bluuebunny/crossref_metadata_2025_split huggingface dataset:
COMPARATIVE EFFECTS OF HYPOPHYSECTOMY AND ADRENALECTOMY UPON PLASMA AND ADRENAL MONOAMINES IN PREGNANT AND NON‐PREGNANT RATS
Authors: ISMAHAN G. , PARVEZ H. , PARVEZ S. , YOUDIM M.B.H. 
Published: July 2012

1 The influence of hypophysectomy and adrenalectomy upon release and storage of adrenaline and noradrenaline during rat oestrous cycle and pregnancy has been studied.2 Hypophysectomy during the pro‐oestrous phase of the oestrous cycle increased plasma noradrenaline concentration which was unchanged, however, by similar treatment in pregnant females. After adrenalectomy during dioestrous and pro‐oestrous phases, as well as on day 15 post‐coitum, plasma noradrenaline showed an increase, although the increase in pregnant females was greater.3 Adrenocorticotrophic hormone (ACTH) administration to non‐pregnant and pregnant females increased plasma adrenaline values significantly, compared with control values. Treatment of adrenalectomized rats with hydrocortisone lowered plasma noradrenaline to control values in both non‐pregnant and pregnant females.4 Hypophysectomy produced a decrease in plasma adrenaline content, whilst ACTH treatment increased it. Plasma adrenaline disappeared completely after adrenalectomy, during the pro‐oestrous phase and pregnancy, but extirpation of adrenals during the dioestrous phase still left appreciable amounts of adrenaline in plasma. Hydrocortisone treatment of both non‐pregnant and pregnant adrenalectomized females resulted in the reappearance of plasma adrenaline5 Adrenal stores of adrenaline and noradrenaline declined after hypophysectomy but the decreases were greater in pregnant females.6 Compensatory administration of ACTH to hypophysectomized females increased adrenaline and noradrenaline content of adrenals to control non‐pregnant female values during the pro‐oestrous phase of the oestrous cycle but similar treatment in pregnant females resulted in an increase in adrenaline.7 Although ACTH administration increased adrenal noradrenaline levels in pregnant hypophysectomized females, the mean value remained below that of non‐operated pregnant females.8 The results suggest that, during oestrous cycle and pregnancy the effects of pituitary and adrenal hormonal deficiency upon storage and release of monoamines differ quantitatively.
ANORECTIC ACTIVITY OF PROSTAGLANDIN PRECURSORS
Authors: DOGGETT N.S. , JAWAHARLAL K. 
Published: July 2012

1 Intraperitoneal and intragastric (i.g.) administration of prostaglandin precursors arachidonic (2 mg, 15 mg/kg, i.p.; 30 mg/kg, i.g.), linolenic (100 mg/kg, i.p.; 200 mg/kg, i.g.) and linoleic (15, 100 mg/kg, i.p.; 100 mg/kg, i.g.) acids to 22 h food‐deprived rats inhibits food intake.2 This anorexia is similar to that induced by prostaglandin F2α (1 mg/kg, i.p.).3 At anorectic doses these fatty acids do not cause pyrexia, in fact arachidonic acid causes hypothermia.4 Prior treatment with indomethacin (15 mg/kg) and paracetamol (50 mg/kg) specifically reverses the anorexia and the behavioural satiety induced by the three fatty acids, while not affecting prostaglandin F2α‐induced suppression of food intake.5 Results of the present experiments suggest that both physiological and pharmacological modification of appetite could be brought about through an effect on prostaglandin generating systems.
C‐FRAGMENT OF LIPOTROPIN—AN ENDOGENOUS POTENT ANALGESIC PEPTIDE
Authors: FELDBERG W. , SMYTH D.G. 
Published: July 2012

1 A series of peptides derived from porcine lipotropin was examined for analgesic and other morphine‐like properties on infusion into the cannulated third ventricle of cats.2 Lipotropin (LPH 1‐91) itself produced no analgesia or other morphine‐like effects when infused in a dose of 150 μg.3 C‐fragment (LPH 61‐91) produced strong long‐lasting analgesia when infused in a dose of 10 or 20 μg; on a molar basis the potency was between 90 and 180 times that of morphine. The following morphine‐like effects were also produced: shivering leading to fever, vasodilatation of the pinnae, mydriasis, opening of the palpebral fissures, tachypnoea with bouts of panting, vocalization, hyperexcitability, restlessness and catalepsy. All the effects, including analgesia, were abolished by an intraperitoneal injection of naloxone (1 mg/kg).4 Hyperglycaemia, another central effect produced by morphine, was obtained with C‐fragment infused in a dose of 60 μg.5 On intravenous injection, C‐fragment produced analgesia with a dose of about 200 μg/kg. Administered by this route, C‐fragment was again more potent than morphine.6 C'‐fragment (LPH 61‐87), LPH 61‐78 and LPH 61‐69, either had no analgesic effect or produced weak short‐lasting analgesia when infused in doses up to 100 μg.7 Methionine enkephalin (LPH 61‐65) either produced very weak short‐lasting analgesia or had no analgesic effect when infused in doses of between 30 and 400 μg.8 N‐methyl methionine enkephalin amide in which both termini of methionine enkephalin were protected against degradation by exopeptidases produced long‐lasting analgesia when infused in doses of 150 to 180 μg; its analgesic potency was approximately 100 times less than that of C‐fragment. Blocking only one terminus of methionine enkephalin did not appear to endow the peptide with analgesic properties. The N‐methyl pentapeptide amide produced other morphine‐like effects of which the most striking was catalepsy. All the effects were abolished by intraperitoneal naloxone (1 mg/kg).
MECHANISMS UNDERLYING GASTRIC MUCOSAL DAMAGE INDUCED BY INDOMETHACIN AND BILE‐SALTS, AND THE ACTIONS OF PROSTAGLANDINS
Authors: WHITTLE B.J.R. 
Published: July 2012

1 The mechanisms by which the bile salt, sodium taurocholate, potentiates the formation of gastric mucosal erosions induced by indomethacin has been investigated in the rat.2 Systemic administration of indomethacin lowered resting mucosal blood flow but had no effect on the acid back‐diffusion across the mucosa.3 Gastric perfusion of taurocholate in acid solution increased acid back‐diffusion and lowered the potential difference. This was accompanied by an increase in mucosal blood flow, which may represent a protective mechanism in the mucosa.4 Administration of indomethacin during acid‐taurocholate perfusion reduced this elevated mucosal blood flow without any further change in acid back‐diffusion.5 The results suggest that although a decrease in mucosal blood flow or an increase in acid back‐diffusion can lead to a low incidence of erosions, a combination of both produces extensive mucosal damage.6 The (15S)‐methyl analogue of prostaglandin E2 reduced erosion formation induced by indomethacin and acid‐taurocholate administration.7 It is suggested that this protective action of the prostaglandin analogue may be linked to changes in gastric mucosal permeability and in mucosal blood flow.
FLUVOXAMINE, A SPECIFIC 5‐HYDROXYTRYPTAMINE UPTAKE INHIBITOR
Authors: CLAASSEN V. , DAVIES J.E. , HERTTING G. , PLACHETA P. 
Published: July 2012

1On the basis of both in vitro and in vivo experiments fluvoxamine has been characterized as a potential anti‐depressant drug with almost exclusively 5‐hydroxytryptamine (5‐HT) uptake inhibiting properties.2 Fluvoxamine is effective in inhibiting 5‐HT uptake by blood platelets and brain synaptosomes. Due to inhibition of the membrane pump the compound prevents 5‐HT depletion by the tyramine‐derivatives H 75/12 and H 77/77. As a result of the interference with the neuronal re‐uptake mechanism for 5‐HT, fluvoxamine produces a decreased 5‐HT turnover in the brain. Effects of 5‐hydroxytryptophan (5‐HTP) are potentiated in mice and in combination with pargyline, fluvoxamine induces 5‐HT‐like behavioural effects.3 In contrast to tricyclic antidepressants, noradrenaline uptake processes are either unaffected or only slightly inhibited by fluvoxamine. The noradrenaline depleting effects of tyramine derivatives are not influenced by fluvoxamine. Reserpine effects, such as ptosis are affected only at very high doses of the test compound. The antagonism by fluvoxamine of the reserpine‐induced lowering of the pentamethylenetetrazole convulsive threshold can be regarded as due to an effect upon 5‐HT uptake. In contrast to the effects of desmethylimipramine and imipramine, no stimulatory effects are found in rats when rapidly acting reserpine‐like compounds are given following a dose of fluvoxamine.
TAMOXIFEN INHIBITION OF AN in vitro OESTRADIOL‐INDUCED SURFACE COAT CHANGE ON MOUSE BLASTOCYSTS
Authors: BLOXHAM P.A. , PUGH D.M. 
Published: July 2012

1 Eighty‐nine hour post‐coitus mouse blastocysts cultured in the presence of oestradiol‐17β underwent a histochemically detectable surface coat change.2 Tamoxifen was found to inhibit this in vitro ‐induced change. The role of Tamoxifen as an inhibitor of implantation is discussed.
THE ANIMAL PHARMACOLOGY OF BUPRENORPHINE, AN ORIPAVINE ANALGESIC AGENT
Authors: COWAN A. , DOXEY J.C. , HARRY E.J.R. 
Published: July 2012

1 The general pharmacology of buprenorphine, a potent analgesic agent derived from oripavine, is described.2 After acute administration of buprenorphine, the spontaneous locomotor activity of mice was increased; rats displayed stereotyped licking and biting movements; behavioural depresssion was marked in guinea‐pigs but mild in rhesus monkeys. The behaviour of cats was unchanged.3 In general, buprenorphine reduced heart rate but had no significant effect on arterial blood pressure in conscious rats and dogs.4 In anaesthetized, open‐chest cats buprenorphine (0.10 and 1.0 mg/kg, i.v.) caused no major haemodynamic changes.5 Buprenorphine (0.01‐10 mg/kg, i.a.) and morphine (0.30‐30 mg/kg, i.a.) increased arterial Pco2 values and reduced Po2 values in conscious rats. With doses of buprenorphine greater than 0.10 mg/kg (a) the duration of respiratory depression became less, (b) ceiling effects occurred such that the maximum effects produced were less than those obtained with morphine.6 Buprenorphine was a potent and long‐lasting antagonist of citric acid‐induced coughing in guinea‐pigs.7 At a dose level 20 times greater than the ED50 for antinociception (tail pressure), morphine suppressed urine output to a greater extent than the corresponding dose of buprenorphine in rats.8 Over the range 0.01‐1.0 mg/kg (s.c.), buprenorphine slowed the passage of a charcoal meal along the gastrointestinal tract in rats. After doses in excess of 1 mg/kg, the meal travelled increasingly further such that the distances measured after 10 and 30 mg/kg did not differ significantly from control values. In contrast, the morphine dose‐response relationship was linear.
LIGATED RENAL PEDICLES AND DURATION OF ACTION OF NEOSTIGMINE AND PYRIDOSTIGMINE
Authors: MILLER R.D. , RODERICK LAURA 
Published: July 2012

1 The duration of neostigmine or pyridostigmine antagonism of a (+)‐tubocurarine (Tc) neuromuscular blockade was determined in the cat anterior tibialis‐peroneal nerve preparation with and without ligated renal pedicles.2 The infusion rate of Tc required to maintain a 90% depression of twitch tension was reduced from 8.8 ± 1.4 (s.e.) to 3.4 ± 0.6 μg kg−1 min−1 by renal pedicle ligation.3 Renal pedicle ligation resulted in an increased duration of antagonism of Tc by both neostigmine and pyridostigmine.
EFFECTS OF Δ9‐TETRAHYDROCANNABINOL ON THE RATES OF OXYGEN CONSUMPTION OF MICE
Authors: PERTWEE R.G. , TAVENDALE R. 
Published: July 2012

1 Experiments with untreated mice confirmed that at ambient temperatures below 30°C, the oxygen consumption rate of mice normally kept at about 23°C varies inversely with ambient temperature.2 At given ambient temperatures in the range 20 to 31°C the oxygen consumption rate was 32 to 43% greater for restrained than for unrestrained mice.3 Hypothermia induced in restrained mice by Δ9‐tetrahydrocannabinol (Δ9‐THC) (1.0 to 4.0 mg/kg i.v.) was accompanied by marked falls in the rate of oxygen consumption. The size of these falls parallelled the degree of hypothermia and increased both with increases in dose and with decreases in the ambient temperature. The oxygen consumption rates of unrestrained mice were also lowered by hypothermic doses (10 to 40 mg/kg i.p.) of Δ9‐THC.4 The maximum falls in oxygen consumption rate occurred at earlier times after drug administration than the maximum falls in rectal temperature.5 At none of the ambient temperatures studied did the oxygen consumption rates of Δ9‐THC‐treated mice fall significantly below the basal levels (59 ± 3 ml 25 g−1 h−1) of unrestrained, resting mice at 30°C.6 The hypothesis that reduced rates of heat production contribute significantly towards the hypothermia induced by Δ9‐THC in our experiments is discussed. The possibility that biological processes responsible for increased heat production in response to cold are more sensitive to Δ9‐THC than those processes governing basal rates of heat production at thermally neutral environmental temperature is also raised.
THE EFFECTS OF ETHER STRESS AND BETAMETHASONE TREATMENT ON THE CONCENTRATIONS OF NORADRENALINE AND DOPAMINE IN VARIOUS REGIONS OF THE RAT BRAIN
Authors: VELLUCCI SANDRA V. 
Published: July 2012

1 The effects of ether stress on noradrenaline (NA) and dopamine levels in different regions of the rat brain were studied.2 Exposure to ether vapour (90 s) caused a significant decrease in the concentration of hypothalamic NA but had no effect on catecholamine (CA) concentrations in the other regions studied.3 Treatment with betamethasone alone (20 μg/ml) given in the drinking water for 24 h, had no effect on CA levels in the cerebral cortex, midbrain or hypothalamus. However, pretreatment with this dose of steroid prevented the decreases in hypothalamic NA which were normally seen after ether stress and also induced significant increases in the concentration of midbrain NA.4 The data provide further support for the involvement of NA in the regulation of stress‐induced corticotropin (ACTH) release and indicate that centres other than the hypothalamus may be involved in mediating the inhibitory action of betamethasone on the response to ether stress.
CARDIOVASCULAR EFFECTS OF Δ9‐TETRAHYDROCANNABINOL IN CONSCIOUS AND ANAESTHETIZED DOGS
Authors: FRIEDMAN E. , GERSHON S. , HINE B. , TORRELIO MARINA , MOSS IMMANUELA RAVE 
Published: July 2012

Temporal effects of Δ9‐tetrahydrocannabinol (THC) on heart rate and blood pressure in conscious dogs were compared to those in anaesthetized dogs.
In conscious dogs, THC in doses of 0.25 and 0.1 mg/kg resulted in maximal heart rate reductions of 48 and 41%, respectively, and in no significant change in blood pressure.
In anaesthetized animals THC in doses of 0.5 and 0.25 mg/kg caused a peak reduction in heart rate of 38 and 34%, and of blood pressure of 24 and 8%, respectively.
The results demonstrate that the bradycardia in response to THC in dogs is independent of the concomitant anaesthesia.
We conclude that the discrepancy between heart rate response to THC in dogs and in man is due to a species difference.
PROFILE OF β‐ADRENOCEPTORS IN FEMORAL, SUPERIOR MESENTERIC AND RENAL VASCULAR BEDS OF DOGS
Authors: TAIRA N. , YABUUCHI Y. , YAMASHITA S. 
Published: July 2012

The homogeneity of β‐adrenoceptors in femoral, superior mesenteric and renal vascular beds was investigated by the use of the regional perfusion technique in dogs.
Isoprenaline and salbutamol produced dose‐related increases in femoral and superior mesenteric blood flow. The dose‐response curves for the two agonists were parallel, but salbutamol was approximately 1/15 as potent as isoprenaline on a weight basis.
Isoprenaline and salbutamol increased renal blood flow in a dose‐related manner. However, salbutamol was approximately 1/240 as potent as isoprenaline on a weight basis, and the slope of the dose‐response curve for salbutamol was less steep than that for isoprenaline.
The dose‐response curves to isoprenaline for increase in femoral and superior mesenteric blood flow were shifted to the right by intravenous pindolol but not by intravenous or intra‐arterial practolol.
The dose‐response curves to isoprenaline for increase in renal bood flow were shifted to the right more markedly by intravenous pindolol than by intravenous or intra‐arterial practolol.
The results indicate that β‐adrenoceptors of the renal vascular bed consist of β1‐type and β2‐type whereas the femoral and superior mesenteric vascular beds contain only β2‐adrenoceptors.
EFFECTS OF Δ9‐TETRAHYDROCANNABINOL AND CANNABIDIOL ON A Mg2+‐ATPase OF SYNAPTIC VESICLES PREPARED FROM RAT CEREBRAL CORTEX
Authors: GILBERT J.C. , PERTWEE R.G. , WYLLIE M.G. 
Published: July 2012

Δ9‐Tetrahydrocannabinol and cannabidiol both exhibited a concentration‐related inhibition of Mg2+‐ATPase of vesicles prepared from synaptosomes isolated from rat cerebral cortex. Cannabidiol was about 3 times more potent than tetrahydrocannabinol.
These results were similar to those obtained previously using drugs with well established anticonvulsant activity.
Tetrahydrocannabinol at a sub‐inhibitory concentration (1 μM) increased the activity of the Mg2+‐ATPase relative to values obtained with vehicle controls.
THE EFFECTS OF LABETALOL (AH 5158) ON ADRENERGIC TRANSMISSION IN THE CAT SPLEEN
Authors: BLAKELEY A.G.H. , SUMMERS R.J. 
Published: July 2012

The competitive α‐ and β‐adrenoceptor blocking agent labetalol, in concentrations up to 10−4 M, produced dose‐dependent increases in transmitter overflow from the isolated blood perfused spleen of the cat following nerve stimulation at 10 and 30 Hz.
At concentrations above 10−4 M labetalol produced a pronounced decrease in transmitter overflow.
Labetalol (1.5 × 10−4M) increased the recovery of 3H label in the venous blood following the close‐arterial infusion of [3H]‐(‐)‐noradrenaline indicating that the drug inhibits uptake of the amine.
Both labetalol (3.8 × 10−5 M) and piperoxan (7.4 × 10−6 M) produced parallel shifts to the right of the dose‐response curves to noradrenaline and oxymetazoline in isolated strips of cat splenic capsule. In this preparation both drugs acted as competitive postsynaptic α‐adrenoceptor blocking agents.
Labetalol (3.3 × 10−5M) increased the transmitter overflow following stimulation of the splenic nerves with 200 impulses at 10 Hz. The overflow could be further increased by subsequent addition of piperoxan (7.2 × 10−6M). Piperoxan (5.7 × 10−6M) alone produced a marked increase in transmitter overflow which could be further increased by subsequent addition of desmethylimipramine (DMI; 3.2 × 10−5M). Cocaine (1.5 × 10−5M) or DMI (5.4 × 10−5M) produced a small increase in transmitter overflow which was not further increased by addition of labetalol (2.8 × 10−5 M).
Labetalol produced a biphasic effect on the responses of the isolated blood perfused spleen of the cat to nerve stimulation. With low doses (up to 10−4M) vascular responses were potentiated and with high doses (greater than 10−4M) inhibited. The potentiation was related to uptake blockade and the inhibition to decreased transmitter overflow and postsynaptic α‐adrenoceptor blockade.
Labetalol appears to act as a postsynaptic α‐adrenoceptor antagonist in the isolated blood perfused spleen of the cat with little effect on presynaptic α‐adrenoceptors. The moderate elevation of transmitter overflow by the drug is related to the inhibitory effect of the drug on neuronal uptake rather than on presynaptic α‐adrenoceptors.
TISSUE BLOOD FLOW AND DISTRIBUTION OF CARDIAC OUTPUT IN CATS: CHANGES CAUSED BY INTRAVENOUS INFUSIONS OF HISTAMINE AND HISTAMINE RECEPTOR AGONISTS
Authors: JOHNSTON BARBARA M. , OWEN D.A.A. 
Published: July 2012

The effects of infusions of histamine on blood pressure, cardiac output, heart rate, total peripheral resistance, stroke volume and tissue blood flow have been determined in anaesthetized cats using radio‐active microspheres to measure cardiac output and tissue blood flow.
Histamine caused dose‐dependent falls in blood pressure and total peripheral resistance over the dose‐range 1 × 10−8 to 3.3 × 10−7 mol kg−1 min−1. Histamine had no effect on cardiac output, heart rate or stroke volume.
Histamine caused vasodilatation in the heart and stomach, with increased blood flow through these organs, and in the small and large intestine where blood flow was maintained despite the falls in arterial blood pressure. Blood flow to the brain, kidneys, liver, adrenal glands, skeletal muscle, spleen and skin was reduced when arterial blood pressure fell. Vascular resistance increased in the skin and spleen, presumably due to reflex vasoconstriction when blood pressure fell.
The selective H1‐receptor agonist 2‐(2‐aminoethyl)pyridine lowered blood pressure and decreased total peripheral resistance but did not change cardiac output, heart rate or stroke volume. 2‐(2‐Aminoethyl)pyridine caused vasodilatation in the heart, small and large intestine and kidneys. Vascular resistance was increased in the spleen and skin.
The selective H2‐receptor agonist 4‐methylhistamine also lowered blood pressure and decreased total peripheral resistance but did not change cardiac output, heart rate or stroke volume. 4‐Methylhistamine caused vasodilatation in the heart, stomach, small and large intestines and skeletal muscle. Vascular resistance was increased in the skin.
AN ELECTROPHYSIOLOGICAL STUDY OF THE ACTION OF CRUDE Enhydrina schistosa VENOM
Authors: FERRY C.B. , GEH SOO LIN 
Published: July 2012

Electrophysiological studies on the rat diaphragm revealed that crude Enhydrina schistosa venom has a blocking action on postjunctional acetylcholine (ACh) receptors.
This venom in concentrations of 0.125‐1.0 μg/ml abolished the extracellular endplate potential (e.e.p.p.) without altering the presynaptic spike. When the phrenic nerve was stimulated at a frequency of 1 Hz the degree of depression of successive e.e.p.ps was approximately the same in records made before and after treatment with venom.
In concentrations of 0.25 and 0.5 μg/ml the venom reduced significantly the amplitude of miniature endplate potentials (m.e.p.ps). The frequency of m.e.p.ps did not increase but was decreased when the amplitude of the m.e.p.ps was much reduced.
The crude venom did not alter the resting membrane potential (RMP) of the muscle cell.
The venom inhibited the depolarization of the muscle membrane caused by carbachol.
It is concluded that an active component in the crude venom is responsible for a blocking action on postjunctional receptors.
CARDIAC ADRENOCEPTORS AT LOW TEMPERATURE AND THE ADRENOCEPTOR INTERCONVERSION HYPOTHESIS
Authors: BENFEY B.G. 
Published: July 2012

The hypothesis that low temperature converts inotropic β‐adrenoceptors to α‐adrenoceptors has been tested in isolated heart preparations of the frog and rat.
The results do not support the adrenoceptor interconversion hypothesis. In the frog ventricle strip lowering the temperature from 24°C to 14°C did not significantly alter the inotropic potency of the sympathomimetic drugs isoprenaline, adrenaline and phenylephrine and did not reduce the potency of the β‐adrenoceptor blocking drug propranolol as an isoprenaline antagonist. In the isolated left atrium of the rat lowering the temperature from 31°C and 24°C to 17–19°C did not significantly alter the inotropic potency of isoprenaline, noradrenaline and phenylephrine, did not diminish the potency of the β‐adrenoceptor blocking drug propranolol and did not increase the potency of the α‐adrenoceptor blocking drug phentolamine.
Phenylephrine acted on α‐ and β‐adrenoceptors in rat left atrium at 31°C and 24°C, but only on β‐adrenoceptors at 17–19°C.