bluuebunny/crossref_metadata_2025_split huggingface dataset:
The nature of the adrenoceptors in the post‐partum rat uterus
Authors: ABDEL‐AZIZ A. , BAKRY N. 
Published: July 2012

Summary
Uteri were removed from rats 0·5 h to 8 days after parturition and were suspended in Locke solution at 37° C.
The agonists isoprenaline, adrenaline, noradrenaline and phenylephrine produced an inhibition of the post‐partum rat uterus.
In the presence of propranolol, the agonists noradrenaline, adrenaline, and phenylephrine had an excitatory effect on the post‐partum rat uterus. This excitatory effect was blocked by phenoxybenzamine indicating that it is mediated through α‐adrenoceptors.
These excitatory α‐adrenoceptors could be demonstrated for 5–6 days after parturition. By the 7th‐8th days their existence was no longer apparent.
Excitatory α‐adrenoceptors were also demonstrated in the late pregnant rat uterus.
The effect of Kö 1173, a new anticonvulsant agent on experimental cardiac arrhythmias
Authors: ALLEN J. D. , EKUE J. M. KOFI , SHANKS R. G. , ZAIDI S. A. 
Published: July 2012

Summary
The effects of the intravenous injection of Kö 1173, a new anticonvulsant drug, phenytoin and procainamide were studied on three types of cardiac arrhythmia in dogs.
Ventricular ectopic beats produced by intravenous injection of adrenaline in anaesthetized dogs respired with halothane were abolished by Kö 1173, 0·6 ± 0·1 mg/kg, phenytoin, 1·1 ± 0·3 mg/kg and procainamide, 4·1 ± 1·8 mg/kg.
Ventricular tachycardia was produced in anaesthetized dogs by the intravenous injection of ouabain and the three drugs infused intravenously at 0·2 (mg/kg)/min until sinus rhythm returned. Kö 1173 was effective in 8 out of 9 dogs after a mean dose of 1·3 ± 0·3 mg/kg; phenytoin in all 3 dogs after 2·7 ± 0·6 mg/kg and procainamide in the 3 dogs tested after 16·6 ± 1·3 mg/kg.
The intravenous injection of Kö 1173, 80 mg/kg, greatly reduced the number of ventricular ectopic beats occurring in conscious dogs 18–44 h after ligation of the anterior descending branch of the left coronary artery, with a resultant increase in the number of sinus beats. Phenytoin, 8·0 mg/kg, had a similar effect but procainamide was much less effective.
These results indicate that Kö 1173 is effective in abolishing experimental cardiac arrhythmias and suggest that its effects should be studied in patients.
Factors influencing the adrenergic neurone blocking action of propranolol
Authors: ELIASH SARAH , WEINSTOCK MARTA 
Published: July 2012

Summary
The reversal by propranolol of its own adrenergic neurone blocking effect in the cat can be prevented by cutting the splanchnic nerves or by ligating the adrenal veins.
In the absence of secretion from the adrenal medulla the nerve blocking action of propranolol is more complete, but can still be reversed by repeated injections or a constant infusion of adrenaline.
Prior treatment with adrenaline or noradrenaline also prevents the development of the blocking action of propranolol in the cat and in the isolated guinea‐pig vas deferens.
It is suggested that in the cat, propranolol stimulates the release of catecholamines from the adrenal medulla which antagonize its nerve blocking effect.
The effect of anti‐inflammatory agents on the changes in local lymph after thermal injury
Authors: BUTLER K. , LEWIS G. P. 
Published: July 2012

Summary
Lymph was collected directly from the hind limbs of rabbits anaesthetized with pentobarbitone and from unanaesthetized rabbits before and after one hind limb was injured by immersion in water at 60° C for 1 minute.
Rabbits were treated with anti‐inflammatory agents hydrocortisone or indomethacin which, in acute experiments, were infused close‐arterially into the limb either at the time of the injury or 90 min later. In chronic experiments hydrocortisone was given intravenously three times a day.
When given at the time of the injury both drugs reduced the subsequent mean increases in the lymph of the intracellular enzymes lactate dehydrogenase and glutamic pyruvate transaminase but not those of β‐glucuronidase and protein; whereas when given 90 min after the injury only the increase in lymph protein concentration was reduced.
The results indicate that these anti‐inflammatory agents probably inhibit the second phase of increase in vascular permeability which occurs after injury and in addition, reduce the leakage of intracellular protein by a non‐specific effect on membrane permeability.
The pronounced variability of the response of individual animals and the complexity of the experiments preclude the method as a suitable model for the estimation of anti‐inflammatory activity.
Effect of prostaglandins E1, E2 and A2 on vascular resistance and responses to noradrenaline, nerve stimulation and angiotensin in the dog hindlimb
Authors: KADOWITZ PHILIP J. 
Published: July 2012

Summary
The relationship between the vasodilator and inhibitory effects of prostaglandin E1 (PGE1), E2 and A2 on responses to nerve stimulation, noradrenaline and angiotensin was evaluated in the dog hindlimb preparation.
PGE1 and PGE2 were equipotent as vasodilators in the hindlimb; however, PGE1 was much more potent as an inhibitor of vasoconstrictor responses to nerve stimulation, noradrenaline and angiotensin.
PGA2 and PGE2 were approximately equal as inhibitors of vasoconstrictor responses to noradrenaline, nerve stimulation and angiotensin; however, PGE2 was far more potent as a vasodilator.
Since there is no relationship between the vasodilator and inhibitory effects of PGE1, E2 and A2, and since the inhibitory effect of PGA2 was present at a time when hindlimb perfusion pressure had returned to control value, it is concluded that the inhibitory action is probably not the result of a physiological antagonism.
Since each prostaglandin inhibited responses to nerve stimulation and noradrenaline to approximately the same extent and responses to angiotensin were also inhibited, it is suggested that these agents antagonize vasoconstrictor responses by a nonspecific depressant effect on smooth muscle cells.
The effect of cold storage on the adrenergic mechanisms of intestinal smooth muscle
Authors: HATTORI K. , KURAHASHI K. , MORI J. , SHIBATA S. 
Published: July 2012

Summary
In the guinea‐pig taenia caecum, fluorescent adrenergic fibres terminate in both muscle layers. The density of these fibres is greater in the taenia than in the underlying circular muscle layer. The myenteric plexus and individual ganglion cells are also densely innervated by intensely fluorescent adrenergic nerve fibres.
After three days of cold storage, the specific fluorescence disappeared from all tissue layers of the taenia caecum and smooth muscle fibres. In contrast, cholinesterase active substances were still demonstrable in all tissue layers even after seven days of cold storage but the density of these substances was decreased.
Cold storage (3–7 days) decreased the tissue noradrenaline content and did not modify the cholinesterase enzyme activity (4 days).
In cold stored strips, the inhibitory response to nicotine, 1,1‐dimethyl‐4‐phenylpiperazinium iodide (DMPP) or electrical transmural stimulation was abolished and enhancement of the contractile response occurred. Cold storage also inhibited the inhibitory action of tyramine. Similar results were observed after reserpine treatment.
In fresh taenia, the relaxation produced by nicotine, DMPP and electrical transmural stimulation was inhibited by adrenoceptor blocking agents and bretylium. In cold storage preparations, contraction produced by these stimuli was blocked by parasympathetic blocking agents and potentiated by anticholinesterase. These results indicate that the inhibitory response to these stimulants is mediated by stimulation of the adrenergic nerve system more than by non‐adrenergic nerves; the excitatory effect is probably due to stimulation of cholinergic nerves.
These results suggest that the adrenergic mechanisms of the taenia caecum are more labile in cold storage than the cholinergic mechanisms. Thus, the inhibitory action of cold storage on the relaxation produced by nicotine, DMPP, and transmural stimulation is probably explained by selective physical degeneration of the adrenergic nerve terminal. Also, enhancement of the contractile response to these stimulants in cold stored preparations is explained by the lack of adrenergic inhibitory mechanisms.
The generation from arachidonic acid of rabbit aorta contracting substance (RCS) by a microsomal enzyme preparation which also generates prostaglandins
Authors: GRYGLEWSKI R. , VANE J. R. 
Published: July 2012

Summary
Sodium arachidonate was incubated with a crude prostaglandin synthetase preparation made from dog spleen. The incubation was made in a dynamic system so that the products could be delivered to strips of rabbit aorta and rat stomach.
A rabbit aorta contracting substance (RCS) and a prostaglandin‐like substance were formed. The RCS had similar properties to that released in anaphylaxis. It was unstable and as the RCS activity declined, so the prostaglandin‐like activity increased. Its formation was prevented by prostaglandin synthetase inhibitors such as indomethacin.
A different rabbit aorta contracting substance was formed by incubation of arachidonate with lipoxygenase, which generates peroxides. This substance was stable and did not lead to prostaglandin production.
We conclude that RCS may be an intermediate in prostaglandin production, such as the postulated cyclic endoperoxide.
The uptake of cardiac glycosides in relation to their actions in isolated cardiac muscle
Authors: GODFRAIND T. , LESNE M. 
Published: July 2012

Summary
The uptake of 3H‐digitoxin, 3H‐ouabain and 3H‐dihydro‐ouabain by isolated guinea‐pig atria has been studied and compared with the inhibition of the sodium pump and with the inotropic effect.
Analysis of the curve relating the uptake of digitoxin and ouabain at equilibrium to the bath concentration enabled a non‐saturable and a saturable binding site to be distinguished.
The uptake of inactive doses of dihydro‐ouabain was only by a non‐saturable mechanism.
The uptake of labelled digitoxin and ouabain was reduced in the presence of another glycoside. The amount of bound glycoside was nearly equivalent to the estimated non‐saturable uptake.
The uptake was reduced at 4° C to the clearance of the non‐saturable site.
ED50 of digitoxin and of ouabain for inhibition of the sodium pump were measured and compared to the ED50 for inotropic effect and to the concentrations producing a half‐saturation of the saturable binding site.
It is concluded that binding to the saturable site may be responsible for the cardiac actions of the glycosides.
Renin‐like activity of the rat submaxillary gland: characterization and the effect of several drugs and stimuli
Authors: GUTMAN Y. , LEVY M. , SHORR J. 
Published: July 2012

Summary
Renin‐like activity was found in rat submaxillary glands.
This activity was destroyed by boiling, was non‐dialyzable and showed an optimum at approximately 50° C.
Renin‐like activity in the submaxillary gland was not diminished 24 h after nephrectomy but was considerably reduced after ligature of the submaxillary duct.
Renin‐like activity in the submaxillary gland was reduced following food‐deprivation, water‐deprivation or hypovolemia.
Renin‐like activity in the rat submaxillary gland was increased after isoproterenol administration but not following pilocarpine.
Renin‐like activity in the rat submaxillary gland was increased considerably by administration of NaCl or KCl, as well as following adrenalectomy.
Chlorothiazide and ouabain increased submaxillary renin‐like activity but diazoxide did not affect this activity.
The effects of diphenylhydantoin and potassium on the biological activity of ouabain in the guinea‐pig heart
Authors: BASKIN S. I. , DUTTA S. , MARKS B. H. 
Published: July 2012

Summary
Diphenylhydantoin (DPH) and potassium significantly prevent ouabain intoxication without preventing the inotropic effects of ouabain in the guinea‐pig isolated heart.
The antiarrhythmic effect of DPH and K on ouabain‐induced toxicity appears to be related to their ability to reduce ouabain accumulation by the myocardium and thereby prevent the intracellular Na and K changes which lead to the arrhythmic state.
Preferential release of newly synthesized 3H‐acetylcholine from rat cerebral cortex slices in vitro
Authors: MOLENAAR P. C. , NICKOLSON V. J. , POLAK R. L. 
Published: July 2012

Summary
Slices of rat cerebral cortex after treatment with the irreversible cholinesterase inhibitor soman, were incubated for 5 min in a Krebs‐Henseleit solution containing 25 mm KCl and 3H‐choline. Subsequently incubation was continued in a medium containing non‐radioactive choline and this medium was replaced at 5 min intervals. The amounts of labelled and total acetylcholine (ACh) released into the medium and extracted from the slices were determined at intervals.
After the initial 5 min contact with 3H‐choline, 44% of the newly synthesized ACh contained a choline moiety originating from the choline in the medium. During the initial 5 min and the subsequent incubation part of the labelled ACh was released. While the rate of total ACh release remained constant, that of the release of labelled ACh was highest in the 5 min period following the initial incubation with 3H‐choline and then declined exponentially.
The ratio of labelled ACh/total ACh in the ACh released during the initial 5 min incubation with 3H‐choline and during the subsequent 5 min was about three times as high as that in the ACh extracted from the slices at the end of these incubation periods.
The ratio of labelled ACh/total ACh in superficial layers of the slices was not higher than that in the total slices.
The rates of release of labelled and unlabelled ACh decreased when calcium was omitted from the incubation medium and were restored when the calcium was added. This suggests that both labelled and unlabelled ACh were released from nerve endings. The efflux of 3H‐choline was not calcium dependent.
It is concluded that labelled ACh newly synthesized from externally applied 3H‐choline does not exchange immediately with all other ACh in the tissue and has a greater chance of being released than unlabelled ACh.
Some pharmacological effects of the nematocide, morantel
Authors: BAMGBOSE S. O. A. , MARQUIS V. O. , SALAKO L. A. 
Published: July 2012

Summary
In isolated nerve‐muscle preparations as well as in nerve‐muscle preparations in intact anaesthetized animals, morantel exhibited neuromuscular blocking properties similar to those of depolarizing blockers. The drug also caused spastic paralysis of 3 day‐old chicks and contracture of the isolated toad rectus abdominis muscle.
Morantel caused contraction of the guinea‐pig and rabbit isolated small intestine. This effect was antagonized by atropine and hexamethonium.
Morantel caused an increase in the blood pressure of the anaesthetized rat and cat and contraction of the nictitating membrane of the anaesthetized cat. These effects were antagonized by hexamethonium.
It was concluded that morantel (like the related compound pyrantel) has acetylcholine‐like action and that its structure is consistent with such action.
Action of several β‐adrenoceptor blocking drugs in the pregnant sheep and foetus
Authors: TRUELOVE J. F. , PETTEN G. R. Van , WILLES R. F. 
Published: July 2012

Summary
The effect of several β‐adrenoceptor blocking drugs on the pregnant ewe and foetus were studied. Bunolol, butidrine, oxprenolol, propranolol and USVP65‐24 all crossed the ovine placenta and produced a β‐adrenoceptor blockade in the ovine foetus. AH3474, AY21011 and sotalol did not cross the ovine placenta as assessed by the absence of a β‐blockade in the foetus when these compounds were administered to the pregnant ewe.
Of the β‐blocking compounds tested, only propranolol and oxprenolol produced a prolonged blockade in the foetus. The β‐blockade with propranolol was of 3 h duration in the ewe and 10 h duration in the foetus. Oxprenolol produced a β‐blockade of 3 h duration in the ewe and 8 h in the foetus.
The β‐blocking drugs which did cross the ovine placenta were more soluble in organic solvents (ether, chloroform, corn oil and olive oil) than those which did not cross the ovine placenta.
Interaction between tyramine and iproniazid on guinea‐pig atria
Authors: DE JALÓN P. D. GARCIA , MARTINEZ‐SIERRA R. , VELASCO A. 
Published: July 2012

SummaryThe inhibition of monoamine oxidase (MAO) by iproniazid may be antagonized by large doses of tyramine as shown by the restoration, or otherwise, of inotropic responses to tyramine in isolated atria from guinea‐pigs that had been treated with reserpine.
Effects of cocaine or denervation on responses of isolated strips of cat spleen to (‐)‐noradrenaline and (‐)‐isoprenaline
Authors: GRANATA A. R. , LANGER S. Z. 
Published: July 2012

Summary
A study has been made of the effects of cocaine and sympathetic denervation on responses of the cat spleen to (–)‐noradrenaline and (–)‐isoprenaline.
Responses of isolated strips of spleen capsule to (–)‐noradrenaline or to (–)‐isoprenaline were not affected by reserpine‐pretreatment.
In adult cats, cocaine (1 and 10 μg/ml) or denervation produced a shift to the left of dose‐response curves to (–)‐noradrenaline, whereas they failed to modify dose‐response curves to (–)‐isoprenaline.
There was an increase in the maximum development of tension to (–)‐noradrenaline after denervation or in the presence of cocaine (10 μg/ml). These procedures did not increase the maximal responses to (–)‐isoprenaline.
Cocaine (10 μg/ml) did not affect dose‐response curves to (–)‐noradrenaline or (–)‐isoprenaline in the denervated spleen.
In the kitten spleen, cocaine (1 and 10 μg/ml) produced a shift to the left of dose‐response curves to (–)‐noradrenaline both in untreated and in reserpine‐pretreated tissues.
There was a small shift to the left in dose‐response curves to (–)‐isoprenaline in the presence of cocaine in the untreated but not in the reserpine‐pretreated kitten spleen.
It is concluded that the potentiation of responses to (–)‐noradrenaline in the cat's spleen is due to a prejunctional effect of cocaine.
The detection of differential β‐adrenoceptor blockade in the cat
Authors: PARKES M. W. 
Published: July 2012

Summary
Tachycardia and bronchodilatation were produced by intravenous dimethyl‐phenylpiperazinium iodide (DMPP) in the spinal or pithed cat. Responses other than those involving β‐adrenoceptors were minimized by appropriate blocking agents.
With intact adrenals, both the tachycardia and bronchodilatation with 10 μg/kg DMPP were equal to those with 1 μg/kg adrenaline.
After adrenalectomy, tachycardia with 100 μg/kg DMPP was equal to that with 1·5 μg/kg adrenaline, but the bronchodilatation was equal to that with only 0·3 μg/kg. This difference may reflect the relative activity of the sympathetic supply to the organs.
After adrenalectomy, propranolol was 3 times as effective against bronchodilatation due to DMPP as against tachycardia. Practolol was inactive against bronchodilatation.
With intact adrenals, propranolol reduced both tachycardia and bronchodilatation due to DMPP equally. Propranolol also antagonized equally both effects of adrenaline in the pithed cat after adrenalectomy.
In the spinal cat, propranolol caused bradycardia and bronchoconstriction that persisted after adrenalectomy or pithing. It was reduced by pempidine and guanethidine and is attributed to spontaneous adrenergic neuronal activity.
The Appendix describes a device for cycle‐by‐cycle spirometry and correction for zero drift of a micromanometer, used in this study for the continuous recording of bronchial resistance.
Central noradrenergic neurones and the cardiovascular actions of clonidine in the rabbit
Authors: DOLLERY C. T. , REID J. L. 
Published: July 2012

Summary
Clonidine (1 μg/kg), given by intracisternal injection to anaesthetized rabbits, lowered mean arterial blood pressure by 33 mmHg and heart rate by 32 beats/min.
In animals pre‐treated with 6‐hydroxydopamine (6‐OHD 500 μg/kg intracisternally) 7–10 days before, intracisternal clonidine (1 μg/kg) reduced mean arterial blood pressure by only 2·5 mmHg and heart rate by 4 beats/minute.
The hypotensive action of intravenous clonidine was reduced to 49% of control by pre‐treatment with intracisternal 6‐OHD. In unanaesthetized normal animals intravenous clonidine (30 μg/kg) lowered mean arterial blood pressure by 19·3 mmHg, while after 6‐OHD it fell only 94 mmHg.
These studies suggest that the central hypotensive effect of clonidine is dependent on the integrity of central monoaminergic neurones.
Effects of histamine on hepatic volume (outflow block) in anaesthetized dogs
Authors: GREENWAY C. V. , OSHIRO G. 
Published: July 2012

Summary
Hepatic volume was recorded by plethysmography in dogs anaesthetized with sodium pentobarbitone. Histamine infusions into the hepatic artery or portal vein increased hepatic volume while hepatic sympathetic nerve stimulation decreased the volume. Simultaneous nerve stimulation and histamine infusion decreased hepatic volume.
The hepatic volume responses to histamine and nerve stimulation could not be explained on the basis of differences in the responses of the larger hepatic veins and the possibility of a histamine‐sensitive sphincter at the junction of the hepatic vein with the inferior vena cava was excluded. Differences in the responses of the hepatic arterial bed contributed to but did not explain the different hepatic volume responses.
It is suggested that histamine produced an intense and specific constriction of the sublobular veins with passive distension of post‐sinusoidal venules, sinusoids and portal venules while hepatic nerve stimulation produced a uniform and generalized constriction of both pre‐ and post‐sinusoidal vessels.
Intravenous infusions of histamine produced a marked hypotension but small variable effects on hepatic volume. It is concluded that hepatic pooling is not the cause of the hypotension produced by intravenous histamine and that significant hepatic pooling will only be produced by mechanisms which release endogenous histamine within the liver.
Changes in plasma levels of vasopressin and renin in response to haemorrhage in dogs
Authors: COUSINEAU D. , GAGNON D. J. , SIROIS P. 
Published: July 2012

Summary
The rabbit rectum superfused with blood or Krebs solution was used to assay vasopressin in circulating blood and in plasma extracts respectively.
Vasopressin was released by a rapid fall in diastolic pressure of as little as 5 mmHg, and the amount of vasopressin released was proportional to the magnitude of the fall in diastolic pressure in the range studied. These results would indicate that vasopressin release follows the magnitude of the fall in diastolic pressure more closely than the actual decrease in blood volume in haemorrhagic hypotension.
It was shown that the time required to induce an increase in circulating vasopressin is inversely proportional to the severity of the fall in diastolic pressure; this suggested that the stimulation of neurosecretory reflex arc varies with the intensity of the stimulus.
The slight changes in plasma renin activity as well as the pattern of renin release suggested the unlikeliness of the influence of renin upon vasopressin secretion under these circumstances. On the contrary, the results suggested that the secretion of large amounts of vasopressin tended to inhibit renin release.