bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of dietary intake of sodium chloride on sugar and amino acid transport across isolated hen colon
Authors: Lind J. , Munck B. G. , Olsen O. 
Published: December 2014

1. Using the isolated mucosa from the colon of the adult hen, transport of galactose, leucine and lysine was studied through measurements of influx across the brush‐border membrane, unidirectional transmucosal fluxes, and of steady‐state mucosal uptake.2. In hens maintained on a NaCl rich diet influx of galactose, leucine and lysine were saturable processes with well defined values for Jmax and Kt. All three substances were actively transported across the epithelium and accumulated in the mucosal tissues to steady‐state concentrations several times higher than in the incubation media.3. In hens maintained on a NaCl poor diet the Kt of the leucine influx was markedly increased and the Jmax moderately decreased, while the epithelium maintained the capability of active transepithelial transport and of establishing a steady‐state tissue/medium distribution ratio well above 1. Galactose and lysine could no longer be actively transported and in the steady state their tissue concentrations did not exceed those of the medium.4. It is proposed that in the low NaCl colon the processes of galactose and lysine co‐transport with Na are abolished and that the transport of galactose proceeds via a phloretin sensitive system like that described for the enterocyte of the chicken small intestine.5. In the high NaCl colon 1 m
M‐leucine increases the mucosa to serosa flux of lysine by a factor 2·8 without affecting the serosa to mucosa flux or the steady‐state mucosal accumulation of lysine. In the low NaCl colon 1 m
M‐leucine induces active transepithelial transport of lysine. Assuming that the active transport of leucine is secondary to the transport of Na, leucine‐induced active transport of lysine is described as a tertiary active transport.6. In the high NaCl colon the mucosa to serosa flux and the steady‐state mucosal accumulation of leucine were inhibited by galactose which had no effect on leucine influx across the brush‐border membrane. Leucine did not affect any of the parameters of galactose transport.
Atropine does not abolish cephalic vagal stimulation of gastrin release in dogs
Authors: Dockray G. J. , Tracy Hilda J. 
Published: December 2014

1. The effect of atropine was studied on serum gastrin responses to feeding in conscious gastric fistula dogs. Intragastric pH was monitored and could be maintained at pH 6·0 by infusion of sodium bicarbonate into the gastric fistula.2. A standard liquid meal was consumed by the dogs in less than a minute. Serum gastrin increased from a basal concentration of 8 pmol/l to a peak of 27 pmol/1 at 4‐7 min, and intragastric pH fell to less than 3·0 after 20 min. Since vagotomy abolished the early gastrin response to feeding, and instillation of the meal directly into the fistula produced only a modest and delayed increase in serum gastrin, we conclude that cephalic vagal stimulation played a major part in mediating the gastrin responses. When intragastric pH was maintained at 6·0 serum gastrin was significantly higher at all times from 4 to 50 min after feeding, indicating the importance of acid inhibition in the control of gastrin secretion.3. After atropine (25 or 100 μg/kg), acid secretion was abolished and intragastric pH was about 6·0 at all times. The low dose of atropine enhanced the gastrin response to feeding, but the time course and magnitude of the response closely resembled that to normal meals pH‐stated to 6·0. The high dose of atropine decreased, but did not abolish serum gastrin responses to feeding.4. When the meal was allowed to drain freely from the gastric fistula (virtually eliminating stimulation of gastrin release by luminal mechanisms) serum gastrin again reached a peak after 4‐7 min, and neither dose of atropine significantly changed the response.5. It is concluded that cephalic vagal stimulation of gastrin release is atropine resistant and so unlikely to be mediated by muscarinic receptors. The enhanced gastrin response to feeding caused by moderate doses of atropine can be attributed to the loss of acid inhibition of gastrin release. The neuropeptide bombesin is a candidate neurotransmitter for the action of post‐ganglionic vagal nerves on gastrin cells.
Increased myometrial blood flow evoked by vasoactive intestinal polypeptide in the non‐pregnant goat
Authors: Carter A. M. , Einer‐Jensen N. , Fahrenkrug J. , Ottesen B. 
Published: December 2014

1. The effect of vasoactive intestinal polypeptide (VIP) on myometrial blood flow was evaluated in anaesthetized goats. A solution of VIP, or vehicle alone, was infused into the right internal iliac artery for a period of 10 min. The myometrial blood flow in both uterine horns was measured from the third to the seventh min of the infusion by the gas clearance technique after local injection of 133xenon in 10 μl. saline solution. Blood samples were collected from both utero‐ovarian veins 5 min from the onset of the infusion and the plasma concentration of VIP determined by radio‐immunoassay.2. During infusion of vehicle before VIP, myometrial blood flow was of the same magnitude in both uterine horns, i.e. 0·06‐0·12 ml./min per g. The blood flow of the right horn increased to 0·20‐0·39 ml./min per g during infusion of VIP (300 p‐mole/min) in the ipsilateral artery, whilst that of the left horn rose to 0·13‐0·26 ml./min per g. The effect was sometimes observed to last for more than 40 min.3. Increased myometrial blood flow was observed with infusion rates down to 3 p‐mole/min. Once a response to VIP had been provoked, however, the vasculature sometimes became refractory to further stimulation.4. The plasma concentration of VIP increased in both utero‐ovarian veins during unilateral infusion of the peptide.5. Methylene blue given through the infusion catheter stained tissue in both uterine horns, further evidencing that their blood supply is not entirely separate.6. Uterine motility was observed to diminish during the VIP infusions.7. During infusion of VIP (300 p‐mole/min) heart rate rose from 146 ± 6 to 158 ± 7 beats/min. No significant change occurred in arterial blood pressure.8. It is concluded that the increase in blood flow is due to a local response and that, since VIP has been demonstrated in uterine nerve endings, it may act as a neuro‐transmitter mediating vasodilatation in the uterus.
Properties of end‐plate channels in rats immunized against acetylcholine receptors
Authors: Alemà S. , Cull‐Candy S. G. , Miledi R. , Trautmann A. 
Published: December 2014

1. Rats injected with purified acetylcholine receptors (AChR) extracted from electric organs of Torpedo marmorata showed clinical symptoms consistent with the development of experimental myasthenia gravis.2. Sera of rats with this disease contain high levels of anti‐AChR antibodies. However, no simple correlation was found between antibody titre and miniature end‐plate current (m.e.p.c.) amplitude.3. M.e.p.c.s. at the end‐plates of rats injected with AChR (Anti‐R), emulsified in complete Freund Adjuvant (CFA), were reduced to about one third the size of controls taken from rats injected only with CFA (Anti‐CFA). Mean m.e.p.c. (Anti‐R) = 0.73 ± 0.06 nA; mean m.e.p.c. (Anti‐CFA) = 2.43 ± 0.12 nA (Vm = ‐80 mV, T = 20 °C).4. The m.e.p.c. decay time constant, τm.e.p.c., is similar at immunized and control rat end‐plates. τm.e.p.c. (Anti‐R) = 1.32 ± 0.06 msec; τm.e.p.c. (Anti‐CFA) = 1.31 ± 0.06 msec (Vm = ‐80 mV, T = 20 °C).5. The end‐plate current decay time constant, τe.p.c., is similar at immunized and control end‐plates and in both cases depends exponentially on membrane potential. The change in membrane potential required to produce an e‐fold change in τe.p.c. is 102.0 ± 5.72 mV at immunized (Anti‐R) end‐plates and 92.3 ± 6.14 mV at control (Anti‐CFA) end‐plates at T = 10 °C.6. Acetylcholine noise was examined at immunized and control rat end‐plates at 10 °C. Analysis of noise indicates that the single channel conductance, γ, and mean channel life‐time, τnoise, are essentially unchanged by immunization against AChR. γ (Anti‐R) = 13.15 ± 0.53 pS; γ (Anti‐CFA) = 12.50 ± 0.50 pS; τnoise (Anti‐R) = 2.9 ± 0.18 msec; τnoise (Anti‐CFA) = 2.68 ± 0.14 msec (Vm = ‐80 mV, T = 10 °C).7. Mean quantal content and Ca2+ dependence of the end‐plate potential are unchanged at immunized end‐plates.8. It is concluded that at immunized end‐plates the number of activated receptor‐channel complexes is reduced without modification of single channel properties. In this respect the immunized rat end‐plate is a good model for myasthenia gravis affected human end‐plates.
Enhancement and diminution of mechanical tension evoked by staircase and by tetanus in rat muscle
Authors: Krarup Christian 
Published: December 2014

1. Potentiation of the isometric twitch tension was compared during and after the staircase and after tetanic stimuli in the fast‐twitch extensor digitorum longus muscle of adult Lewis rats at 37‐38°C.2. With up to 250 stimuli the potentiation rose with an increase in both the frequency and number of stimuli in the staircase (2‐5/sec) and the tetanus (100‐167/sec). After a tetanus of 375 stimuli (125/sec) the potentiation was smaller. The potentiation 2 sec after a tetanus of 250 stimuli (167/sec) was + 132 ± 5% (n = 21,
s.e. of mean) which was greater (P < 0·001) than at the 250th stimulus at 5/sec, +92±3% (n = 21,
s.e. of mean).3. After the staircase the decay of potentiation was initially slow and later more rapid. This was taken to indicate both the recovery of a process that diminished twitch tension and the decay of a process causing potentiation. After 250 stimuli (5/sec) the rate of decay of the processes causing diminution and potentiation had time constants of 34·5 ± 3·8 sec (n = 18,
s.e. of mean) and 102·2 ± 6·6 sec (n = 20,
s.e. of mean) respectively. Compared with the potentiation, the process causing diminution became relatively more pronounced the greater the frequency of stimuli.4. The decay of post‐tetanic potentiation showed an initial rapid and a later slower phase of decay. After a tetanus of 250 stimuli (167/sec) the rates of decay had time constants of 5·7 ± 0·8 sec (n = 16,
s.e. of mean) and 113·5 ± 8·7 sec (n = 19,
s.e. of mean) respectively.5. Compared with the unpotentiated response the time course of the twitch was shortened initially in the staircase and when the post‐tetanic potentiation was low. The contraction time was then increasingly prolonged the greater the potentiation and the greater the number of stimuli in the staircase and in the tetanus. The half‐relaxation time was the more prolonged the greater the number of stimuli.6. Potentiation can be described in terms of a two‐compartment model of processes which show saturation. Both compartments were activated in a tetanus whereas only the compartment with a slow rate of decay was activated in the staircase. It is speculated that the two compartments are related to the excitation—contraction coupling. The process that caused diminution of twitch tension during the staircase may be due to fatigue. It is suggested that the energy consumption in 250 twitches is about 10 times greater than in a tetanus of 250 stimuli which may explain the presence of fatigue after the staircase whereas it was absent after the tetanus.
Temperature dependence of enhancement and diminution of tension evoked by staircase and by tetanus in rat muscle
Authors: Krarup Christian 
Published: December 2014

1. The effect of temperature (20‐37·5 °C) on the potentiation of twitch tension was examined during and after the staircase (250 stimuli, 5/sec) and after the tetanus (188 stimuli, 125/sec) in the extensor digitorum longus muscle of adult Lewis rats.2. During the staircase at 20°C the twitch tension decreased (negative staircase) by 10‐20%. At 25‐30°C the staircase was initially negative and later positive. At 37·5°C the staircase was positive throughout the train. Both at the end of the staircase and 2 sec after the tetanus the potentiation increased linearly with increasing temperature.3. After the staircase and the tetanus at 20‐30°C the twitch tension increased initially rapidly and later after the staircase at a slower rate. Maximal potentiation at 20°C was attained 3 min after the staircase (+ 30 ± 3%, n = 10,
s.e. of mean) and 1 min after the tetanus (+ 16 ± 1%, n = 10,
s.e. of mean). At 37·5°C the potentiation decayed rapidly after the staircase and the tetanus.4. During the staircase the time course of the twitch was shortened twice as much at 20 as at 37·5°C. At the end of the staircase and 2 sec after the tetanus the contraction time was the more prolonged the greater the potentiation. At maximal potentiation the contraction time was prolonged three times as much at 20°C (+ 19 ± 3%, n = 10,
s.e. of mean) as at 37·5°C (P < 0·005). The half‐relaxation time at the end of the staircase was prolonged 10 times more at 20 than at 37·5°C (P < 0·02).5. When extrapolated to time zero after the staircase and the tetanus the potentiation at 20°C was still marked (20‐50%). The rate of decay of potentiation (time constant, 20°C, 561·2 ± 37·4 sec, n = 20,
s.e. of mean) increased with increasing temperature (Q10 = 2·6). The event of potentiation with a fast rate of decay, present after the tetanus but not after the staircase at 37·5°C, was abolished below 30°C.6. The increase in twitch tension after the staircase and the tetanus at 20‐30°C was taken to indicate the recovery of events that diminished the twitch, occurring simultaneously with potentiation.7. (i) One process of diminution, present after the staircase but not after the tetanus, increased on cooling and was assumed to be due to fatigue. The rate of recovery of the process (time constant, 20°C, 79·6 ± 7·4 sec, n = 10,
s.e. of mean) increased with increasing temperature (Q10 = 1·9). The half‐relaxation time of the last twitch in the staircase was the more prolonged the greater the process. (ii) Another process causing diminution was present after the staircase and the tetanus at 20‐30°C. It recovered at 20°C with a time constant of 14·9 ± 2·2 sec (n = 10,
s.e. of mean). This process, possibly responsible for the initially negative staircase, was not thought to be due to fatigue. It may reflect a diminished depolarization of the transverse tubules by repetitive stimuli.
The effect of dantrolene on the enhancement and diminution of tension evoked by staircase and by tetanus in rat muscle
Authors: Krarup Christian 
Published: December 2014

1. The effect of Dantrolene on the potentiation of isometric twitch tension was examined during and after the staircase (5/sec, 250 stimuli) and after the tetanus (167/sec, 250 stimuli) in the extensor digitorum longus muscle of adult Lewis rats at 37‐38°C.2. The study confirmed that Dantrolene decreased the twitch tension much more than the tetanic tension. The drug shortened the contraction time of the twitch. The rate of force development of the twitch was diminished by only half that of the twitch tension. The findings may suggest that the drug both shortened and diminished the activation of the muscle during the twitch.3. Dantrolene decreased the potentiation produced by a given number of stimuli early in the staircase. At the 250th stimulus the staircase was about 25% larger after than before application of the drug. Dantrolene increased the potentiation 2 sec after the tetanus by about 60%.4. After application of Dantrolene, the decay of potentiation after the staircase indicated that the process that diminished the twitch during the staircase, present before application of the drug, was absent. The size of the process causing potentiation was the same with and without the drug. Both events of potentiation after the tetanus were increased by Dantrolene. Both after the staircase and after the tetanus, Dantrolene increased the slow phase of decay by 60‐70%. The fast rate of decay after the tetanus was unchanged by the drug.5. The contraction time was prolonged less in the potentiated twitch after than before application of Dantrolene. This was presumably due to a greater relative increase in activation rather than to a prolongation of the time during which the muscle was activated.6. A model is proposed where the delay in potentiation during the staircase and the increase in potentiation after the tetanus are due to the proportion of sites in the excitation—contraction coupling occupied by Dantrolene being reduced by repetitive depolarizations of the transverse tubules during trains of repetitive stimuli.
The inotropic actions of adrenaline on frog ventricular muscle: relaxing versus potentiating effects
Authors: Morad Martin , Sanders Chris , Weiss James 
Published: December 2014

1. In frog ventricle, adrenaline increases the size of the action potential, potentiates twitch tension, and enhances relaxation. Because tension development is directly controlled by membrane potential in frog ventricle, experiments were designed to separate the effects of adrenaline on the action potential from its effects on the development of tension.2. Comparison of the tension—voltage relations in the presence and absence of adrenaline showed that during the initial portion of the voltage clamp step, adrenaline potentiated tension, but beyond 1 sec into the clamp pulse tension was depressed.3. The time and voltage dependence of the positive inotropic effect of adrenaline during voltage clamp pulses were compatible with the kinetics of the slow inward current, which is known to be augmented by adrenaline in frog and mammalian ventricle.4. Ni2+, which has been shown to block the slow inward current in frog ventricle, also inhibited the positive inotropic effect of adrenaline.5. The relaxant effect of adrenaline was demonstrated to be present at least as early as 600 msec after the onset of membrane depolarization. However, generally 1 sec or more of membrane depolarization was required before the relaxant effect of adrenaline predominated over its positive inotropic effect.6. In catecholamine depleted strips, the augmentation of the action potential and twitch tension in the presence of adrenaline was found to occur at a sixty‐fold lower concentration than the relaxant effect as judged by suppression of KCl‐induced contractures.7. Pure β‐receptor agonists reproduced completely the electromechanical effects of adrenaline on the frog ventricle. α‐receptor agonists or antagonists had no effect on action potential or development of tension.8. Cyclic AMP and dibutyryl cyclic AMP were found to augment the frog ventricular action potential and potentiate twitch tension in reserpinized or β‐blocked frog ventricular strips. However, none of the relaxant effects of catecholamines could be reproduced by these agents alone.9. Theophylline produced changes in the action potential similar to those induced by adrenaline and mimicked both the positive inotropic and relaxant effects of the drug.10. The results suggest that the positive inotropic effects of adrenaline results mainly from changes induced in the action potential plateau. The changes are both time and voltage dependent, and if inhibited, leave the relaxant effect of adrenaline unopposed.11. The findings are consistent with a cyclic AMP‐mediated mechanism of the positive inotropic effect of adrenaline. However, the role of cyclic AMP in mediating the relaxant effects of adrenaline is less clear.
The effect on salt appetite and the renin—aldosterone system on replacing the depleted ions to sodium‐deficient cattle
Authors: Bell F. R. , Drury P. L. , Sly Jennifer 
Published: December 2014

1. Sodium depletion which occurred in cattle following exteriorization of a parotid duct produced depression of both plasma and salivary sodium, acidosis, elevated plasma aldosterone and renin activity. Increased sodium appetite, characteristic of sodium depletion, was assessed by operant behaviour where scoring of panel pressing for NaHCO3 rewards showed change in sodium appetite.2. Sodium‐depleted calves readily drank the calculated ionic deficit as a hypertonic solution (4 l.) in a few minutes, or as an isotonic solution (16 l.) usually within 30 min.3. When the ionic deficit was restored by either
i.v. infusion or drinking, sodium appetite was reduced significantly. The suppression of sodium appetite was more rapid when the depleted ions were replaced by drinking (30 min) than by
i.v. infusion (2 hr) but in both circumstances the effect was short lived since sodium appetite redeveloped within 3 hr.4. The rapid return of sodium appetite following restoration of the ionic deficit occurred even when the plasma sodium level was normal. Other biochemical changes resulting from sodium depletion, such as acidosis and reduced salivary sodium, could not be correlated with variation in sodium appetite.5. Rapid infusion of Ringer saline (4 l.) did not inhibit the sodium appetite, which suggests that neither vascular volume changes per se nor vascular baroreceptors control sodium appetite in sodium‐deficient calves.Plasma aldosterone fell rapidly following infusion of the hypertonic solution but only slightly with the isotonic infusion. The change in plasma hormone level was not related to changes in sodium appetite.6. Drinking the hypertonic solution produced a marked reduction in panel pressing for NaHCO3 with a rapid rise in plasma sodium. Consumption of the larger volume of isotonic solution also inhibited sodium intake but plasma sodium remained low. A secondary increase in plasma renin activity (p.r.a.) occurred following ingestion of the hypertonic solution, but both p.r.a. and aldosterone fell to normal levels over the next 6 hr when the cattle again showed marked sodium appetite. It is possible that these effects may be due to ion and fluid movement between gut and extracellular fluid and reflect osmolality changes or tissue dehydration.7. It is concluded that the sodium appetite of sodium deficient cattle is only temporarily alleviated by restoration of the depleted ionic loss, and that the behavioural response to seek sodium rewards is independent of plasma sodium, p.r.a., aldosterone and volume changes in the gut and vascular system.8. Recent reports suggest that sodium appetite may be controlled by receptors in the hypothalamus or by angiotensin II in the brain. In cattle the capacious gut may also be involved, since sodium appetite is inhibited more rapidly when the depleted ions are taken orally than by
i.v. infusion.
Responses of pontine units to skin‐temperature changes in the guinea‐pig
Authors: Hinckel P. , Schröder‐Rosenstock K. 
Published: December 2014

1. The responses of fifty‐five single units to changes in skin temperature were recorded in twenty‐three guinea‐pigs anaesthetized with urethane. Skin‐temperature changes were induced by changing the temperature of the water‐perfused support plate of the stereotaxic apparatus and that of the double‐walled Perspex jacket that was put on the support plate.2. Thirty‐three units were stereotaxically and histologically verified as being within a circumscribed area of the pontine dorsomedial reticular formation (subcoeruleus region). Twenty‐one units were located in the surrounding areas, and one unit in the nucleus raphé magnus region.3. Twenty‐seven of thirty‐three recorded subcoeruleus units were specifically excited by cooling of the abdominal or leg skin, whereas only five units were non‐thermoresponsive and one unit was warm‐responsive. The cold‐responsive units had peak activity at skin temperatures between 22 and 29 °C, in accordance with the maximum activity in cutaneous cold‐receptors.4. A markedly different distribution of units was found in the surrounding areas. Only four units were cold‐responsive. Thirteen units were non‐thermoresponsive, and four units were warm‐responsive.5. The cold‐responsive subcoeruleus units were situated in regions which are known to contain accumulations of noradrenergic cell bodies, and to project to hypothalamic neurones. Electrical stimulation of these regions is known to cause excitatory metabolic responses in unanaesthetized guinea‐pigs. It is concluded that part of the cutaneous cold‐afferents projects to hypothalamic thermointegrative neurones via noradrenergic pathways that ascend from these subcoeruleus regions.