDUCED AMYLASE SECRETION FROM GUINEA‐PIG SUBMANDIBULAR GLAND
Authors: BLOOM G.D. , CARLSÖÖ B. , DANIELSSON Å. 
Published: July 2012

The effects of dopamine, 5‐hydroxydopamine (5‐OHDA) and noradrenaline on amylase secretion from the guinea‐pig submandibular gland were investigated under in vitro conditions.
All three amines greatly enhanced amylase secretion. Blockade of dopamine β‐hydroxylase did not inhibit the response to dopamine.
Noradrenaline and dopamine stimulated amylase release from salivary glands of reserpine‐treated animals, whereas 5‐OHDA had no stimulatory effect on secretion in guinea‐pigs pretreated with reserpine.
Haloperidol completely inhibited dopamine‐induced enzyme discharge, but did not affect noradrenaline‐initiated secretion.
Apomorphine caused a slight enzyme release by itself; it diminished the dopamine secretory effect, but did not modify that of noradrenaline.
Pimozide and fluspirilene attenuated the dopamine‐induced enzyme discharge, but compared with haloperidol they were less effective.
It is concluded that dopamine exerts a secretagogic action different from that of noradrenaline. The possible presence of a specific dopamine receptor in salivary glands is discussed.
A QUANTITATIVE MICROIONTOPHORETIC ANALYSIS OF THE RESPONSES OF CENTRAL NEURONES TO NORADRENALINE: INTERACTIONS WITH COBALT, MANGANESE, VERAPAMIL AND DICHLOROISOPRENALINE
Authors: FREEDMAN R. , HOFFER B.J. , WOODWARD D.J. 
Published: July 2012

A new experimental procedure has been devised for the study of pharmacological antagonism in the central nervous system using automated microiontophoresis to deliver pulses of agonists and computer‐generated histograms to quantify the neuronal response. The system allows study of potential antagonists having direct depressant effects and also of neurones with irregular or slow discharge rates.
The histogram analysis reveals the necessity for regular, periodic delivery of agonists during the assessment of agonist‐antagonist interactions. Without regular repetitive delivery, many agonists, such as noradrenaline, exhibit an apparent but artifactual decrease in inhibitory potency after an interruption of agonist pulses. Examples of this phenomenon are shown, using cerebellar Punkinje cells and cerebral cortical neurones in rats anaesthetized with halothane.
Preliminary results with these computer‐generated drug response histograms revealed manganese, cobalt, and verapamil to be generally ineffective as antagonists of noradrenaline, despite their direct depressant effects.
Conversely, dichloroisoprenaline (DCI), a β‐adrenoceptor antagonist, was effective in blocking noradrenaline‐induced depressions of firing in the cerebral cortex at doses which caused over 50% decrease in spontaneous discharge.
SOME PHARMACOLOGICAL EFFECTS OF p‐CHLOROPHENYLALANINE UNRELATED TO TRYPTOPHAN HYDROXYLASE INHIBITION
Authors: MARLEY E. , WHELAN JENNIFER E. 
Published: July 2012

Experiments were performed on a variety of tissues from different species to establish whether or not the properties of p‐chlorophenylalanine methyl ester (PCPA) included a 5‐hydroxytryptamine (5‐HT)‐like action which might explain the soporific action of PCPA in chicks.
PCPA, like 5‐HT, contracted the rat fundal preparation (as did PCPA base), and in cats enhanced twitch tension of a lower limb flexor reflex, evoked adrenal medullary secretion and attenuated histamine‐induced gastric secretion; the effects on the rat fundal strip and the adrenal medulla were prevented by methysergide.
Like 5‐HT, PCPA elicited bronchoconstriction of guinea‐pig lungs, isolated or in vivo; this was not prevented by methysergide but reduced by polyphloretin and by indomethacin. Perfusate collected from the lungs during PCPA‐induced bronchoconstriction and applied to superfused isolated tissues contained a substance with prostaglandin‐like activity.
In contrast, the effect of PCPA on the guinea‐pig isolated ileum differed from that of 5‐HT, since it relaxed the ileum when contracted by transmural excitation, by acetylcholine, histamine or 5‐HT and contracted the ileum on wash‐out.