Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “EXTRACELLULAR SPACE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,675 records · Page 93Linked to original sources
PubMed1975

Diffusion of horseradish peroxidase perfused through the lateral ventricle of the chick telencephalon.

Horseradish peroxidase, perfused into the lateral ventricle of chick brain, freely and slowly diffuses through the cerebral extracellular spaces. The layer of astrocytic end-feet surrounding blood capillaries does not consitute a barrier to the tracer which permeates the basal lamina, diffuses between the pericytic cells and finally accumulates in the intercellular space beneath the tight junctions between contiguous endothelial cells. No evidence was found for transport by micropinocytotic vesicles from the cerebral parenchyma to the capillary lumen.

Animals↗
PubMed1978

Ultrastructural detection of Haemophilus ducreyi in biopsies of chancroid.

During an endemic appearance of chancroids (26 cases) in Berlin (West) coccobacilli were disclosed in biopsies by electron microscopy. The bacteria were aggregated predominantly in groups in the extracellular space. Their cell wall is approximately 120 A thick and trilaminar as in Gram-negative bacteria. Concerning the cell wall structure and the cytoplasmic composition, the detected coccobacilli are identical to culturally grown Haemophilus ducreyi obtained from chancroids.

Chancroid↗
PubMed1993

Effect of extracellular ATP on contraction, cytosolic calcium activity, membrane voltage and ion currents of rat mesangial cells in primary culture.

1. The effects of extracellular ATP on contraction, membrane voltage (Vm), ion currents and intracellular calcium activity [Ca2+]i were studied in rat mesangial cells (MC) in primary culture. 2. Addition of extracellular ATP (10(-5) and 10(-4) M) to MC led to a cell contraction which was independent of extracellular calcium. 3. Membrane voltage (Vm) and ion currents were measured with the nystatin patch clamp technique. ATP induced a concentration-dependent transient depolarization of Vm (ED50: 2 x 10(-6) M). During the transient depolarization ion currents were monitored simultaneously and showed an increase of the inward- and outward current. 4. In a buffer with a reduced extracellular chloride concentration (from 145 to 30 mM) ATP induced a depolarization augmented to -4 +/- 4 mV. 5. ATP-gamma-S and 2-methylthio-ATP depolarized Vm to the same extent as ATP, whereas alpha,beta-methylene-ATP (all 10(-5) M) had no effect on Vm. 6. The Ca2+ ionophore, A23187, depolarized Vm transiently from -51 +/- 2 to -28 +/- 4 mV and caused an increase of the inward current. 7. The intracellular calcium activity [Ca2+]i was measured with the fura-2 technique. ATP stimulated a concentration-dependent increase of [Ca2+]i (ED50: 5 x 10(-6) M). The increase of [Ca2+]i was biphasic with an initial peak followed by a sustained plateau. 8. The [Ca2+]i peak was still present in an extracellular Ca(2+)-free buffer, whereas the plateau was abolished. Verapamil (10(-4) M) did not inhibit the [Ca2+]i increase induced by ATP. 9. The data indicate that extracellular ATP contracts MC and is able to increase [Ca2+]i by the release of Ca2+ from intracellular stores and recruitment from the extracellular space. In addition ATP depolarizes Vm of MC by activating a Cl- conductance. The ATP-induced depolarization is mediated by a P2y receptor.

Adenosine Triphosphate↗
PubMed1992

Stimulus-evoked slow potential shifts and changes in [K+]0 of the frog optic tectum.

In 17 frogs (Rana esculenta var ridibunda) immobilised with succinyl choline the optic tectal surface was stimulated by trains of electrical pulses or by a flash to the contralateral eye. Sustained potential shifts (SPSs) and changes in extracellular potassium concentration (delta[K+]0) were simultaneously recorded. In response to electrical stimulation SPSs of maximal amplitudes (1.19 +/- 0.1 mV) were recorded between 50 and 200 microns in depth and maximal delta[K+]0 (0.69 +/- 0.08 mM) between 100 and 350 microns. The changes of SPS and delta[K+]0 showed a close similarity in experiments with changes in voltage, pulse duration and frequency of stimuli within a train. The induced SPS had a duration of 28 +/- 1.54 s, the delta[K+]0 of 32 +/- 1.23 s. The flash stimulus induced an SPS and delta[K+]0 of maximal amplitudes between 50 and 200 microns in depth with values of 0.57 +/- 0.1 mV and 0.29 +/- 0.03 mM respectively. An additional wave with a latency of ca 1 s and a duration of ca 3 s arose on the background of the SPS to a flash stimulus, associated with an additional increase in [K+]0. It is considered that the accumulation of K+ in extracellular space, with neuronal activity, results in depolarization of radial processes of ependymal glia. This is reflected in the neuropil of the upper layers of the optic tectum as an SPS.

Animals↗
PubMed1975

Fine structure of a cerebellar "fibroma".

The fine structure of an intracerebellar "fibroma" has been examined. The tumor consists of irregularly-shaped cells connected by well developed junctional complexes. Unusual, fenestrated capillaries with extremely narrow and irregular lumens are frequent. Collagen fibers are not common but the wide extracellular spaces contain large amounts of dense, granular or fibrillar material. The dense material coats the tumor cells and is a apparently secreted from small vesicles found within these cells.

Adult↗
PubMed1993

Origin of intracellular Ca2+ elevation induced by in vitro ischemia-like condition in hippocampal slices.

Microfluorometry was used to investigate the origin of intracellular Ca2+ ([Ca2+]i) elevation in field CA1 of gerbil hippocampal slices perfused with a glucose-free physiological medium equilibrated with a 95% N2/5% CO2 gas mixture (standard in vitro ischemia-like condition). Large [Ca2+]i elevation was detected about 4 min after the beginning of standard in vitro ischemia-like condition, which was accompanied with a negative shift of extracellular DC potential. When slices were perfused with Ca(2+)-free in vitro ischemia-like medium, large [Ca2+]i elevation was observed about 3.5 min after the beginning of Ca(2+)-free in vitro ischemia-like condition, however, the increase in [Ca2+]i was more gradual and of a lesser extent compared with that detected in the slices perfused with the standard in vitro ischemia-like medium that contained Ca2+. When slices were perfused with the Ca(2+)-free in vitro ischemia-like medium that contained dantrolene (50 microM) which is known to prevent Ca(2+)-induced Ca2+ release from intracellular Ca2+ stores, the increase in [Ca2+]i was more gradual and of a lesser extent compared with that detected in the slices perfused with the Ca(2+)-free in vitro ischemia-like medium that did not contain dantrolene. These results indicate that large [Ca2+]i elevation induced by in vitro ischemia-like condition in field CA1 of the hippocampus was caused by both Ca2+ influx from extracellular space and Ca2+ release from intracellular Ca2+ stores, and that a part of the Ca2+ release was due to Ca(2+)-induced Ca2+ release from intracellular Ca2+ stores.

Animals↗
PubMed1985

The effect of reserpine treatment on the extraneuronal uptake of [3H]-isoprenaline into rat atria.

Treatment of rats with reserpine (1 mg kg-1 day-1) for up to 7 days resulted in a marked decrease in a corticosterone-sensitive component of the extraneuronal accumulation of [3H]-isoprenaline into their atria. The change in extraneuronal uptake did not appear to be due to a direct action of reserpine on the uptake mechanism, since it was several days before the treatment had a significant effect on the accumulation of [3H]-isoprenaline. Further, reserpine in vitro did not inhibit extraneuronal uptake. The reserpine-induced change in the accumulation of [3H]-isoprenaline was not an artifact due to changes in water balance, ion distribution, extracellular space or tissue atrophy. Nor was the change due to an increase in the efflux of [3H]-isoprenaline from the tissue. These experiments support the suggestion that the extraneuronal uptake is dependent upon a functional adrenergic innervation.

Animals↗
PubMed2006

Extracellular chelation of zinc does not affect hippocampal excitability and seizure-induced cell death in rats.

In the nervous system, zinc can influence synaptic responses and at extreme concentrations contributes to epileptic and ischaemic neuronal injury. Zinc can originate from synaptic vesicles, the extracellular space and from intracellular stores. In this study, we aimed to determine which of these zinc pools is responsible for the increased hippocampal excitability observed in zinc-depleted animals or following zinc chelation. Also, we investigated the source of intracellularly accumulating zinc in vulnerable neurons. Our data show that membrane-permeable and membrane-impermeable zinc chelators had little or no effect on seizure activity in the CA3 region. Furthermore, extracellular zinc chelation could not prevent the accumulation of lethal concentrations of zinc in dying neurons following epileptic seizures. At the electron microscopic level, zinc staining significantly increased at the presynaptic membrane of mossy fibre terminals in kainic acid-treated animals. These data indicate that intracellular but not extracellular zinc chelators could influence neuronal excitability and seizure-induced zinc accumulation observed in the cytosol of vulnerable neurons.

Animals↗
PubMed1997

Removal of osteoclast bone resorption products by transcytosis.

Osteoclasts are multinucleated cells responsible for bone resorption. During the resorption cycle, osteoclasts undergo dramatic changes in their polarity, and resorbing cells reveal four functionally and structurally different membrane domains. Bone degradation products, both organic and inorganic, were endocytosed from the ruffled border membrane. They were then found to be transported in vesicles through the cell to the plasma membrane domain, located in the middle of the basal membrane, where they were liberated into the extracellular space. These results explain how resorbing osteoclasts can simultaneously remove large amounts of matrix degradation products and penetrate into bone.

Actins↗
PubMed1995

Extracellular nucleotides stimulate leukocyte adherence to cultured pulmonary artery endothelial cells.

Adenosine, ATP, and various nucleotides were examined for their effects on the adherence of leukocytes to bovine pulmonary artery endothelial cells. Extracellular ATP enhanced adherence of HL-60 cells and human neutrophils to endothelial cells in a dose-dependent fashion. Maximal adherence occurred after 15 min coincubation of ATP and HL-60 cells or neutrophils with endothelial cells. ATP stimulation was mediated by direct effects on both HL-60 cells and endothelial cells. The potency profile of various nucleotides was ATP = 2-MeSATP > beta,gamma-CH2ATP, indicative of a P2y receptor. Interestingly, UTP was as potent as ATP in stimulating HL-60 cell adherence, suggesting the presence of a pyrimidine nucleotide receptor. Photoaffinity labeling of endothelial cells with 8-Az-[alpha-32P]ATP showed the presence of two ATP binding proteins of 48 and 87 kDa. ATP and 2-MeSATP inhibited binding by both proteins. Labeling of the 87-kDa protein was inhibited by beta,gamma-CH2ATP, whereas UTP blocked binding by the 48-kDa protein. Thus photoaffinity labeling experiments support the proposal that endothelial cells possess two ATP receptors, one of which is a P2u nucleotide receptor. These findings show that extracellular nucleotides enhance leukocyte adherence to endothelial cells. Nucleotide release into the extracellular space may be one mechanism of exacerbating vascular cell injury relevant to conditions such as adult respiratory distress syndrome and septic shock.

Adenosine Triphosphate↗
PubMed1993

Muscle glucose uptake in the rat after suspension with single hindlimb weight bearing.

This study was designed to examine the effect of non-weight-bearing conditions and the systemic influences of simulated microgravity on rat hindlimb muscles. For this purpose, rats were suspended (SUS) in a head-down position (45 degrees) with the left hindlimb non-weight bearing (NWB) and the right hindlimb bearing 20% of presuspension body mass (WB). Weight bearing by the SUS-WB limb was accomplished by using a platform connected to a rod in sleeve, cable, and pulley apparatus to which weight could be added. Rats (250-325 g) were assigned to SUS or cage control (CC) conditions for 14 days. The angle between the foot and leg for SUS-WB and CC remained similar (20-30 degrees) throughout the experiment while the SUS-NWB hindlimbs extended to approximately 140 degrees by day 12. On day 14, the soleus, plantaris, and gastrocnemius muscles from the SUS-NWB limbs exhibited significantly lower (P < or = 0.05) masses than presuspension mass values (29, 11, and 21%, respectively). Weight bearing by the SUS-WB limbs prevented the loss of mass by these muscles. In separate groups of SUS and CC rats, 2-deoxyglucose uptake during hindlimb perfusion was significantly higher in both SUS-NWB and SUS-WB hindlimbs at 24,000 microU/ml of insulin compared with CC for all the muscles examined (21-80%). In addition, extracellular space (ml/g) was significantly greater in the soleus muscles from both the SUS-NWB and SUS-WB hindlimbs (64%) compared with CC muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

High extracellular potassium, and not extracellular glutamate, is required for the propagation of spreading depression.

1. Cortical spreading depression (SD) is a propagating transient suppression of electrical activity associated with depolarization, which may contribute to the pathophysiology of important neurological disorders, including cerebral ischemia and migraine. The purpose of this study is to ascertain whether SD propagation depends on local accumulation of extracellular K+ or glutamate. 2. Propagating SD recorded through microdialysis probes perfused with artificial cerebrospinal fluid (ACSF) was much smaller than that recorded with conventional glass microelectrodes, presumably because some SD-induced transient changes in the extracellular fluid composition were buffered by ACSF. We have exploited this effect to determine whether perfusion with a medium containing increasing amounts of K+ and/or glutamate favors SD propagation. 3. Increasing the concentration of K+ (15-60 mmol/l) in the perfusion medium dose-dependently restored SD propagation, whereas application of 100-250 mumol/l glutamate through the microdialysis probe had no effect. Superimposing 200 mumol/l glutamate onto 15 and 30 mmol/l K+ did not further improve the restoration of SD propagation by K+. 4. Because potent uptake mechanisms may efficiently clear exogenous glutamate from the extracellular space, the effect of local inhibition of high-affinity glutamate uptake was also studied. Perfusion of the recording microdialysis probe with 1 mmol/l L-trans-pyrrolidine-2,4-dicarboxylate (L-trans-PDC), either alone or together with 200 mumol/l glutamate, had no effect. In addition, L-trans-PDC did not potentiate the positive effect of 30 mmol/l K+ on SD propagation. 5. These results strongly suggest that high extracellular K+, and not extracellular glutamate, is the driving force sustaining SD propagation.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1977

An anatomical basis for the resistance and capacitance in series with excitable membrane of the squid giant axon.

To correlate periaxonal tissue layer resistance with Schwann cell layer anatomy, cross and longitudinal sections of giant axons of Loligo pealei were examined by transmission electron microscopy. Measurements were made of the width and frequency of mesaxonal clefts entering the Schwann cell layer from the periaxonal space and leaving the cell layer adjacent to the basal lamina. The average mesaxonal cleft width is 10.5 nm. One cm2 of the giant axon surface is enclosed by a single cell layer containing about 690 000 Schwann cells. One cm2 of axon surface has a sheath mesaxonal area of 0.002 cm2 at the periaxonal surface and 0.016 cm2 at the basal lamina, the mesaxons branching frequently as they cross the sheath. The volume of the Schwann cell layer extracellular space was estimated to be roughly 1% of the Schwann cell layer volume. Several models were used to predict the resistance R, across the Schwann cell layer. Assuming the mesaxonal clefts contain seawater, and can be lumped into volume conductors having simple geometries, then (normalized for one cm2 of axon surface) R was estimated to be between 0.4 and 0.9 omega cm2. This compares favourably with electrophysiological estimates of the periaxonal tissue resistance (current clamp value = 0.9 omega cm2 and the voltage clamp value = 1.4 omega cm2) as these electrically measured values include the resistance across the outer connective tissue layer as well as the Schwann cell layer. The value of the Schwann cell membrane capacity was estimated to be approximately 0.7 muF/cm2.

Animals↗
PubMed1992

Anoxia-induced changes in extracellular K+ and pH in mammalian central white matter.

In gray matter (GM), anoxia induces prominent extracellular ionic changes that are important in understanding the pathophysiology of this insult. White matter (WM) is also injured by anoxia but the accompanying changes in extracellular ions have not been studied. To provide such information, the time course and magnitude of anoxia-induced changes in extracellular K+ concentration ([K+]o) and extracellular pH (pHo) were measured in the isolated rat optic nerve, a representative central WM tract, using ion-selective microelectrodes. Anoxia produced less extreme changes in [K+]o and pHo in WM than are known to occur in GM; in WM during anoxia, the average maximum [K+]o was 14 +/- 2.9 mM (bath [K+]o = 3 mM) and the average maximum acid shift was 0.31 +/- 0.07 pH unit. The extracellular space volume rapidly decreased by approximately 20% during anoxia. Excitability of the rat optic nerve, monitored as the amplitude of the supramaximal compound action potential, was lost in close temporal association with the increase in [K+]o. Increasing the bath glucose concentration from 10 to 20 mM resulted in a much larger acid shift during anoxia (0.58 +/- 0.08 pH unit) and a smaller average increase in [K]o (9.2 +/- 2.6 mM). The increased extracellular glucose concentration presumably provided more substrate for anaerobic metabolism, resulting in more extracellular lactate accumulation (although not directly measured) and a greater acid shift. Enhanced anaerobic metabolism during anoxia would provide energy for operation of ion pumps, including the sodium pump, that would result in smaller changes in [K+]o. These effects were probably responsible for the observation that the optic nerve showed significantly less damage after 60 min of anoxia in the presence of 20 mM glucose compared to 10 mM glucose. Under normoxic conditions, increasing bath K+ concentration to 30 mM (i.e., well beyond the level shown to occur with anoxia) for 60 min caused abrupt loss of excitability during the period of application but minimal change in the amplitude of the compound action potential following the period of exposure. The anoxia-induced increase in [K+]o, therefore, was not itself directly responsible for irreversible loss of optic nerve function. These observations indicate that major qualitative differences exist between mammalian GM and WM with regard to anoxia-induced extracellular ionic changes.

Action Potentials↗
PubMed1969

Calculation of the membrane potential in smooth muscle cells of the guinea-pig's taenia coli by the Goldman equation.

1. The intracellular K(+), Cl(-) and Na(+) concentrations in the taenia coli cells of the guinea-pig have been estimated from the total ion content or the extrapolated intracellular tracer content, the sorbitol space and the dry wt./wet wt. ratio.2. The exchange of K(+), Cl(-) and Na(+) was studied by following the uptake and the efflux of these ions with radioactive isotopes. The following efflux values have been calculated: m(K), 4 p-mole.cm(-2).sec(-1); m(Cl), 8.4 p-mole.cm(-2).sec(-1) and m(Na), 7.2 p-mole.cm(-2).sec(-1). These flux values agree well with the influx values, obtained under the same experimental conditions.3. The slowness of diffusion in the extracellular space reduces the Na flux by about 2.5% and the K flux by about 30%. A correction factor of 1.3 has to be introduced to obtain the true K flux.4. The values for the permeability constants calculated by the constant field assumptions are for P(K), 11 x 10(-8) cm/sec; P(Cl), 6.7 x 10(-8) cm/sec and for P(Na), 1.8 x 10(-8) cm/sec. The introduction of these values and of the ion concentrations in the Goldman equation gives a resting potential of -37 mV.5. One of the possible explanations for the discrepancy between the measured resting potential and the calculated one, is that the resting potential of these smooth muscle cells is partly a diffusion potential and partly due to the operation of an electrogenic Na pump.

Animals↗
PubMed1979

Nature of the disturbance in the body fluid compartments during and after surgical operations.

Haematocrit and plasma protein concentrations have been measured in patients undergoing surgical operations in order to estimate relative changes in the volumes of the extracellular and plasma compartments. That these provide valid estimates of volume changes has been shown by applying them to patients known to have lost extracellular fluid. Further confirmation that changes in haematocrit, as indices of falls in plasma volume, are valid even after surgery is provided by measurements of red cell mass, using red cells labelled with 99Tcm. When these methods were applied to patients undergoing abdominal and non-abdominal operations, only the abdominal group showed a significant fall in plasma volume. This fall was caused not by a loss of crystalloid from the extracellular space as a whole, but by a loss of plasma; the magnitude of this loss correlated significantly with the duration of operation. These changes were also demonstrated using the radioisotope dilution indicators 125I (RISA) and 131I (RISA).

Abdomen↗
PubMed1994

Relaxographic imaging.

A fundamental extension of NMR imaging is described. The distribution of relaxation times, the relaxogram, is considered as the third (or fourth) dimension of a set of 2D (or 3D) image data. There is a relaxographic dimension for each type of relaxation: longitudinal, transverse, rotating frame, etc. It is the formal inverse Laplace transform of the relaxation decay data set. Thus, combined relaxography and imaging (CRI) approaches are defined. CRI data can be displayed in two fundamental ways: localized relaxograms (relaxograms from any part of an image) or relaxographic images (images produced from discrete portions of a relaxogram). Relaxographic images are elemental components of the true spin-density image. The CRI concept is demonstrated with longitudinal relaxation data from samples of yeast cells suspended in media containing the contrast agent (CR) GdDTPA2-. This allows the discrimination of subvoxel intra- and extracellular 1H2O signals in the relaxograms from very small image voxels (about 400 nl). It is possible to isolate the intracellular 1H2O resonance from as few as a million cells. Relaxographic images are shown of the extracellular space (i.e., the distribution space of the CR) and the cytoplasmic space of a cell suspension with a cytocrit gradient. These have important potential applications in the in vivo situation. Also, the extent of equilibrium transcytolemmal water exchange can be detected and quantified.

Body Water↗
PubMed1986

The influence of extracellular buffer concentration and propionate on lactate efflux from frog muscle.

Lactate efflux from frog sartorius muscles was measured following a lactate load of about 18 mumol X g-1 induced by a 4-min period of stimulation. Lactate efflux rate was buffer concentration dependent. The initial efflux rate increased from about 150 nmol X g-1 X min-1 in 1 mM MOPS buffer to 400 nmol X g-1 X min-1 in 25 mM MOPS buffer. The addition of 20 mM propionate reduced mean intracellular pH by about 0.2 units and increased lactate efflux rate by 70% at the highest buffer concentration and 400% at the lowest buffer concentration. The observed results are in reasonable agreement with predictions based on a model in which net efflux is limited by diffusion of both buffer and lactate in the extracellular space. Transmembrane lactate efflux appears to consist of two components, one of which is proton linked and carried either by undissociated lactic acid or coupled proton-lactate transport, the other being carried by independent lactate ions.

Animals↗