bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inward movement of sodium ions in resting and stimulated frog's sartorius muscle
Authors: Venosa R. A. 
Published: December 2014

1. Paired frog sartorius muscles were exposed to Ringer solutions labelled with 22Na+ for about 20 min. At the end of this exposure one of them was stimulated supramaximally one hundred to two hundred times. Immediately after the stimulation both members of the pair were washed in a series of tubes filled with a Na+‐free medium containing 3 × 10−5
M strophanthidin.2. Under the above conditions the intracellular component of the efflux was exponential with an average time constant (τ) of 388 min, that is, approximately four times longer than in the presence of normal Ringer. On the other hand the mean τ for the washout of the interfibre space was 3·2 min.3. From the extrapolation to time zero of the intracellular component of the washout curve the initial intracellular radioactivity of both muscles was obtained and the resting and extra Na+ influx were calculated.4. The mean surface membrane area/muscle weight ratio was found to be 552 cm2.g−1 and the mean fibre diameter 53·4 μm for muscles weighing on the average 60 mg.5. The average resting Na+ influx in the presence of normal Ringer was 4·7 p‐mole.cm−2.sec−1. As the external Na+ concentration ([Na+]0) was reduced the Na+ influx diminished in a non‐linear fashion. This non‐linearity could be accounted for by the presence in the influx of a Na+ for Na+ exchange fraction which saturates at low [Na+]0.6. The mean extra Na+ influx in the presence of normal Ringer was 27·4 p‐mole.cm−2.impulse−1 and was not significantly affected either by halving [Na+]0 or by varying the frequency of stimulation. When [Na+]0 was reduced to 45 m
M by partial replacement of Na+ by Tris+ the extra influx was significantly higher than when choline+ instead of Tris+ was used to substitute for Na+.
Evidence for the involvement in the baroreceptor reflex of a descending inhibitory pathway
Authors: Coote J. H. , Macleod Valerie H. 
Published: December 2014

1. The onset and time course of baroreceptor inhibition of pre‐ and post‐ganglionic sympathetic reflex activity has been examined in the anaesthetized cat.2. The shortest time to the onset of inhibition of an intercostal evoked reflex response in cardiac and renal nerve was less than 90 msec following a rise in pressure in a carotid sinus blind sac, and around 55 msec following stimulation of the ipsilateral sinus nerve. The cardiac nerve response was completely inhibited before the renal nerve response.3. Because of the long delays in the somato‐sympathetic reflex pathway it is argued that these minimum times will be much less than the real central delay of baroreceptor inhibition. These were estimated by adding on the central times for the somato‐sympathetic reflexes to give latencies of 94–143 msec for the inhibition.4. A spinal sympathetic reflex was inhibited by 30–75% following a rise in pressure in a carotid sinus blind sac or sinus nerve stimulation. The minimum time for this inhibition was around 100 msec.5. The baroreceptor inhibition of the spinal sympathetic reflex was abolished following section of a restricted region in the dorsolateral part of the lateral funiculus of the cervical spinal cord.6. Both pre‐ and post‐ganglionic reflexes could be inhibited when stimulating within three regions of the medulla oblongata. The latency to inhibition elicited from the ventromedial reticular formation was short, some 5‐30 msec, whereas that elicited from a ventrolateral region or the mid line raphe nucleus was long, some 90–160 msec.7. The possibility is discussed that the baroreceptor inhibition of both the pre‐ and post‐ganglionic reflexes examined in this study is occurring at the spinal level via a pathway from either the raphe nuclei or ventrolateral medulla.
Renin and angiotensin‐like levels in foetal, new‐born and adult sheep
Authors: Pipkin Fiona Broughton , Kirkpatrick S. Margaret L. , Lumbers Eugenie R. , Mott Joan C. 
Published: December 2014

1. Plasma renin (measured as rate of formation of angiotensin I ng/ml.hr−1 in the presence of added substrate at pH 7·5 and 37° C) was much lower in recently nephrectomized foetal, new‐born and older lambs than in intact siblings or other similar lambs.2. Angiotensin II‐like concentrations were measured using a superfusion technique in an extracorporeal circuit. Resting concentrations in acute experiments under anaesthesia were deduced by comparison of carotid blood of intact lambs with that from recently nephrectomized lambs.3. Angiotensin II‐like activity (mean ±
S.E. of mean, 315 ± 117 pg/ml.) was readily detectable in foetal blood at 123–138 days gestation. The highest concentrations (mean ±
S.E. of mean 839 ± 96 pg/ml.) were found in lambs less than 8 hr old, delivered vaginally. The lowest concentrations of angiotensin II‐like activity occurred in lambs delivered by Caesarean section (mean ±
S.E. of mean < 123 ± 12 pg/ml.). Concentrations declined with post‐natal age.4. Hypovolaemia as a result of haemorrhage evoked an increase in angiotensin II‐like concentrations in foetus, new‐born lambs and adult sheep. The greatest increase of angiotensin‐like concentrations was seen in new‐born lambs. This rise was associated with increase of plasma renin.5. The rise of arterial pressure during bilateral carotid occlusion in new‐born lambs was accompanied by an increase of angiotensin II‐like concentration.6. It is concluded that the renin‐angiotensin system is functional and can be stimulated during intra‐uterine life. The increase of angiotensin II‐like concentration following parturition is probably transient and associated with the trauma of delivery. This contrasts with observations made in the rabbit which suggest that full functional maturity of the renin angiotensin system is delayed until the second week of life.
Circulatory effects of deep inspirations, blocked expirations and positive pressure inflations at equal transpulmonary pressures in conscious dogs
Authors: Charlier André A. , Jaumin Pierre M. , Pouleur Hubert 
Published: December 2014

1. Circulatory effects of deep inspirations, blocked expirations and constant endotracheal positive pressure inflations were studied in six conscious dogs under comparable geometries of the pulmonary vascular bed, i.e. at equal transpulmonary pressures (around 10·2 cm H2O) and similar lung volumes.2. In order to characterize these effects, we measured beat‐by‐beat left and right ventricular ejections, pulmonary arterial, left atrial and aortic mean transmural pressures, and concomitant intrathoracic and tracheal pressures. Changes in pulmonary—left heart blood volume were also computed.3. During inspiration when intrathoracic pressure became more negative, there was a slight increase in right ventricular output (+15%; P < 0·1) and always a net decrease in left ventricular output (−25%; P < 0·01) despite a significant increase in mean transmural left atrial pressure (+3 cm H2O, i.e. +40%; P < 0·005). It is concluded that the more negative intrathoracic pressure increases the left ventricular outflow impedance and that an inspiratory increase in pulmonary vascular capacity cannot explain the observed reduction in left ventricular output since this reduction occurs together with an increase in left ventricular filling pressure.4. During blocked expiration when intrathoracic pressure was positive, decreases in right ventricular output (−17%; P < 0·05) and in pulmonary‐left heart blood volume (−12 ml.; P < 0·05) were observed while right ventricular outflow impedance increased. After an initial augmentation in left ventricular output (despite a concomitant progressive decrease in mean transmural left atrial pressure), left ventricular output also decreased (−17%; P < 0·05). Such circulatory changes were similar but less marked than those observed under constant positive pressure inflations. These observations suggest that the decrease in venous return (and consequently in right ventricular output) following the increase in intrathoracic pressure is the leading factor which overshadows the augmentation in left ventricular output associated with the simultaneous decrease in left ventricular outflow impedance.5. Similar experiments performed on two additional dogs in acute conditions showed the same circulatory effects before and after pharmacological blockade. These observations therefore confirm that mechanical factors play a leading part during these respiratory manoeuvres.
A microinjection study of the control of antidiuretic hormone release by the supraoptic nucleus of the hypothalamus in the cat
Authors: Milton A. S. , Paterson Anna T. 
Published: December 2014

1. The release of antidiuretic hormone (ADH) has been studied in the chloralose anaesthetized cat after microinjection of various agents directly into the brain, in particular the supraoptic nucleus of the hypothalamus (SON). The concentration of ADH in jugular venous blood was determined using the waterloaded, alcohol anaesthetized rat assay. The position of the microinjection cannula was located post mortem in stained brain sections.2. Nicotine, noradrenaline (NA) and hypertonic saline caused release of ADH, whereas microinjections of isotonic saline did not affect the blood level of the hormone.3. Nicotine administered to other sites in the central nervous system (
C.N.S.) could also cause ADH release. Hypertonic saline proved to be an ineffective stimulus at all the tested sites outside the supraoptic region.4. The ganglion‐blocking agents hexamethonium and pempidine inhibited the releasing action of nicotine at the SON in most of the experiments. These blocking drugs had no effect on osmotic release. When administered alone, both hexamethonium and pempidine had variable, but analogous effects on the hormone output.5. The α‐adrenoreceptor blocking drug, phentolamine, stimulated ADH release, but the β‐receptor blocking drug, propranolol, had no such effect. Both drugs appeared to have inhibitory action on noradrenergic release of ADH, but neither had a consistent effect on the osmotic release of the hormone.
Role of cations, anions and carbonic anhydrase in fluid transport across rabbit corneal endothelium
Authors: Fischbarg J. , Lim J. J. 
Published: December 2014

1. A small electrical potential difference (541 ± 48 μV, aqueous side negative) across rabbit corneal endothelium has been recently found. Its dependence on ambient [Na+], [K+], [H+] and metabolic and specific inhibitors was examined.2. Changes in concentration of the ions above either were known or were presently shown to affect the rate of fluid transport across this preparation (normal value: 5·2 ± 0·4 μl./hr.cm2). Ionic concentration changes were also found here to influence potential difference in the same way as fluid transport. In the cases tested, the effects on both fluid transport and potential difference were reversible.3. Fluid transport and potential difference were both decreased or abolished in absence of Na+, K+ and HCO3−, and when [H+] was decreased. Fluid transport and potential difference were saturable functions of [HCO3−] and half‐saturation occurred in both cases at about 13 m
M‐HCO3−. The potential difference was also a saturable function of [Na+] (half‐saturation around 15 m
M). There was a pH optimum for potential difference in the range 7·4–7·6. Lower pH values decreases the potential difference and the fluid transport, and a small (−100 μV) reversed potential was observed in the range of 5·3–5·5.4. Total replacement of Cl− by HCO3− or SO42− produced no impairment on either fluid transport or potential difference.5. Carbonic anhydrase inhibitors (ethoxyzolamide 10−5 or 10−4
M and benzolamide 10−3
M) produced a 40–60% decrease in the rate of fluid pumping. In contrast, ethoxyzolamide 10−4
M or acetazolamide 10−3
M did not produce any change in the potential difference. NaCN and Na iodoacetate (both 2 m
M) eliminated the potential difference in 1‐1·5 hr while in controls it lasted for 5‐6 hr.6. Ouabain (10−5
M) abolished the potential difference in less than 10 sec when added to the aqueous side, which suggests the existence of an electrogenic pump. This extremely fast time transient can be accounted for by the accessibility and simple geometry of the present monocellular layer. Ouabain abolished also the reversed potential difference observed at low pH.7. The data are interpreted in terms of a scheme similar to that advanced for other epithelia and in which (a) H+ would be pumped into the intercellular spaces, while Na+ and CO2 would enter into the cells, and (b) Na+ would be subsequently pumped into the aqueous humour, producing as a result the fluid movement observed. The actual origin of the potential difference is further discussed in terms of two contrasting possibilities: (i) one or more electrogenic pumps, and (ii) a neutral pump which would create a diffusion potential across ‘leaky’ intercellular junctions.
The relation of oxygen intake and speed in competition cycling and comparative observations on the bicycle ergometer
Authors: Pugh L. G. C. E. 
Published: December 2014

1. The relation of V̇O2 and speed was determined on six competition cyclists riding at speeds ranging from 12 km/hr to 41 km/hr on the runway of an airfield. Comparative measurements were made on the bicycle ergometer to determine the corresponding work rates, and from this information rolling resistance and air resistance were derived.2. V̇O2 was a curvilinear function of cycling speed, and increased from 0·88 l./min at 12·5 km/hr to 5·12 l./min at 41 km/hr, mean body weight being 72·9 kg.3. On the ergometer, V̇O2 was a linear function of work rate; maximum values up to 5·1 l./min (74·4 ml./kg min) and work rates up to 425 W (2600 kg m/min) were observed.4. Data are presented on the relation of pedal frequency and speed in cycling, and on the relation of mechanical efficiency and pedal frequency, as determined on the ergometer.5. The estimated rolling resistance for four subjects was 0·71 kg f. The drag coefficient was 0·79 and the drag area 0·33 m2. The values agreed well with results obtained by other methods.6. The energy expenditure (power developed) in cycling increased approximately as the square of the speed, and not as the cube of the speed as expected. This was explained by the varying contribution of rolling resistance and air resistance to over‐all resistance to motion at different speeds.
Metabolic and ionic requirements for the axoplasmic transport of dopamine β‐hydroxylase
Authors: Garcia A. G. , Kirpekar S. M. , Prat J. C. , Wakade A. R. 
Published: December 2014

1. Metabolic and ionic requirements for the intra‐axonal transport of dopamine β‐hydroxylase (DBH) were investigated in the cat hypogastric nerve‐inferior mesenteric ganglion preparation in vitro by monitoring the enzyme accumulation above a crush, 2‐2·5 cm distal to the ganglion.2. DBH accumulation in the proximal segment immediately above the crush increased linearly up to 6 h, during incubation in normal Krebs solution at 37° C. The rate of transport of the enzyme was about 4 mm/h.3. Removal of the ganglion, electrical stimulation or reserpine pretreatment (1–6 days before the experiment) did not modify the rate of DBH accumulation.4. Anoxia and glucose deprivation, singly, did not affect accumulation of DBH; however, the combined treatment of anoxia plus glucose deprivation, or dinitrophenol plus glucose deprivation, very markedly interfered with accumulation.5. Removal of sodium or potassium from Krebs solution markedly inhibited the transport of DBH. Preincubation of the nerve in a high‐calcium Krebs solution at 4° C, and then reincubation at 37° C, prevented the enzyme accumulation.6.
N‐ethylmaleimide, ouabain and oligomycin markedly inhibited the transport of DBH.7. The results suggest that transport of DBH, and therefore of noradrenaline storage vesicles, within the hypogastic nerve is dependent on metabolic energy derived from either glycolysis or oxidative phosphorylation. It is also suggested that the sodium‐potassium‐activated ATPase may play an important role in the intra‐axonal transport of storage vesicles.
On the role of vasopressin and angiotensin in the development of irreversible haemorrhagic shock
Authors: Errington M. L. , e Silva M. Rocha 
Published: December 2014

1. Long‐lasting haemorrhagic hypotension (4·5 hr at 35 mmHg) leading to irreversible haemorrhagic shock, has been studied in normal dogs, in dogs treated with a bradykinin potentiating nonapeptide (BPP9a), which blocks the conversion of angiotensin I to angiotensin II, and in dogs with experimental chronic diabetes insipidus (DI dogs). BPP9a was given by
I.V. injection before the start of bleeding (BPP pre‐treated group), 45 min after blood pressure had reached 35 mmHg (BPP early treated group) or 2 hr after blood pressure had reached 35 mmHg (BPP late‐treated group). After retransfusion of blood all dogs were allowed to recover and observed for a further period of 3 days.2. Untreated control dogs developed haemorrhagic shock with tachycardia, low cardiac output, low total peripheral conductance and low stroke volume. All died within 24 hr of retransfusion, with pathological lesions typical of irreversible haemorrhagic shock.3. BPP pre‐treated dogs developed haemorrhagic shock with bradycardia (during early shock), high cardiac output, high peripheral vascular conductance and high stroke volume when compared with the untreated controls. All pre‐treated animals survived the 3 day observation period. They were then killed and on post‐mortem showed no signs of irreversible haemorrhagic shock.4. BPP early‐treated animals behaved like controls before BPP, but like pre‐treated animals after the drug. Only one out of eight died within the 3 day observation period.5. BPP late‐treated dogs behaved like controls before BPP. They responded to the drug with a rise in cardiac output, peripheral vascular conductance and stroke volume, and with a fall in heart rate. These responses were, however, short‐lived. Four out of these eight animals died within the 3 day observation period, with lesions of irreversible haemorrhagic shock.6. DI dogs developed haemorrhagic shock with tachycardia (like controls), but with high cardiac output and peripheral vascular conductance (like BPP pre‐treated dogs). The stroke volume of DI dogs was intermediate between those of controls and pre‐treated groups. All six dogs survived the 3 day observation period.7. BPP9a had no measurable effect on the course of endotoxic shock.8. It is suggested that the normally severe vasoconstriction of the mesenteric vascular bed, which is thought to be responsible for irreversible haemorrhagic shock, is absent or attenuated in the absence of vasopressin or angiotensin. The consequences of this on the development of irreversibility are discussed.
Current spread in the smooth muscle of the rabbit aorta
Authors: Mekata F. 
Published: December 2014

1. The electrical responses of the smooth muscle cells of the rabbit aorta to both extracellular and intracellular stimulation were studied using the partitioned chamber and Wheatstone bridge method.2. No spontaneous electrical activity was recorded when the tissue was soaked in either isotonic or hypertonic Krebs solutions, and strong depolarizing currents also failed to trigger action potentials in either solution.3. The circular muscle of the aorta has cable properties. Mean values in isotonic Krebs solution were 2·1 mm for space constant and 433 msec for time constant.4. The input resistance (mean 12 MΩ) measured with the Wheatstone bridge method was considerably smaller than that calculated from values measured with the partitioned chamber method.5. Electrotonic potentials could be recorded from the smooth muscle of ‘injury bundles’ although their amplitude was smaller than that from the intact bundle.6. High concentrations of noradrenaline readily induce oscillatory potentials from the aorta in both isotonic and hypertonic Krebs solutions. It was estimated by simultaneous recording with two micro‐electrodes that noradrenaline‐induced oscillatory potential can conduct in both longitudinal and transverse directions of the smooth muscle.7. These results suggest that the smooth muscle of the aorta behaves like a syncytium or single unit muscle and activation of cells on the inner surface of the media can be induced both by electrotonic current spread and by propagation of oscillatory potentials from the outer cells directly activated by the transmitter.
Electrophysiological evidence for the activation of supraoptic neurones during the release of oxytocin
Authors: Lincoln D. W. , Wakerley J. B. 
Published: December 2014

1. Antidromically identified supraoptic (SO) units were recorded in lactating rats anaesthetized with urethane (1·1 g/kg), and their activity was studied during milk ejection evoked by the suckling of the young. Fifty‐eight SO units were recorded through 174 milk ejections. Each milk ejection was the result of a neurohypophysial release of an oxytocin pulse of 0·5–1·5 m‐u.2. Fifty‐five of the SO units displayed background activity and three were silent. The firing rates ranged from 0 to 15·4 spikes/sec, the distribution was exponential with 26% of the units firing at < 1 spike/sec. Sixteen (28%) of the SO units displayed a phasic pattern of activity characterized by periods of activity (6–132 sec) and silence (4–71 sec).3. Twenty‐five of the non‐phasic units displayed a large and stereotyped acceleration in spike activity some 10·5–17·4 sec before the rise in intramammary pressure at milk ejection. Units accelerated to rates between 9–66 spikes/sec, an increase of about thirtyfold (median) on background activity. The response was brief (0·9–4·7 sec) and was followed by a period of after‐inhibition.4. It was concluded from studies of double recordings and observations of multi‐unit activity that all the responsive units were synchronously activated. The mean latency of 13·3 sec between the onset of the neurosecretory response and milk ejection was similar to that observed following the experimental release of endogenous oxytocin by electrical stimulation of the neurohypophysis (50 pulses/sec for 2‐4 sec).5. Four of the phasically active units were correlated with the oxytocin release for milk ejection. Three of these units displayed a burst of activity superimposed on the terminal portion of an active phase, some 10·2–14·7 sec before milk ejection. The fourth unit, recorded in conjunction with a responsive non‐phasic unit, consistently switched from silence to activity coincident with the onset of the SO activation.6. The remaining SO units and a further ten units that were not antidromically activated by neurohypophysial stimulation displayed no change in activity during either the period of neurosecretory activation or the period of after‐inhibition.7. This activation of the SO neurones, in the formulation of oxytocin release and milk ejection, is the same as that we have previously observed in recordings from the paraventricular (PV) region, and the proportion of neurones displaying the response is similar: 48% in the SO nuclei, 58% in the PV nuclei. We conclude, since the SO nuclei contain 80% of the neurosecretory cells that project to the neurohypophysis, that the SO nuclei are as important, if not more so, than the PV nuclei in the control of oxytocin release.