bluuebunny/crossref_metadata_2025_split huggingface dataset:
Functional electrical properties of the endothelium in lymphatic vessels of the guinea‐pig mesentery
Authors: von der Weid Pierre‐Yves , Van Helden Dirk F. 
Published: September 2004

The resting and agonist‐stimulated properties of endothelial cells and electrical communication between the endothelium and smooth muscle were investigated in open segments of guinea‐pig mesenteric lymphatic vessels using intracellular microelectrodes.
Endothelial cells had a mean resting membrane potential (RMP) of – 71.5 ± 0.5mV (n= 100) which was significantly different from the value of −60.8 ± 1.1 mV (n= 75) recorded in smooth muscle.
Acetylcholine (ACh, 5–1 μm) generally evoked an initial hyperpolarization followed by depolarization (mean 3.4 ± 0.5 mV and 15.4 ± 1.0 mV, respectively, n= 75).
Ca2+‐activated K+ channels were likely to underlie the ACh‐induced hyperpolarization as this response exhibited an increase in membrane conductance, was larger in 0.5 mm K+ solution and was blocked by charybdotoxin (50 nm).
The endothelium did not exhibit a response to nitric oxide (NO) as the NO‐donor sodium nitroprusside did not alter the RMP and the electrical responses to ACh were not affected by the NO‐synthase inhibitor Nω‐nitro L‐arginine at a concentration which markedly inhibited smooth muscle hyperpolarization.
Electrical coupling between the endothelium and smooth muscle was not functional as there was extremely limited electrical continuity (1 in 12, endothelial/smooth muscle cell simultaneous recordings) and bradykinin, noradrenaline and isoprenaline caused different electrical responses in the two cell types.
These results provide the first description of RMP and electrical responses to various agonists in the lymphatic endothelium and its lack of functional electrical coupling with the smooth muscle.
The Roles of Adenosine in Regulating the Respiratory and Cardiovascular Systems in Chronically Hypoxic, Adult Rats
Authors: Thomas Teresa , Marshall Janice M. 
Published: September 2004

We have investigated the roles of adenosine in regulating the respiratory and cardiovascular systems of rats that were made chronically hypoxic for 3–4 weeks from 6 weeks of age (CH rats) in an hypoxic chamber at 12% O2. They were studied under anaesthesia while breathing 12% O2 and during acute hypoxia (breathing 8% O2 for 5min) before and after addition of the adenosine receptor antagonist 8‐phenyltheophylline (8‐PT, 10 mg kg−1). The results were compared with those obtained from normoxic (N) rats in a previous study.
CH rats breathing 12% O2 had greater minute ventilation (V̇E) than N rats breathing air, but their levels of arterial blood pressure (ABP), heart rate (HR), femoral vascular conductance (FVC) and cerebral vascular conductance (CVC) were fully comparable. 8‐PT increased tidal volume (VT) in CH rats indicating a greater tonic central inhibitory influence of adenosine on VT than in N rats. However, 8‐PT had no effect on cardiovascular variables, indicating no tonic cardioinhibitory or vasodilator influence of adenosine in CH rats.
Acute hypoxia in CH rats increased V̇E such that at the 5th minute of 8% O2 absolute V̇E was comparable to that of N rats breathing 8% O2. Moreover, in CH rats 8‐PT increased VT at the 5th minute of 8% O2 indicating that the central inhibitory influence of adenosine limits the ability to maintain VT in acute hypoxia as it does in N rats.
Eight per cent O2 also produced a fall in ABP in CH rats that was comparable to that induced in N rats by the larger change from air to 8% O2. However, the changes in HR were similar in CH and N rats while the increases in FVC and CVC were smaller in CH rats. This suggests that the ability of the secondary effects of hyperventilation and of the baroreceptor reflex to maintain cardiac output and thereby ABP is reduced in CH rats.
Whereas 8‐PT substantially reduced the hypoxia‐induced increases in FVC and CVC in N rats, it had a small effect in CH rats (P= 0.054 and 0.06, respectively). Further, acute hypoxia in CH rats had no effect on the K+ concentration in the venous efflux of hindlimb K+ (Kv+) before or after 8‐PT treatment. We suggest that in CH rats, the dilator influence of adenosine in acute hypoxia occurs via actions on the blood vessel walls: there was no evidence that adenosine can release dilator concentrations of K+ from skeletal muscle fibres in CH rats as proposed for N rats.
Assessment of the reliability of amplitude histograms from excitatory synapses in rat hippocampal CA1 In Vitro
Authors: Larkman A. U. , Jack J. J. B. , Stratford K. J. 
Published: September 2004

Excitatory postsynaptic potentials (EPSPs) were evoked using minimal extracellular stimulation and recorded from pyramidal cells from the CA1 region of slices taken from adult rats and maintained in vitro.
Segments of data were selected that gave EPSP amplitude frequency histograms that showed approximately equally spaced peaks. Selection was performed either on the basis of stationarity of the EPSP mean and standard deviation, or on the trajectory of a graph of the (coefficient of variation)−2 against mean for the EPSP, or, in some cases, by trial and error.
For each histogram, we determined the likelihood that peaks of similar sharpness and equality of spacing could have arisen by sampling artifact from a smooth distribution, using a method based on autocorrelation and Monte Carlo simulation.
Thirty‐three histograms were analysed. For twenty‐six of these, the likelihood of sampling artifact was estimated at 1 in 100 or less, and for eleven histograms the likelihood was less than 1 in 1000. For the histogram with the clearest peaks, the likelihood was less than 1 in 350000. Histograms judged to be reliable by this method could occur when the EPSP mean amplitude was changing.
We conclude that random sampling artifact is very unlikely to be the explanation for the peaks in our data histograms. It seems more likely that they are due to a quantal synaptic transmission mechanism with low quantal variability.
The autocorrelation method also gives a measure of the mean peak spacing, and hence the mean quantal size, for each histogram. Quantal sizes ranged from 93 to 285 μV, with a mean ±s.d. of 172 ± 47 μV.
From these quantal sizes and the EPSP mean amplitudes we calculated the mean number of quanta released per trial for each histogram. This ranged from 0.36 to 6.9, with a mean of 3.3 ± 1.67.
Effect of cardiopulmonary C fibre activation on the firing activity of ventral respiratory group neurones in the rat
Authors: Wilson Christopher G. , Bonham Ann C. 
Published: September 2004

Cardiopulmonary C fibre receptor stimulation elicits apnoea and rapid shallow breathing, but the effects on the firing activity of central respiratory neurones are not well understood. This study examined the responses of ventral respiratory group neurones: decrementing expiratory (Edec), augmenting expiratory (Eaug), and inspiratory (I) neurones during cardiopulmonary C fibre receptor‐evoked apnoea and rapid shallow breathing.Extracellular neuronal activity, phrenic nerve activity and arterial pressure were recorded in urethane‐anaesthetized rats. Cardiopulmonary C fibre receptors were stimulated by right atrial injections of phenylbiguanide. Neurones were tested for antidromic activation from the contra‐ and ipsilateral ventral respiratory group (VRG), spinal cord and cervical vagus nerve.Edecneurones discharged tonically during cardiopulmonary C fibre‐evoked apnoea and rapid shallow breathing, displaying increased burst durations, number of impulses per burst, and mean impulse frequencies. Edecneurones recovered either with the phrenic nerve activity (25 s) or much later (3 min).By contrast, the firing activity of Eaugand most I neurones was decreased, featuring decreased burst durations and number of impulses per burst and increased interburst intervals. Eaugactivity recovered in ˜3 min and inspiratory activity in ˜1 min.The results indicate that cardiopulmonary C fibre receptor stimulation causes tonic firing of Edecneurones and decreases in Eaugand I neuronal activity coincident with apnoea or rapid shallow breathing.
Quantal analysis of excitatory synapses in rat hippocampal CA1 In Vitro during low‐frequency depression
Authors: Larkman A. U. , Jack J. J. B. , Stratford K. J. 
Published: September 2004

We have performed a detailed quantal analysis of excitatory postsynaptic potentials (EPSPs) evoked by minimal extracellular stimulation in the CA1 region of slices of adult rat hippocampus maintained in vitro.
EPSPs were evoked at 2–5 Hz, and the eight that were analysed all showed at least a 50 % depression of mean peak amplitude during recording.
EPSP amplitude fluctuations were analysed by three methods: the use of amplitude frequency histograms with clear and reliable peaks where available, graphs of the EPSP (coefficient of variation)−2 against EPSP mean, and analysis of EPSP mean and standard deviation assuming simple binomial statistics with the number of release sites (N) kept constant but the quantal size (Q) and the release probability (Pr) allowed to vary over time.
The results of the three analysis procedures were in good agreement. Seven EPSPs showed a substantial reduction in the mean number of quanta released per trial, and in three cases this was the predominant mechanism of the depression. Five EPSPs showed a substantial decrease in Q. Values for N ranged between 3 and 18, with a median of 6; Pr ranged between 0.14 and 0.81 and Q between 66 and 275 μV.
We used the Q estimates from the binomial method to correct the recorded EPSP amplitudes for changes in quantal size over time. For seven out of the eight EPSPs, this rescaling procedure allowed histograms with clear peaks to be obtained from longer runs of data, or improved the sharpness of the peaks in histograms from all the recorded data. The improvement in peak sharpness was assessed using an autocorrelation‐based method. The correction was much less successful if the Q estimates were obtained with a variant of the binomial method in which Pr was held constant and N was allowed to vary.
The only simple explanation for the success of the correction procedure is that changes in quantal size were a major factor in obscuring peaks in histograms based on large numbers of trials, and that the quantal size estimates from the binomial method with N held constant were reasonably accurate.
We conclude that transmission at these synapses was quantal with relatively low quantal variance, but repetitive stimulation often induced substantial changes in the quantal parameters that might prevent the success of conventional quantal analysis approaches.
Paraesthesiae Induced by Prolonged high Frequency Stimulation of Human Cutaneous Afferents
Authors: Kiernan Matthew C. , Hales John P. , Gracies Jean‐Michel , Mogyoros Ilona , Burke David 
Published: September 2004

The present study has explored the behaviour of human cutaneous afferents following conduction of prolonged trains of impulses at 200 Hz for 10–20 min, correlating the resultant changes in excitability with the perception of paraesthesiae.
Tetanization for 10 min resulted in activity‐dependent changes in axonal excitability, with an initial period of hyperexcitability, followed by a long‐lasting subexcitability. All subjects experienced paraesthesiae soon after cessation of the tetanic train, and these subsided gradually over 16 min.
Longer tetanic trains of 20 min duration resulted in greater changes in axonal excitability, but with paraesthesiae of a similar time course. The post‐tetanic increase in excitability was abolished when short tetanic trains were delivered > 30 min before long trains, but all subjects still experienced paraesthesiae.
Threshold distributions following tetanic stimulation for both 10 and 20 min established that all axons contributing to the sensory volley underwent a uniform pattern of post‐tetanic threshold changes. There was no evidence of a bimodal distribution with some axons hyper‐polarized and others depolarized, as occurs with motor axons. However, the excitability changes were graded, with axons of lowest threshold undergoing a proportionately greater increase in excitability than axons of higher threshold.
The post‐tetanic excitability changes were greater at the site of stimulation than elsewhere along the peripheral nerve. However, DC polarizing currents applied at this site failed to alter the sensation of paraesthesiae in the post‐tetanic period. Furthermore, local anaesthetic block of the peripheral nerve proximal to the stimulation site failed to suppress the paraesthesiae.
The uniform pattern of post‐tetanic threshold changes for cutaneous afferents differs from the bimodal distribution seen with post‐ischaemic and post‐tetanic motor axons. This difference in behaviour may reflect greater inward rectification and greater expression of a non‐inactivating threshold conductance in cutaneous afferents. It is suggested that the ectopic activity responsible for paraesthesiae in the post‐tetanic period arises from a more central site than the peripheral nerve.
Relationship Between Venous Pressure and tissue Volume During Venous Congestion Plethysmography in Man
Authors: Christ F. , Gamble J. , Baschnegger H. , Gartside I. B. 
Published: September 2004

Venous congestion strain‐gauge plethysmography enables the non‐invasive assessment of arterial blood flow, fluid filtration capacity (Kf), venous pressure (Pv)and isovolumetric venous pressure (Pvi)in man. One of the major assumptions of this technique, that cuff pressure (Peuff) applied to the limb equals Pv at the level of the strain gauge, was tested in this study.
In nine healthy male volunteers (mean age, 29.3 ± 1.2 years) the saphenous vein was cannulated with an 18‐gauge catheter proximal to the medial malleolus. The subjects were supine and Pv was continuously measured during the application of small step (8–10 mmHg) increases in congestion Pcuff (up to 70 mm Hg). Pcuff, changes in limb circumference and Pv were recorded by computer for off‐line analysis. Since the determination of Pv is influenced by the changes in plasma oncotic pressure, venous blood samples were obtained at the start of the study, when P& was raised to 30 mmHg and again to 65 mmHg and 4 min after deflation of the cuff.
The relationship between Pv and Pcuff was linear over the range of 10–70 mm Hg (n= 9, 69 measurements, slope 0.9.1, r= 0.97, P. <<0.001). The non‐invasively measured calf Pv based on the intercept of the relationship between the vascular compliance component (Vv) and Pcuff, was 8.0±0.4mmHg, which was not significantly different from the corrected invasively measured Pv value of 8.8±0.3 mmHg P= 0.08).
Venous blood lactate and haemoglobin concentrations, as well as colloid osmotic pressure, total protein and albumin concentrations were unchanged throughout the protocol, whereas significant decreases in Po2 and blood glucose concentration were observed when Pcuff reached 65 mmHg. Assuming a constant oxygen consumption, this may suggest a reduction in tissue perfusion.
This study demonstrates the close correlation between Pcuff and Pvin the saphenous vein. Since the small congestion Pcuff step protocol does not cause significant increase in plasma oncotic pressure, we conclude that Pv as well as Kf can be accurately determined with this venous congestion plethysmography protocol.
Longitudinal distribution of Na+ and Ca2+ channels and β‐adrenoceptors on the sarcolemmal membrane of frog cardiomyocytes
Authors: Jurevičius Jonas , Fischmeister Rodolphe 
Published: September 2004

The distribution of L‐type Ca2+ and tetrodotoxin‐sensitive Na+ channels and of β‐adrenergic receptors was examined in frog ventricular myocytes using the whole‐cell patch‐clamp technique and a double capillary for extracellular microperfusion.
Rod‐shaped cells (250–300 μm long) were sealed at both ends to two patch‐clamp pipettes and positioned transversally at different positions between the mouths of two micro‐capillaries separated by a thin wall. A combination of nifedipine (1 μm) and tetrodotoxin (0.3 μm) (blocking solution) was added to one capillary in order to inhibit macroscopic Ca2+ and Na+ currents (ICa and INa, respectively) in the part of the cell exposed to this capillary.
Moving the cell in 10–20 μm steps from the control capillary to the capillary containing the blocking solution induced step decreases in ICa and INa amplitudes. Complete block of both currents occurred when the entire cell was exposed to the blocking solution.
Each step decrease in current was due to the loss of activity of the functional Ca2+ and Na+ channels present in the slice of sarcolemmal membrane newly exposed to the blocking solution. These step current changes allowed longitudinal mapping of current density for Ca2+ and Na+ channels on the sarcolemmal membrane.
Addition of a submaximal concentration of isoprenaline (10 nm) to the control capillary induced a local increase in ICa which enabled examination of the distribution of functional β‐adrenergic receptors as well.
Our results demonstrate that Ca2+ and Na+ channels and β‐adrenergic receptors are equally and essentially uniformly distributed on the sarcolemmal membrane of frog ventricular myocytes.
Evidence Suggesting a Transcortical Pathway from Cutaneous Foot Afferents to Tibialis Anterior Motoneurones in Man
Authors: Nielsen J. , Petersen N. , Fedirchuk B. 
Published: September 2004

Stimulation of the superficial peroneal or the sural nerve (3 shocks, 3 ms interval, 1 ms duration, 2.5 × perception threshold) evoked a reflex activation of the tibialis anterior muscle at a latency of approximately 70–95 ms in all of nine healthy human subjects. Stimulation of the medial plantar nerve only rarely produced similar effects. The possibility that a transcortical pathway contributes to these late reflex responses was investigated by combining the cutaneous stimulations and a transcranial magnetic stimulation of the contralateral motor cortex.
A significant facilitation of short‐latency peaks in the post‐stimulus time histogram of single tibialis anterior motor units evoked by the transcortical magnetic stimulation was observed in eight out of nine subjects following stimulation of the superficial peroneal or sural nerves at the latency of the long‐latency reflex. In contrast such a facilitation was only rarely seen when the medial plantar nerve was stimulated.
With the same timing for the stimuli, the superficial peroneal and sural nerve stimulations also produced a significant increase in the short‐latency, presumed monosynaptic, facilitation of the tibialis anterior H reflex produced by the brain stimulation.
Similar facilitatory effects of the cutaneous stimuli could not be demonstrated when the magnetic stimulation of the cortex was replaced with electrical stimulation, implying that cortical excitability is affected by a conditioning cutaneous stimulation.
It is suggested that the long‐latency reflexes in the tibialis anterior muscle evoked by activation of cutaneous afferents from the human foot are, at least partly, mediated by a transcortical pathway.
Drastic facilitation by α‐latrotoxin of bovine chromaffin cell exocytosis without measurable enhancement of Ca2+ entry or [Ca2+]i
Authors: Michelena Pedro , de la Fuente María‐Teresa , Vega Teresa , Lara Baldomero , López Manuela G. , Gandía Luis , García Antonio G. 
Published: September 2004

Latrotoxin (LTX, 1–3 nm) caused a gradual increase of the supontaneous catecholamine release rate in bovine adrenal chromaffin cells superfused with normal Krebs–Hepes solution containing 2.5 mm Ca2+. Ca2+ removal abolished this effect. LTX enhanced also the secretory responses to high K+ (35 or 70 mm) and to acetylcholine (ACh, 30 μm).
The application of Ca2+ pulses to cells previously superfused with a 0 Ca2+ solution (Krebs–Hepes deprived of CaCl2) induced secretory responses that gradually reached 400–800 nA of catecholamines, provided that LTX was present. The responses to ACh or 35 mm K+ pulses (in the presence of Ca2+) were also enhanced by LTX, from around 100–200 nA to over 1000 nA. Though such enhancement remained in the presence of Ca2+ channel blockers, it disappeared upon the lowering of [Na+]0 or in electroporated cells.
Using protocols similar to those of secretion, LTX did not enhance basal 45Ca2+ uptake, whole‐cell Ca2+ currents or basal [Ca2+]j. In fact, LTX attenuated the K+‐ or ACh‐evoked increases in 45Ca2+ uptake and [Ca2+]1.
It is proposed that the secretory response to brief periods of Ca2+ reintroductions is triggered by local subplasmalemmal Ca2+1 tranMents, produced by the Na+‐Ca2+ exchanger of the plasma membrane working in the reverse mode. This situation might be physiologically reproduced during ACh stimulation of chromaffin cells, which is followed by the firing of Na+‐dependent action potentials.
Angiotensin II Inhibition of ATP‐Sensitive K+ Currents in Rat Arterial Smooth Muscle Cells Through Protein Kinase C
Authors: Kubo M. , Quayle J. M. , Standen N. B. 
Published: September 2004

The effects of the vasoconstrictor angiotensin II (Ang II) on whole‐cell ATP‐sensitive K+currents (Ik,atp) of smooth muscle cells isolated enzymatically from rat mesenteric arteries were investigated using the patch clamp technique.
Ang II, at a physiological concentration (100 nm), reduced Ik,atp activated by 0.1 mm internal ATP and 10 μm levcromakalim by 36.4 ± 2.3%.
The protein kinase C (PKC) activator 1‐oleoyl‐2‐acetyl‐sn‐glycerol (OAG, 1 μm) reduced Ik,atp by 44.1 ± 2.7%. GDPβS (1 mm), included in the pipette solution, abolished the inhibition by Ang II, while that by OAG was unaffected.
Pretreatment with the PKC inhibitors staurosporine (100 nm) or calphostin C (500 nm) prevented the Ang II‐induced inhibition of Ik,atp.
Ang II inhibition was unaffected by cell dialysis with PKA inhibitor peptide (5 μm), and the PKA inhibitor Rp‐cAMPS (100 μ) did not reduce Ik,atp.
Our results suggest that Ang II modulates Katp channels through activation of PKC but not through inhibition of PKA.