bluuebunny/crossref_metadata_2025_split huggingface dataset:
An electrophysiological study of the innervation of the smooth muscle of the colon
Authors: Furness J. B. 
Published: December 2014

1. Micro‐electrodes were used to examine transmission from intrinsic and extrinsic nerves to single cells of the longitudinal and circular muscle coats of colons from guinea‐pigs and rabbits.2. When intrinsic nerves were stimulated, inhibitory junction potentials (IJPs) were observed in over 90% of the cells of the longitudinal coat and nearly all of the cells of the circular coat. The characteristics of IJPs in the guinea‐pig and rabbit were similar. Facilitation of two or three successive IJP's was sometimes observed. The IJPs were unaffected by guanethedine but were blocked by procaine. IJPs could not be elicited by stimulation of either the pelvic parasympathetic or periarterial sympathetic nerves. In some cells, the IJP was preceded by a brief depolarization, which probably results from the stimulation of excitatory nerves to the same cell.3. Excitatory junction potentials (EJPs) were observed in about 5% of cells of the longitudinal coat in response to stimulation of the intramural nerves. When the pelvic nerves were stimulated, EJPs were observed in most cells of both the longitudinal and circular muscle coats. The EJP in the guinea‐pig colon was blocked by hyoscine.4. The interaction of the IJP evoked by intrinsic nerve stimulation and the EJP evoked by pelvic nerve stimulation was examined. When both nerve supplies were stimulated together, only an IJP was observed.5. The nature of the innervation of the colon and the origin of intrinsic non‐adrenergic inhibitory neurones is discussed.
Ionic, histological and vascular factors in the reaction of the sheep's parotid to high and low mineralocorticoid status
Authors: Blair-West J. R. , Coghlan J. P. , Denton D. A. , Nelson J. , Wright R. D. , Yamauchi A. 
Published: December 2014

1. The blood capillaries from the alveolar areas of the sheep's parotid gland drain into a sinusoidal portal venous system which is in close relation to the striated intralobular ducts.2. The alveoli of the gland are surrounded by a mesh of muscular processes of myoepithelial cells: there are no myoepithelial structures in relation to the ducts.3. In close relation to the alveoli are nerve fibres, some containing noradrenaline and some with cholinesterase at their cellular contact area. Stimulation of the cervical sympathetic trunk for 1–2 min (or intra‐arterial injection of noradrenaline) causes expulsion from each gland of a regular amount of saliva without changing the long term appearance rate of saliva. Stimulation of the secretomotor nerve (or acetylcholine
I.A.) causes an increase in saliva production.4. It is proposed that the saliva which appears due to sympathetic stimulation is expelled from the alveoli by contraction of the myoepithelial network and is little changed during its rapid transit through the duct system.5. The results indicate that the alveolar cells react to increasing aldosterone status by increasing concentration of K+ in alveolar fluid with inverse change of Na+ in alveolar secretion over a wide range of flow rates.6. No histological evidence of innervation of the intralobular striated ducts by sympathetic or secretomotor nerves was obtained.7. The secretory ducts appear to be the site of exchange of HCO3− and phosphate, Na+ and K+, and for enrichment of SCN− and I− in the alveolar fluid.8. During stimulation of the secretomotor nerve supply, the gland, whether in adrenally insufficient or in hyperaldosterone status, shows the initial transient of discharge of K+ into saliva and blood and then maintains K+ intake from plasma as near to output in saliva as does the gland in the replete animal with basal aldosterone status.
Influence of prehydration on the changes in renal tissue composition induced by water diuresis in the rat
Authors: Hai M. A. , Thomas S. 
Published: December 2014

1. The composition of renal tissue was determined in rats before and immediately after intravenous infusion of dextrose (2·5 g/100 ml.) in amounts sufficient to administer a positive fluid load of 4% body weight over 2 hr. The rats were classified into three groups, according to the preinfusion urine osmolality: hydropaenia, normal and moderately diuretic (over 2400, 800‐1500 and below 800 μ‐osmoles/g H2O, respectively).2. In non‐infused rats, the steepness of the corticomedullary osmolal gradient varied, due to differences in both water and solute (sodium and urea) contents, and was related to urinary osmolality. Whereas differences in medullary and papillary solute contents occurred between all three groups, papillary water content was significantly higher only in the moderately diuretic animals.3. Dextrose infusion caused the induction of water diuresis, the lowest urinary osmolalities being produced in the previously moderately diuretic animals.4. Dextrose infusion caused a considerable reduction in the steepness of the corticomedullary osmolal gradient in all rats, particularly in the previously hydropaenic animals, due to changes in both solute (sodium and urea) and water contents. Whereas reductions in medullary and papillary solute contents occurred in all three groups, there was no further increase in papillary water content from the already high values seen in the noninfused diuretic animals.5. Thus, dextrose infusion largely abolished any previous differences in tissue water content, whereas significant, though small, differences in osmolal (particularly urea) content persisted.6. These data are discussed in terms of changes and differences in endogenous antidiuretic hormone (A.D.H.) release.7. Changes in the magnitude and direction of the urinary‐papillary urea concentration difference are discussed in terms of passive transport, with probable A.D.H.‐induced changes in nephron urea permeability.
Use of a miniature GM counter and a whole body counter in the study of potassium transport by the colon of normal, sodium‐depleted and adrenalectomized rats in vivo
Authors: Barnaby C. F. , Edmonds C. J. 
Published: December 2014

1. A method is described employing a whole‐body counter and a miniature GM counter placed within the lumen of the gut which can be used to study the absorption rates and kinetics of labelled substances in the mucosal epithelium in vivo. The method was applied to the study of K transport by the mucosa of the descending colon of normal, Na‐depleted and adrenalectomized rats.2. The K influx rate was linearly related to luminal [K] over the range 5–80 m
M. NaCN in the lumen produced a fall of electrical potential difference (p.d.) and of K secretion rate but did not reduce K influx rate. The findings were consistent with passive K influx.3. The mucosal 42K content reached a steady value after 60–90 min of exposure to 42K in the lumen. The value was similar in normal and adrenalectomized rats but was greater in Na‐depleted rats.4. After replacement of luminal solution by a non‐radioactive solution the fall of mucosal 42K content could be described, in the majority, by a curve having two exponential components with half‐times of 8–10 and 65–106 min. Approximately half of the 42K outflow passed to the lumen. The rate constants were similar in all groups of rats.5. The results analysed on the basis of representing the mucosal K as in two compartments, indicated that the observed absorption rate could not be accounted for by transport through these compartments alone and that most of the 42K crossed the mucosa by a fast pathway not detectable by the miniature GM counter. Most of the mucosal K was relatively inaccessible from the lumen.6. Na depletion raised the transmucosal p.d., increased the K secretion rate and appeared to increase K permeability of the mucosa but the kinetics were unaltered. Accumulation of 42K in the mucosa was greater, suggesting that the permeability of the luminal face had increased. Adrenalectomy produced only one change, namely a reduction of K secretion rate.
The effects of hypophysial portal plasma on the content of immunoreactive growth hormone in the anterior pituitary
Authors: Buse M. G. , Fulmer J. D. , Kansal P. C. , Worthington W. C. 
Published: December 2014

1. Blood plasma obtained from the hypophysial portal vessels of rats has been tested in assay animals for effects on the content of growth hormone in the anterior pituitary.2. Growth hormone was estimated by radioimmuno‐assay at 15 min, 30 min, 1 hr and 2 hr after intracarotid or intravenous infusion of portal plasma. There was a significant increase in growth hormone content at 15 min after infusion, but not at 30 min, 1 hr and 2 hr.3. Insulin, cold stress, haemorrhage and treatment with growth hormone had no effect on growth hormone content of the pituitary under the conditions of application of these stimuli.4. Growth hormone was measured in plasma obtained from the pituitary of control and insulin‐treated animals. In control animals the amount of growth hormone in this plasma was higher than in base line samples and in the insulin‐treated animals it was lower than in base line samples. A calculation based on the growth hormone content of blood obtained directly from the pituitary indicates a daily rate of synthesis and release of about 10 μg.5. The hypothesis that portal plasma stimulated the synthesis of immuno‐assayable growth hormone by the anterior pituitary is considered.6. Discrepancies between our results using immuno‐assay and those of others using bio‐assay are discussed.
Release of acetylcholine by chick embryo heart before innervation
Authors: Coraboeuf E. , Le Douarin G. , Obrecht‐Coutris G. 
Published: December 2014

1. In chick embryo hearts, 3‐day‐old and not yet innervated, repetitive direct stimulation causes a transitory inhibition of the spontaneous rhythm.2. The degree of post‐stimulation inhibition depends on the frequency and duration of the artificial stimulation and on the concentration of K and Ca ions in the extracellular solution.3. After treatment with atropine (10−5 g/ml.) post‐stimulation inhibition is no longer observed. The spontaneous rhythm is accelerated by atropine. The findings therefore suggest that an ACh‐like substance is released from the non‐innervated embryonic heart during activity.4. By use of the dorsal muscle of the leech for biological assay the liberation of an ACh‐like substance from the non‐innervated embryonic heart was confirmed.
Hypothalamic control of adrenaline secretion in response to insufficient glucose
Authors: Himsworth R. L. 
Published: December 2014

1. The rise of plasma glucose consequent upon the release of adrenaline following the systemic administration of 3‐O‐methylglucose is prevented by previous infiltration with lignocaine of the lateral hypothalamic area on both sides.2. The similarity between this effect and that of the same procedure in preventing the hypersecretion of gastric acid in response to the same stimulus, together with the known fact that hypoglycaemia or the systemic administration of some glucose analogues produce both gastric and adrenal medullary hypersecretion, provides strong presumptive evidence that there exists in the lateral hypothalamic area a chemoreceptor which controls the release of adrenaline. The cells of this receptor like those of the chemoreceptor controlling gastric acid secretion, are activated by an insufficiency of metabolizable glucose.
The involvement of the complement system in the pressor response to the injection of Forssman antibody in the guinea‐pig
Authors: Darlow G. , Gough G. F. , Tanalp R. 
Published: December 2014

1. When the hind limbs of the guinea‐pig were perfused at constant volume inflow with undiluted pooled blood, an intra‐arterial injection of the Forssman antibody caused a rapid and long‐lasting pressor response.2. In the whole animal the pressor response was accompanied by a fall in the number of circulating platelets, but perfusion experiments suggest that serotonin was not responsible for the pressor response.3. When decomplemented serum was perfused through the hind‐limb preparation the Forssman antibody failed to produce a rise in pressure, but a pressor response developed when unheated serum was subsequently introduced. This suggests that the actual combination of antibody with its tissue antigen is not the immediate cause of the pressor reaction.4. The cause of the pressor response is still unknown but apparently depends on the activation of the complement system. The effectiveness of serum shows that polypeptides split off from fibrinogen are not involved.
Sympathetic denervation of the smooth muscle of the vas deferens
Authors: Birmingham A. T. 
Published: December 2014

1. The post‐ganglionic nerve fibres to the vas deferens of the guinea‐pig and rat were interrupted in vivo by stripping one vas deferens of its serous coat; the other vas deferens was left intact as a control.2. Four to eight days later the stripped vas deferens did not contract in response to electrical transmural stimulation in vitro at 0·1 msec pulse duration. Pulses of 1·0 msec duration produced small contractions which were not abolished by local anaesthetic or adrenergic neurone‐blocking drugs.3. Log dose—response curves to noradrenaline were, for stripped vasa deferentia, to the left of those for control vasa. The increase in sensitivity to noradrenaline at 8 days was about sixteenfold for rat vasa and about tenfold for guinea‐pig vasa. Tyramine did not contract stripped vasa from guinea‐pigs or rats.4. The noradrenaline and adrenaline content of guinea‐pig and rat vasa was greatly reduced or abolished 8 days after the stripping operation.5. Fluorescent nerve terminals were usually absent when transverse sections of stripped vasa were examined by fluorescence microscopy after treatment by the formaldehyde condensation method for demonstrating catecholamines.6. It is concluded that post‐ganglionic sympathetic denervation is achieved by stripping the vas deferens in vivo of its serous coat and mesenteric attachments.
The effect of diet and acute starvation on the deiodination of thyroxine and triiodothyronine in the thyroidectomized rat
Authors: Nathanielsz P. W. 
Published: December 2014

1. General agreement exists that the level of thyroid function is depressed by starvation. The virtually complete cessation of biliary‐faecal thyroxine loss in the starved animal makes the significance of this reduction difficult to assess in physiological terms.2. Deiodination of [131I]thyroxine was investigated in thyroidectomized rats. Thus central feed‐back effects were eliminated and the changes in peripheral utilization of thyroxine could be observed. The simultaneous use of [125I] sodium iodide permitted changes in renal handling of iodide to be taken into consideration.3. Rats fed oxoid (Oxo Ltd. diet 41 B) deiodinated a significantly greater proportion of thyroxine in the 24 hr after injection of a tracer dose of [131I]thyroxine than did the starved or glucose‐fed rat. [131I]triiodothyronine was also probably deiodinated at a faster rate in oxoid‐fed rats than in starved or glucose‐fed rats.4. Thyroxine was deiodinated at a faster rate by starved rats than by rats fed glucose.5. Thyroxine disappeared significantly faster from the blood in oxoid‐fed than in the starved or glucose‐fed rat. Thyroxine also disappeared faster from the blood in the starved rat than in the glucose‐fed rat over 24 hr.6. These results are discussed in relation to previous findings of depressed pituitary—thyroid function in starvation.
The effects of distension of the pulmonary vein—atrial junctions upon peripheral vascular resistance
Authors: Carswell F. , Hainsworth R. , Ledsome J. R. 
Published: December 2014

1. Small balloons were inserted through the left pulmonary veins so as to lie at the pulmonary vein—left atrial junctions.2. Distension of the balloons caused a reflex increase in heart rate. The afferent path was in the vagus nerves and the efferent path was in the cardiac sympathetic nerves.3. Only small and variable changes in vascular resistance in a perfused hind limb accompanied the increase in heart rate when a steady state had been reached.4. In about half of the experiments a transient vasodilatation was observed in the perfused hind limb, occurring immediately after distension of the pulmonary vein—atrial junctions and lasting about 22 sec.5. The transient dilatation was due to a decrease in sympathetic vasoconstrictor nervous activity.6. Stimulation of left atrial receptors causes an increase of sympathetic nervous activity to the heart but does not cause a corresponding increase in sympathetic nervous activity to the hind limbs.
The relation between membrane potential, membrane currents and activation of contraction in ventricular myocardial fibres
Authors: Beeler G. W. , Reuter H. 
Published: December 2014

1. Membrane currents and contractile responses have been measured in ventricular myocardial preparations under voltage clamp conditions.2. In Tyrode solution, steady‐state contraction was obtained only after 5‐8 depolarizations to a given potential level. The threshold of steady‐state tension was identical to the potential where the calcium inward current, ICa, was activated (about −35 mV). Both thresholds were shifted in the same direction along the voltage axis and by the same amount by changing [Ca]o or [Na]o. Maximum tension was obtained at inside positive potentials.3. The time courses of steady‐state tension and of activation of ICa were different by more than one order of magnitude in Tyrode solution. But in order to achieve any appreciable steady‐state tension, ICa had to flow during several identical depolarizations. Tension decreased again at potentials above ECa. This suggests that calcium inward current must flow in order to fill intracellular calcium stores from which calcium can be released by an unknown mechanism.4. The ability of a fibre bundle to contract again after a preceding twitch is greatly dependent on the membrane potential between two equal depolarizations. In Tyrode solutions with 1·8 and 7·2 m
M‐CaCl2 half restoration of this ability occurred at −45 ± 3 mV (±
S.E. of mean) and −23 ± 4 mV, respectively.5. In sodium‐free bathing solutions, steady‐state tension was attained upon the first depolarization provided ICa was activated. Furthermore, at different potentials, the time courses of activation of tension and of activation of ICa were identical, i.e. tension reached its maximum when ICa was fully activated. This suggests that in sodium‐free solutions the flow of calcium ions into the fibre directly activates contraction.
Signals from cones
Authors: Alpern M. , Rushton W. A. H. , Torii S. 
Published: December 2014

1. We have studied red and green cones by contrast flash inhibition and found them both to be very similar to rods in their response to flash energy, except that all light quantities must be some 100‐fold greater in cones for the same effect.2. Using the methods of a previous paper (A.R.T. a) where no backgrounds were employed, we plotted log test flash λ against log surround flash ϕ with criterion that λ should just be detected. The experiment was repeated with a ‘windmill stop’ interposed in the ϕ flash which reduced its area symmetrically to ⅛. From these two curves it is possible to extract the relation between N, the inhibitory signal, and ϕ, the test flash. It isN = ϕ/(ϕ+σ),where σ, the semi‐saturation constant, is about 4·5 log td sec.3. Using the methods of (A.R.T. b) where backgrounds were studied, we measured the increment threshold for the surround flash ϕ against its background θ using as criterion not that ϕ should just be seen but that it should generate a fixed inhibitory signal N so that the fixed test flash λ could just be seen.4. This increment threshold curve resembled the Aguilar & Stiles (1954) curve for rods, showed saturation and a complete symmetry about the 45° line through the point with co‐ordinates (log θD, log σ).5. These results imply that the cone signal N is related to flash ϕ and steady background θ by [Formula: see text], where θD is receptor noise (= eigengrau), and ϕ and θ are expressed in units of quantum catch.6. The ordinary increment threshold for cones does not show saturation because a steady saturating background bleaches all the pigment away. When the background is presented for only 100 msec with dark pauses between, no great bleaching occurs and saturation is seen.
On the degeneration of rat neuromuscular junctions after nerve section
Authors: Miledi R. , Slater C. R. 
Published: December 2014

1. A study was made of functional and structural changes during degeneration of end‐plates in the rat diaphragm after phrenic nerve section at two levels.2. For 8–10 hr after cutting the nerve in the neck, all end‐plates retain the ability to transmit impulses. During the following 8–10 hr, an increasing number of end‐plates lose this ability so that after a total of about 20 hr, no end‐plates can transmit.3. Transmission failure occurs abruptly at most end‐plates. This failure is usually accompanied by cessation of spontaneous miniature end‐plate potentials (min.e.p.p.s), though in a few cases min.e.p.p.s persist after junctional transmission has failed. Several degenerating junctions were observed where the frequency of min.e.p.p.s was very low, suggesting an intermediate stage in min.e.p.p. failure.4. The time of junctional failure depends on the length of the degenerating nerve stump. For each additional centimetre of nerve, failure is delayed about 45 min.5. Changes in ultrastructure of nerve endings closely parallel those of function. For about 8–12 hr after cutting the nerve, nearly all end‐plates appear normal. During the period when transmission is failing, some end‐plates are clearly undergoing structural break‐down. By the time functional failure is complete, all end‐plates appear grossly abnormal.6. During degeneration, the contents of the axoplasm undergo disruption and the nerve terminal breaks up into small fragments. In contrast, the Schwann cell appears to become very active and its processes extend into the synaptic cleft to surround fragments of the nerve terminal. Ultimately, the Schwann cell completely replaces the axon at the end‐plate.7. Increasing the length of the peripheral nerve stump delays the onset of structural break‐down. Disruption of end‐plates near the site of nerve entry into the muscle occurs before those farther away.8. It is suggested that end‐plate degeneration is triggered by a signal which passes from the site of injury to the nerve terminal. The duration of the period after transection when end‐plates appear to be normal would then reflect the time required for this signal to travel the length of the isolated nerve stump.
Action of kinins on salivary myoepithelial cells
Authors: Emmelin N. , Garrett J. R. , Ohlin P. 
Published: December 2014

1. Bradykinin and kallidin were injected close‐arterially into the submaxillary glands of dogs and the effects on the pressure in the salivary ducts were recorded.2. Both kinins in very low dosage (threshold about 0·001 μg/kg) caused a pressure rise in the salivary duct without eliciting any salivary secretion, indicating that they produced contraction of the salivary myoepithelial cells.3. This effect was obtained even after administration of atropine, dihydroergotamine and propranolol.