bluuebunny/crossref_metadata_2025_split huggingface dataset:
On the presynaptic acetylcholine receptor in sympathetic ganglia of the frog
Authors: Ginsborg B. L. 
Published: December 2014

1. Action potentials have been recorded extracellularly from individual preganglionic nerve terminals in the lumbar sympathetic chain of frogs (cf. Koketsu & Nishi, 1968).2. The action potentials were unaffected by changes in external Mg2+ or Ca2+ concentration, but were attenuated or even abolished by acetylcholine or carbachol. The effect on the presynaptic action potential was transient, in contrast to the blockade of synaptic transmission caused by these drugs, which as is well known persists indefinitely in their presence.3. In the presence of tubocurarine (5 × 10−5
M), acetylcholine and carbachol had no effect on the presynaptic action potential.4. The action potentials were reduced by an increase in external K+ concentration and abolished at between 9 and 16 m
M K+. Synaptic transmission persisted until the amplitude of the action potential was reduced to less than one third of its control value.5. It is concluded that although the presynaptic nerve is endowed with acetylcholine receptors, they are not the source of the long lasting blockade of synaptic transmission caused by cholinergic substances.
Evidence against adrenergic motor transmission in the guinea‐pig vas deferens
Authors: Ambache N. , Zar M. Aboo 
Published: December 2014

1. Field stimulation of desheathed preparations of guinea‐pig vas deferens, treated with a ganglion‐blocking agent, has revealed the presence of two tetrodotoxin‐susceptible components in the motor response, suggesting the existence of two sets of post‐ganglionic motor nerve fibres of different excitability: one set responding maximally to pulses of 0·1–0·4 msec; the other, to pulses of 2 msec. No distinction could be made pharmacologically between the two components.2. Cooling potentiated that component in the twitch‐responses which was due to stimulation of the more excitable fibres.3. The sensitivity of the longitudinal muscle to the motor action of noradrenaline was low and was subject to considerable animal variation. But normal responses to post‐ganglionic field stimulation were elicited in noradrenaline‐insensitive preparations, in which the twitches elicited by 5 pulses could not be matched with noradrenaline, even 100–125 μg/ml.4. In some forty experiments, small doses of noradrenaline inhibited the twitch‐responses evoked by either set of motor fibres. This inhibition differed from that produced by isoprenaline in two respects. Firstly, propranolol did not antagonize the noradrenaline inhibition, thus excluding an action on β‐adrenoceptors; and secondly, noradrenaline did not depress contractions elicited by muscarine or by 5‐methylfurmethide.5. Phenoxybenzamine, 10−6 g/ml., produced a thousandfold reduction in the sensitivity of the muscle to the motor action of noradrenaline, without any decrease in the height of the twitches elicited by 0·1 or 1 msec pulses.6. The twitch‐responses were not affected by combined α + β adrenoceptor blockade with phentolamine and propranolol.7. Tyramine, amphetamine, tranylcypromine and prostaglandin E2 inhibited the twitches but potentiated the contractile effect of noradrenaline.8. The twitch‐responses and their inhibition by noradrenaline were present in preparations taken from reserpinized animals.9. Although the twitch‐responses could be paralysed by bretylium or guanethidine, the foregoing results excluded adrenergic transmission at the motor endings. Cholinergic transmission was also excluded by negative findings with anticholinesterases, atropine, nicotine and (+)‐tubocurarine.10. Motor transmission by histamine, 5‐hydroxytryptamine, γ‐aminobutyric acid or ATP was also excluded.
Stimulation of amylase secretion from the perfused cat pancreas by potassium and other alkali metal ions
Authors: Argent B. E. , Case R. M. , Scratcherd T. 
Published: December 2014

1. In the isolated cat pancreas, stimulated maximally with secretin, increasing the perfusate potassium concentration (at the expense of sodium ions) caused a copious secretion of amylase from the gland, reduced the volume rate of secretion and caused vasoconstriction.2. Rubidium and caesium had similar effects to potassium: lithium, though depressing secretory rate, had no effect on enzyme secretion or vasoconstrictor action.3. Amylase secretion was detected at potassium concentrations of 30 m
M and was maximal at 80–90 m
M, output declining as the concentration was raised to 120 m
M.4. Amylase secretion was maximal during the first few minutes of exposure to excess potassium, but remained above basal levels throughout the test period. Secretory rate was depressed by a constant amount during the test period.5. Atropine sulphate blocked the effect on enzyme secretion without affecting the reduction in secretory rate.6. During perfusion with excess potassium a vasodepressor material with the properties of acetylcholine was detected in the effluent from the gland.7. The reduction in secretory rate, when perfusate sodium was replaced by potassium, was equal to that obtained when sodium was replaced by sucrose.8. It is concluded that potassium stimulates amylase secretion indirectly by releasing acetylcholine from nerve terminals in the gland, and that the reduction in secretory rate is due not to excess potassium but to sodium deficiency.
Studies on the translocation of noradrenaline‐containing vesicles in post‐ganglionic sympathetic neurones in vitro. Inhibition of movement by colchicine and vinblastine and evidence for the involvement of axonal microtubules
Authors: Banks P. , Mayor D. , Mitchell Mary , Tomlinson D. 
Published: December 2014

1. Methods are presented for studying axonal transport mechanisms in preparations of constricted hypogastric nerve/inferior mesenteric ganglia maintained in vitro for periods up to 48 hr. Under these conditions the ultrastructure of the tissue is excellently preserved.2. The proximo‐distal movement of noradrenaline and noradrenaline storage vesicles in the non‐myelinated axons of these preparations is inhibited by both colchicine (10 μg/ml.) and vinblastine sulphate (1 μg/ml.) whilst the movement of mitochondria appears to be unaffected.3. Neither colchicine nor vinblastine sulphate depletes accumulated dense‐cored vesicles of their stores of noradrenaline.4. These drugs reduce the accumulation of noradrenaline and densecored vesicles against a constriction when they are in contact with the nerve trunks only, and are denied direct access to the nerve cell bodies in the ganglion.5. The only other morphological change that can be attributed to the action of colchicine and vinblastine is a marked reduction in the number of axonal microtubules.6. The experiments provide strong support for the view that the axonal system of microtubules is closely involved in the proximo‐distal movement of noradrenaline storage vesicles within noradrenergic neurones. The microtubular system does not appear to be involved in mitochondrial movement.
The hyperpolarization of frog skeletal muscle fibres induced by removing potassium from the bathing medium
Authors: Akiyama T. , Grundfest H. 
Published: December 2014

1. The time course of changes in resting potential after removing K0 was studied in twenty‐four single fibres and in 136 fibres from small bundle (two to four fibres) preparations of frog semitendinosus muscles.2. The initial resting potentials in the control saline ranged between −88 and −98 mV. The potentials returned to nearly the initial values when control conditions were reinstated after 3‐8 hr of experimentation. All the fibres twitched at the end of the experiment.3. Only about one third of the fibres hyperpolarized for any length of time on exposure to a K‐free saline at room temperature (20–28° C). The hyperpolarization was reversed to depolarization after a variable delay. The resting potential could fall to −50 or −40 mV.4. The remainder of the fibres depolarized with little or no prior hyperpolarization.5. Both patterns of response could be replicated in the different fibres.6. Hyperpolarization induced by K‐free solution was reduced or abolished on cooling to ca 10°C; on substitution of Tris or Li for Na; and upon inhibition of the Na pump with DNP (0·025–0·2 m
M) or ouabain (0·05 m
M). The latter agent was not as effective as the other conditions.7. Only small, slowly developing depolarization occurred when Na was replaced with Tris or Li.8. The various effects in K‐free solutions were reversed on returning to the control conditions.9. It is suggested that removal of K0 itself has little or no direct effect on the resting potential and that the initial hyperpolarization is due to the pumped efflux of Na without a compensatory influx of K. Block of the pump electrogenesis is manifested by depolarization of the fibres as K1 is depleted and Na1 increased.10. The Na pump appears to be dependent upon the nutritional status of the frogs and variations of the latter probably cause the different responses of fibres to removal of K0.
Methyl histamines and gastric secretion
Authors: Code C. F. , Maslinski S. M. , Mossini F. , Navert H. 
Published: December 2014

1. The previous findings that N‐methylhistamine and N‐dimethylhistamine are more potent stimulators of gastric secretion than histamine have been confirmed in dogs with Heidenhain pouches or gastric fistulas.2. In cats with gastric fistulas, doses of N‐methylhistamine of 0·25 or 0·5 μmole/hr produced 1·4–1·6 times as much HCl as equimolar doses of histamine.3. The maximal HCl outputs of dogs with Heidenhain pouches to histamine, N‐methylhistamine, and N‐dimethylhistamine were not significantly different, though lesser doses of the N‐methyl derivatives were required to produce the maxima. At the one‐half maximal level, N‐dimethylhistamine showed a twofold greater potency than histamine.4. When given slowly or quickly via arteries supplying blood to the stomach of dogs or cats with gastric fistulas or via the artery to a Heidenhain pouch in a dog, 0·1–1·0 μmole N‐methylhistamine or N‐dimethylhistamine produced 4·1–13·9 times as much HCl as equimolar doses of histamine.5. Injection of histamine or N‐methylhistamine via the portal vein in two dogs with gastric pouches stimulated less secretion of HCl than injection of the same doses via a systemic vein.6. The results allow the conclusion that N‐methylhistamine and N‐dimethylhistamine are more potent stimulators of acid gastric secretion than histamine in dogs and cats, particularly when delivered directly via the arterial route to the gastric mucosa, and support the prospect that N‐methylhistamine or N‐dimethylhistamine or both are natural chemostimulators of the parietal cells.
Some properties of a preparation of rat colon perfused in vitro through the vascular bed
Authors: Parsons D. S. , Powis G. 
Published: December 2014

1. A technique is described for the perfusion of the isolated colon of the rat, involving the infusion of an appropriate fluid through both the inferior and the superior mesenteric arteries. During neither the preparation nor the subsequent perfusion is the colon without an adequate supply of oxygen. The preparation remains histologically intact and metabolically viable and is capable of actively transporting ions for up to 5 hr.2. The addition of at least 3 g albumin/100 ml. perfusate is necessary to prevent the formation of large quantities of serosal exudate. With erythrocytes added to the vascular perfusate the preparation appears to be adequately oxygenated as judged by measurements of the rate of glycolysis. The mean rate of oxygen utilization over 4 hr is 9·2 ± 0·3 (4) μmole. hr−1.g−1 fat free dry weight.3. Ion transport rates approaching those found in vivo are found only after the administration of an antihistamine substance to the colon donor rat before operation. In the absence of an antihistamine substance there appears to be an ultrafiltration of the plasma fluid into the lumen.4. Vasodilatory substances accumulate in the recycled perfusate. In a ‘single pass’ perfusion, the transport capacity of the preparation decreases at high perfusion pressures. It is suggested that this is due to some form of autoregulation whereby perfusate is shunted away from the epithelium into deeper layers as the pressure is increased.5. With CO2 absent from the vascular infusate there is an increase in the net lumen to blood flux of total CO2. This increased flux is accompanied by an equivalent amount of cation, comprising Na+ and K+ in the ratio of 12:1.6. The presence of ammonium in the lumen, a physiological constituent of the contents of rat distal colon in vivo, has a marked inhibitory effect upon the secretion of CO2 into the contents of the lumen of the colon.
Storage of ATP and 5‐hydroxytryptamine in blood platelets of guinea‐pigs
Authors: Da Prada M. , Pletscher A. , Tranzer J. P. 
Published: December 2014

1. By density gradient centrifugation of homogenized blood platelets of guinea‐pigs, subcellular organelles have been isolated which exhibit much higher concentrations (μmole/μg protein) of ATP than the whole platelets.2. The organelles also store endogenous 5‐HT whose concentration is, however, considerably inferior to that of ATP.3. Investigated by electron microscopy most of the isolated organelles look empty and only very few show dense osmiophilic cores indicating the presence of 5‐HT. Accordingly the occurrence of dense osmiophilic organelles in the whole platelets is also very rare.4. Exogenous 5‐HT taken up by the platelets markedly accumulates in the subcellular fraction containing the organelles storing ATP. Concomitantly, the platelets show a rise in the number of osmiophilic organelles and the frequency of osmiophilic cores in the isolated organelles is increased.5. From these and previous in vitro experiments it is concluded that the so called 5‐HT storage organelles of blood platelets primarily store ATP and only subsequently accumulate 5‐HT.
Effect of microcirculation changes on brain tissue oxygenation
Authors: Bicher H. I. , Bruley D. , Knisely M. H. , Reneau D. D. 
Published: December 2014

1. A new, 2 μ tip, oxygen micro‐electrode and a constantly circulated Beckman oxygen gas analyser were used to measure tissue and blood PO2 in anaesthetized, curarized cats under positive pressure breathing. As a parameter for the ability of the circulation to oxygenate tissue, the ‘reoxygenation time’ (defined as the time required to reach the previous PO2 level after a short period of anoxic anoxia) was determined on blood and cerebral cortex.2. First, it was found that haemorrhage (from 15–25 c.c./kg) alone or haemorrhage combined with sludging of the blood (by the
I.V. administration of high molecular weight Dextran, 1 g/kg) markedly diminished PO2 levels in blood and tissue.3. Further, the reoxygenation time was significantly affected by these procedures. Sludging markedly prolonged the reoxygenation time, an effect counteracted by the use of an anti‐adhesive drug breaking up the red cell aggregates.4. Bleeding prolonged the reoxygenation time up to four times that found in the same animals previous to the bleeding.
Induction of the action potential mechanism in slow muscle fibres of the frog
Authors: Miledi R. , Stefani E. , Steinbach A. B. 
Published: December 2014

1. The electrical and structural characteristics of ‘slow’ muscle fibres of the frog were studied in normal and denervated muscles, and in muscles undergoing re‐innervation by a mixed nerve containing large and small motor axons.2. In agreement with previous studies, slow fibres in normally innervated muscles were incapable of producing action potentials.3. Approximately 2 weeks after the sciatic nerve was transected or crushed, slow muscle fibres acquired the ability to generate action potentials. These fibres were positively identified as belonging to the slow type, because their passive‐electrical and ultrastructural characteristics remained essentially unchanged after the operations.4. The action potential mechanism induced in slow fibres is sodium‐dependent, and is blocked by tetrodotoxin.5. After long‐term re‐innervation by a mixed nerve, slow fibres lose their acquired ability to generate action potentials, presumably because small motor axons re‐establish connexion with the fibres.6. It is concluded that the action potential mechanism of slow muscle fibres is under neural control, and is normally suppressed by small motor axons.
The effect of calcium on the force‐velocity relation of briefly glycerinated frog muscle fibres
Authors: Julian F. J. 
Published: December 2014

1. Twitch fibres were isolated from the semitendinosus muscles of frogs. The sarcolemma was made more permeable by a 30 min soak in a solution containing 47·3% glycerine (v/v), 2 m
M‐EGTA and 10 m
M phosphate buffer, pH 7. This was followed by a 30–60 min soak in a solution containing the non‐ionic detergent Lubrol‐WX. The fibres were then placed in a relaxing medium containing (in m
M): KCl, 100; MgCl2, 1; ATP, 4; EGTA, 2; imidazole buffer, 10; pH 7·0.2. A piece of fibre about 1‐2 mm long treated as described in (1) was attached to a servo apparatus. This apparatus made it possible either to hold fibre length constant giving isometric conditions, or alternatively to hold the force constant while measuring isotonic length changes. A special network made it possible to switch control from isometric to isotonic conditions so that afterloaded contractions with a shortening stop could be carried out.3. Contractions were induced at about 4° C by lowering the pCa in the relaxing solution to various levels determined by the ratio of calcium and EGTA added. Contractions were never observed above pCa 7. The steady force generated reached a maximum over the range of pCa 6·09 to 5·49. The relationship between steady force generated and pCa is S‐shaped and very steep, implying that multiple interacting binding sites for calcium are involved in the force generating process.4. The relative force—velocity relation is the same at pCa 6·09 and 5·49 where the steady force is at a maximum. The data points can be well fitted by a hyperbola in which the extrapolated value for Vmax is 2·39 muscle lengths/sec. The values obtained for the Hill parameters a/P0 and b are within the range of those reported for living electrically excited frog muscle.5. The relative force—velocity points obtained at higher pCa values at which the steady force was on average 37% of that developed at pCa 5·49 can also be fitted by a hyperbola. However, the extrapolated value for Vmax is only 1·12 muscle lengths/sec. The value for a/P0 is increased slightly and the value for b is markedly decreased.6. Evidence is presented against the possibility that an unrecognized fixed internal load is responsible for the change in the relative force—velocity relation obtained at high pCa.7. The relative force—velocity relation does not change appreciably over at least part of the range of sarcomere lengths in which the force generated varies linearly with overlap provided the pCa is held constant.8. The results support the view that lowering the pCa produces a mechanical state equivalent to that produced by tetanic electrical stimulation.9. Some models for calcium activation are discussed. It is concluded that a model based on calcium binding to troponin on the thin filaments is difficult to reconcile with all of the experimental evidence. There is additional evidence for believing that activating calcium may directly influence the cross‐bridges.
Enhancement of the post‐occlusive oscillation in the splenic circulation by adenosine
Authors: Hashimoto Koroku , Satoh Susumu 
Published: December 2014

1. The blood flow to the splenic artery of dogs anaesthetized with sodium pentobarbitone was measured under constant pressure perfusion with the animal's own blood led from the femoral artery.2. Immediately after release of occlusion there was a rapid increase of inflow rate above the pre‐occlusion level which then oscillated up and down. In a majority of cases such oscillatory responses continued for a while but progressively diminished during a period of about 6 min.3. This post‐occlusive oscillatory response was not modified by either neural or autonomic receptor blocking agents such as tetrodotoxin, guanethidine, phentolamine, propranolol, atropine and methysergide.4. In the cases with a relatively short‐lasting response, the selective administration of adenosine into the splenic artery caused a distinct enhancement of the oscillation.5. These results suggest that adenosine may play an important role in the post‐occlusive oscillatory response of the splenic circulation.
Thermoregulation around a new ‘set‐point’ established in the monkey by altering the ratio of sodium to calcium ions within the hypothalamus
Authors: Myers R. D. , Yaksh T. L. 
Published: December 2014

1. The cerebral ventricles of the unanaesthetized monkey were perfused at a rate of 50–100 μl./min with artificial cerebrospinal fluid (c.s.f.) containing 11·0–34·0 m
M excess sodium or 23·9–47·9 m
M excess calcium ions. By repeated perfusions, a marked hyperthermia elicited by excess sodium or deep hypothermia by excess calcium was sustained for up to half a day.2. During the sodium‐induced hyperthermia or calcium‐induced hypothermia, the monkey thermoregulated adequately around the new level of temperature in response to either 50 or 150 ml. water heated to 58° C or chilled to 0° C and given by the intragastric route. Cold water produced a transient hypothermia after which temperature returned to the pre‐load level; hot water given in the same way evoked a short‐lasting hyperthermia, and again the temperature returned just to the new setpoint level.3. Perfusions at 50 μl./min of isolated areas of the diencephalon by means of push‐pull cannulae with a solution containing 11·0–34·0 m
M excess sodium ions or 11·3–47·9 m
M excess calcium ions altered the body temperature of the monkey only when the sites of perfusion were located in the mammillary region of the posterior hypothalamus. Following the prolonged hyperthermia produced by excess sodium ions or the deep hypothermia evoked by excess calcium ions in the push‐pull perfusion fluid, the monkey thermoregulated around the new temperature level again in response to 150 ml. of either hot or cold water given in the stomach.4. Chelation of calcium ions within the ventricles by perfusing EGTA through the cerebral ventricles caused a long‐lasting elevation in temperature. When EGTA was perfused directly in the posterior hypothalamus by means of push‐pull cannulae, a profound hyper‐pyrexia ensued which could be abolished immediately by perfusing a solution of excess calcium at the same diencephalic site.5. During the calcium‐induced hypothermia, the heart rate declined but the electrical activity of the cortex was relatively unchanged. Feeding was also elicited in the hypothermic monkey by noradrenaline microinjected at a site in the hypothalamus at which eating was evoked when the body temperature was normal.6. The evidence supports the hypothesis that in the primate, the inborn mechanism which establishes the set‐point for body temperature at 37° C is the constancy in the intrinsic ratio between sodium and calcium ions within the posterior hypothalamus. If the set‐point is elevated or lowered by a disturbance of the balance between these two cations, the monkey nevertheless can thermoregulate normally around the new level of body temperature.