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At least 1,063 records · Page 59Linked to original sources
PubMed1991

Perpetuation of misinterpretations due to lack of methodical insight. A critical re-evaluation of the determination of 45Ca release from intact guinea-pig atria.

1. The evaluation of still more pretentious and complicated methods is accompanied by a decline of methodical knowledge outside of the own technical field. Interpretations or extrapolations are taken as granted without critical examination of the methodical steps applied. An example is given by re-evaluating the 45Ca release from isolated cardiac tissue and the possible interpretations. 2. 45Ca release and tissue Ca content were measured in isolated guinea-pig left atria during Ca equilibrium and under conditions known to induce net Ca movements. 3. At equilibrium condition (1.8 mM Na2+0) 3 exponential phase of 45Ca release from the atria were observed. The compartments contained 61%, 29% and 10% of total 45Ca; the t1/2 were 2, 12 and 90 min, respectively. 4. The release of 45Ca from the slowly exchanging compartment (t1/2 90 min) decreased during incubation in nominal Ca-free solution, although a net loss of tissue Ca occurred. Addition of EGTA (5 x 10(-5) M) to the washout medium abolished this retardation of 45Ca release. 5. At external Na+ concentrations below 40 mM (substituted by sucrose), the 45Ca release from the slowly exchanging compartment decreased. Simultaneously, the tissue Ca content increased massively. The 45Ca release was further reduced in Na-poor, nominal Ca-free solution. Under both conditions, the presence of EGTA in the washout medium normalized the rate of 45Ca release. 6. The results suggest that the apparent decline of 45Ca release from intact atria upon reduction of the external Ca and Na concentration does not reflect a decrease of the cellular efflux rate, but is the consequence of an enhanced re-uptake of 45Ca from the extracellular space into the myocardial cells. The probability for the released 45Ca either to escape into the organ bath or to become reabsorbed depends on the specific radioactivity of 45Ca in the extracellular space during the washout phase. Thus, this experimental procedure is not suited to demonstrate a Na-Ca exchange at the cardiac sarcolemma.

Animals↗
PubMed1961

Morphological and chemical studies of collagen formation. I. The fine structure of guinea pig granulomata.

This paper describes electron microscopic studies of developing connective tissue in granulomata induced by the subcutaneous injection of carrageenin into guinea pigs. Seven days after injection the granulomata contained many fibroblasts and exhibited rapid production of collagen. The fibroblasts were characterised by an extensively developed endoplasmic reticulum and showed numbers of fine, unstriated filaments in the outer regions of the cytoplasm. The filaments, about 50 A in diameter, tended to lie parallel to and closely adjacent to the cell boundary. The cytoplasmic membrane was frequently ill defined or disrupted, particularly bordering regions in which filaments occurred. In longitudinal sections of extended cell processes, filaments were abundant and, in some instances, the cytoplasmic membrane was barely detectable. In the extracellular space striated collagen fibrils were usually accompanied by filaments, 50 to 100 A in diameter, and these often exhibited the characteristic periodicity of collagen, particularly after intense electron bombardment. Much cellular debris was present in the extracellular space. These observations have led to the suggestion that connective tissue precursors are released from fibroblasts by the disintegration or dissolution of the cytoplasmic membrane and the shedding of cytoplasmic material, as in the apocrine gland cells. In some instances this release may take the form of the elongation from the cell of extended processes; disintegration of the cytoplasmic membrane surrounding these processes then leaves the contents in the extracellular phase.

Animals↗
PubMed1977

Penetration of systemically injected horseradish peroxidase into ganglia and nerves of the autonomic nervous system.

HRP given intravenously to rats and guinea-pigs passes within 5 minutes into the extracellular spaces of the superior cervical and coeliac ganglia, reaching the spaces between neurons and their associated satellite cells and the equivalent spaces between neuronal processes and satellite cells. The sympathetic nerve trunks have a blood-nerve barrier. The myenteric plexus does not contain blood vessels, but is permeable to tracer from the extracellular spaces of the adjacent muscle layers.

Adrenal Medulla↗
PubMed1992

Peripheral injury and anterograde transport of wheat germ agglutinin-horse radish peroxidase to the spinal cord.

Previous observations have revealed labeling in the extracellular space surrounding boutons and unmyelinated fibers in superficial laminae of the spinal cord after injection of the tracer wheat germ agglutinin conjugated to horseradish peroxidase in dorsal root ganglia. The degree of extracellular labeling appeared related to the extent of the damage to the ganglia at the time of the injection. To determine whether injury might produce extracellular labeling, we investigated the effects of unilateral nerve crush or transection on spinal labeling after bilateral injections of the tracer into sciatic nerves. Confirming previous reports, labeling was confined to small dorsal root ganglion cells and to spinal laminae I and II, suggesting a selective affinity of this tracer for unmyelinated fibers. Labeling of both ganglion neurons and superficial spinal laminae was increased on the injured side, probably as a result of increased efficiency of receptor-mediated endocytosis. Electron microscopical observations revealed that the tracer was largely confined to unmyelinated dorsal root fibers bilaterally; a higher percentage of these fibers were labeled on the injured side. In the dorsal horn, the tracer was predominantly within unmyelinated axons and their terminals on the control side, whereas most of the labeling was extracellular and transneuronal on the injured side. The extracellular labeling surrounded unmyelinated fibers and their terminals in the spinal cord, but was excluded from the synaptic cleft. The demonstration that injury is accompanied by significantly increased release of this tracer from the terminals of unmyelinated fibers into the extracellular space suggests that endogenous substances may be released after peripheral lesions as a central signal of injury.

Animals↗
PubMed1995

N-methyl-D-aspartate-induced 45Ca2+ release from pre-labelled adult rat hippocampus in vivo.

We report the results of microdialysis experiments investigating the NMDA-induced release of intracellular Ca2+ in different brain regions. Microdialysis probes were implanted stereotaxically into the striatum, thalamus and hippocampus dentate gyrus (DG) of adult rats. Dialysates were analysed for alterations in the concentration of ionized Ca2+ in an initially calcium-free medium and for changes in 45Ca efflux from the pre-labelled endogenous Ca2+ pools. The application of 5 mM of NMDA to the dialysis medium for 20 min in the striatum, resulted in increases in Ca2+ and 45Ca concentrations by 25% and 35% respectively. After NMDA perfusion in the hippocampus DG and in the thalamus, decreases in the Ca2+ concentration to 65.6% and 38.6% of the basal level respectively, were accompanied by increases in 45Ca efflux, exceeding 1,500% of the basal level in the hippocampus. Cell swelling, and the corresponding reduction of the extracellular space volume was insufficient to explain the huge increase in 45Ca efflux. Thus, our experiments demonstrated that in vivo in the rat hippocampus DG, NMDA induces the release of 45Ca to the extracellular space from unidentified intracellular calcium stores.

Animals↗
PubMed1996

Glioma invasion in the central nervous system.

Invading glioma cells seem to follow distinct anatomic structures within the central nervous system. Tumor cell dissemination may occur along structures, such as the basement membranes of blood vessels or the glial limitans externa, that contain extracellular matrix (ECM) proteins. Frequently, invasive glioma cells are also found to migrate along myelinated fiber tracts of white matter. This behavior is most likely a consequence of using constitutive extracellular ligands expressed along the pathways of preferred dissemination. The extracellular space in anatomic structures, such as blood vessel basement membranes or between myelinated axons, is profoundly different, thus suggesting that glioma cells may be able to use a multiplicity of matrix ligands, possibly activating separate mechanisms for invasion. In addition, enzymatic modification of the extracellular space or deposition of ECM by the tumor cells may also create a more permissive environment for tumor spread into the adjacent brain. Tumor cell invasion is defined as translocation of neoplastic cells through host cellular and ECM barriers. This process has been studied in other cancers, in which a cascade of events has been described that involves receptor-mediated matrix adhesion, degradation of matrix by tumor-secreted metalloproteinases, and, subsequently, active cell locomotion into the newly created space. Although some of these mechanisms may play an important role in glioma invasion, there are some significant differences that are mainly the result of the profoundly different composition of the extracellular environment within the brain. This review focuses on the composition of central nervous system ECM and the recent evidence for the use by glioma cells of multiple invasion mechanisms in response to this unique environment.

Central Nervous System↗
PubMed1985

Cytotactin, an extracellular matrix protein of neural and non-neural tissues that mediates glia-neuron interaction.

An extracellular matrix protein, cytotactin, with widespread tissue distribution has been identified, isolated, and partially characterized. Cytotactin mediates glia-neuron adhesion in vitro, but unlike Ng-CAM, the neuron-glia cell-adhesion molecule, it is absent from neurons. Cytotactin was isolated from 14-day embryonic chicken brains as structurally related polypeptides of Mr 220,000, 200,000, and 190,000. These polypeptides were efficiently extracted in the absence of detergent and appeared to be disulfide-linked into higher polymers. Immunofluorescence staining with specific antibodies indicated that cytotactin is found in extracellular spaces and in basement membranes of a variety of non-neural tissues including smooth muscle, lung, and kidney. In the cerebellum, it appears on glial end-feet, on Bergmann glial fibers, and in extracellular spaces. The molecule is synthesized by glia and cells from smooth muscle, lung, and kidney. It is found at the surface of glia in culture in a cell-associated fibrillar pattern. A survey of the times and sites of its appearance during embryogenesis is consistent with the hypothesis that cytotactin is a cell-substrate adhesion molecule that may mediate cell migration in a site-restricted fashion.

Animals↗
PubMed2003

Distribution of biglycan and decorin in rat dental tissue.

Biglycan and decorin are small leucine-rich proteoglycans that play several biological and structural roles in different tissues and organs. Several reports have indicated that biglycan participates in odontoblast and ameloblast differentiation and in the calcification process. In the present study we show that the expression of biglycan changes from within the ameloblasts and odontoblasts to the extracellular space according to the stage of animal development. In predentin and in the pulp space, however, biglycan was continually expressed throughout the period of investigation. In contrast, decorin was absent in odontoblasts and in ameloblasts and was exclusively expressed in predentin throughout the period of observation. In young rats, however, decorin was expressed in the extracellular spaces of the pulp, where it was concentrated mainly in the peripheral pulp.

Ameloblasts↗
PubMed1990

Fluid flow rates in human peritumoural oedema.

Five patients with various types of brain tumours were infused with x-ray contrast material in a schedule designed to maintain a constant plasma concentration of tracer over a period of 3 hours. CT scans from an equatorial section of the tumour were taken at frequent intervals the first hour; then at 2 and 3 hours, and when possible up to 14 hours. Two different mathematical models-1. simple diffusion, and 2. transport by bulk flow plus diffusion were used to analyze the changes in tracer amount along profiles placed radially from the tumour center into the oedematous white matter. We found that the simple diffusion model could not account for the spread of contrast material in 3 cases. Adding bulk flow transport gave a very good fit to the measurements, also for the late scans. This model gave bulk flow rates of 0.0005 to 0.005 ml cm-2 min-1 for the extratumoural tissue close to the tumour, and values from 0.25 to 0.55 for the extracellular space in this region. We conclude that the peritumoural tissue is "perfused" by oedema fluid at relatively high flow rates and that this flow transports tracer and other components of plasma into the extracellular space.

Body Fluids↗
PubMed1979

Electrical properties of structural components of the crystalline lens.

The electrical properties of the crystalline lens of the frog eye are measured with stochastic currents applied with a microelectrode near the center of the preparation and potential recorded just under the surface. The stochastic signals are decomposed by Fourier analysis into sinusoidal components, and the impedance is determined from the ratio of mean cross power to input power. The data are fit by an electrical model that includes two paths for current flow: one through the cytoplasm, gap junctions, and outer membrane; the other through inner membranes and the extracellular space between lens fibers. The electrical properties of the structures of the lens which appear as circuit components in the model are determined by the fit to the data. The resistivity of the extracellular space within the lens is comparable to the resistivity of Ringer. The outer membrane has a normal resistance of 5 kohm . cm(2) but large capacitance of 10 muF/cm(2), probably because it represents the properties of several layers of fibers. The inner membranes have properties reminiscent of artificial lipid bilayers: they have high membrane resistance, 2.2 megohm . cm(2), and low specific capacitance, 0.8 muF/cm(2). There is so much membrane within the lens, however, that the sum of the current flow across all the inner membranes is comparable to that across the outer surface.

Animals↗
PubMed1995

Endothelin-1 and endothelin-3 regulate differently vasoconstrictor responses of smooth muscle of the porcine coronary artery.

1. Using front-surface fluorometry of fura-2 and medial strips of the porcine coronary artery, we investigated mechanisms by which endothelin-1 (ET-1) and ET-3 function as vasoconstrictors. 2. In the presence of extracellular Ca2+(1.25 mM), ET-1 (10(-10)-10(-7) M) increased cytosolic Ca2+ concentrations ([Ca2+]i) and tension, in a concentration-dependent manner. ET-1, at concentrations greater than 10(-8) M, induced an abrupt elevation of [Ca2+]i which reached a transient peak (the first component, [Ca2+]i-rising phase) and subsequently declined ([Ca2+]i-declining phase) to reach a lower sustained phase (the second component, steady-state phase), while the tension rose monotonically to reach a peak and then slightly and gradually declined. ET-1, at concentrations lower than 10(-8) M, induced slowly developing and sustained increases in [Ca2+]i and tension ([Ca2+]i-rising phase followed by steady-state phase). All concentrations of ET-1 increased tension more slowly than [Ca2+]i. 3. In the presence of extracellular Ca2+, ET-3 (10(-8)-10(-5) M) induced concentration-dependent increases in [Ca2+]i and tension. However, the maximal elevations of [Ca2+]i and tension induced by ET-3 were substantially smaller than those induced by ET-1, indicating the involvement of an ETA receptor subtype. ET-3, at concentrations greater than 6 x 10(-7) M, caused biphasic slowly developing increases in [Ca2+]i and tension. At concentrations lower than 10(-6) M, ET-3 caused monophasic increases in [Ca2+]i and tension. At all concentrations of ET-3, the time courses of increases in [Ca2+]i and tension were similar. 4. The biphasic increases in [Ca2+]i and tension induced by 10-5 M ET-3 and by 1O-7M ET-1 were significantly inhibited by pretreatment with 10-5 M of the Ca2+ entry blocker, diltiazem, although the inhibition of the first component of ET-l-induced [Ca2+]i increase was partial.5. In the absence of extracellular Ca2+, ET-1 induced a concentration-dependent transient increase in[Ca2+]i, possibly due to release of Ca2+ from intracellular stores, and a sustained contraction. In contrast, ET-3 ( 10-6 M) caused little, if any, transient increase in [Ca2+]i and a small sustained contraction.6. Temporal changes in the relationships between [Ca2+]i and tension ([Ca2+]1-tension relationship)during contractions induced by ET-1 and ET-3 were compared with the [Ca2+]i-tension relationship of Ca2+-induced contractions (Ca2+-contractions) obtained by cumulative applications of extracellular Ca2+(0-7.5 mM) to tissues depolarized in the presence of 118 mMK+. In the [Ca2+]i-rising phase, ET-1 increased tension more slowly than [Ca2+]i, thereby shifting the [Ca2+]i-tension relation to the right from that for Ca2+-contractions. In the [Ca2+I-declining and the steady-state phases, ET-1, at concentrations higher than 10-9 M, produced greater tension development than that expected from a given change in[Ca2+ji, resulting in a leftward shift of the [Ca2+]i-tension relation. During ET-3-induced contractions,([Ca2+]i-rising, [Ca2+]i-declining and steady-state phases), the [Ca2+]i-tension relation was similar to that of Ca2+-contractions.7. BQ-123, a selective ETA receptor antagonist, completely inhibited the increases in [Ca2+1]i and tension induced by ET-1 and ET-3.8. These results suggest: (1) That ET-1 elicits vasoconstriction by increasing [Ca2+]i through the activation of Ca2+ influx from the extracellular space and Ca2+ release from intracellular storage sites,and by increasing the Ca2+ sensitivity of the contractile apparatus, whereas ET-3 induces vasoconstriction by increasing [Ca2+1] mainly through Ca2+ influx from the extracellular space. (2) Distinct mechanisms of time-dependent modulation of the Ca2+ sensitivity function in the vasoconstrictor responses to ET-1 and ET-3. (3) That both ET-1- and ET-3-induced contractions seem to be mediated via ETA-receptors in porcine coronary artery, and that the ETA-receptor-mediated effects of ET-1 and ET-3 can be dissociated at the sub-receptor levels of the signal transduction pathway.

Animals↗
PubMed1981

Impedance of the amphibian lens.

1. The electrical resistance of the perfused frog lens was measured using separate internal current passing and voltage measuring electrodes. 2. The resistance values obtained using voltage clamp and direct and alternating current techniques were in good agreement. 3. The voltage transients induced in response to current steps were multi-exponential in form. Increasing the external K concentration reduced both the amplitude of the voltage response and the rise time. 4. The impedance characteristics were investigated in more detail using alternating current analysis techniques. 5. In an equivalent-circuit modelling study it was assumed that there were two major pathways for current flow in the lens. The first through the surface membranes and the second through the inner fibre membranes via the narrow extracellular spaces. 6. The experimental impedance loci could not be adequately fitted by a simple two time constant model and a third time constant was introduced which may represent diffusion polarization effects in the extracellular spaces. 7. The three time constant model gave good and consistent fits to impedance data from a number of preparations. 8. The form of the impedance loci was also dependent on the external K concentration, but the only fitted parameter which changed consistently with external K was the surface membrane resistance (Rs).

Animals↗
PubMed1993

Renal function in patients at risk of contrast material-induced acute renal failure: noninvasive, real-time monitoring.

Real-time changes in renal function were studied in a group of 20 patients at risk of contrast-material-induced acute renal failure during different angiographic procedures. Renal function was evaluated with an ambulatory renal monitor (ARM) after a single injection of the glomerular filtration agent technetium-99m diethylenetriaminepentaacetic acid (DTPA). The ARM was used to continuously monitor the clearance of Tc-99m DTPA activity from the extracellular space in the arm of the patient during angiography. A one-compartment model was used to calculate on-line the rate constant for clearance of Tc-99m DTPA from the extracellular space. Changes in the rate constant were compared with changes in plasma creatinine level measured 1-4 days after angiography. The results showed that the ARM measured rapid changes in renal function during angiography with a resolution time of 5-10 minutes in patients with normal to moderately decreased renal function and 15-20 minutes in patients with severe renal dysfunction. The sensitivity of this technique was superior to that of plasma creatinine level analysis.

Acute Kidney Injury↗
PubMed1974

Pancreatic acinar cells: effects of lanthanum ions on amylase release and calcium ion fluxes.

1. The effect of La(3+) on amylase release and Ca(2+) fluxes in mouse pancreatic fragments in vitro was studied.2. Amylase release was increased by 0.1 mM-La(3+) and progressively inhibited by 1.0-10 mM-La(3+). Non-stimulated and bethanecol stimulated secretion were altered in an identical manner. Inhibition of amylase release was rapid and reversible.3. Uptake of (45)Ca(2+) was multiphasic with equilibrium with stable Ca(2+) still not complete after 2 hr. La(3+) (10 mM) limited uptake of (45)Ca(2+) to the extracellular space and slightly decreased total Ca(2+) content. Lower concentrations of La(3+) affected (45)Ca(2+) uptake and total Ca(2+) content in a biphasic manner which paralleled effects on amylase release.4. La(3+) restricted washout of (45)Ca(2+) to isotope in the extracellular space and abolished the bethanecol-stimulated increase in (45)Ca(2+) efflux.5. Uptake of (45)Ca(2+) into intracellular space, as measured by the ;lanthanum' method, was not affected by bethanecol.6. Tissue ultrastructure and Na(+) and K(+) content were not affected by La(3+).7. It is concluded that an influx of extracellular Ca(2+) is not important for triggering of secretion and that La(3+) may inhibit amylase release by acting on the release process rather than on Ca(2+) influx.

Amylases↗
PubMed1984

The application of EDXS to the biological sciences.

The distribution of chemical elements in soft tissues may be faithfully preserved by very rapid freezing. Most often the material is then cryosectioned and the sections frozen-dried prior to analysis, but direct analysis in the hydrated state is an established alternative. For bulk specimens, the shape of the analysed volume is uncertain. But whichever current model is accepted, analytical spatial resolution must generally be limited to the order of 1 micron. Such specimens can be suitable for the specific analysis of cytoplasm, cell nuclei and large extracellular spaces but not for study on a finer scale. Analytical spatial resolution in the range 200-500 nm is obtainable with sections cut approximately 1 micron thick. In the frozen-hydrated state, small extracellular spaces can be analysed but multiple scattering obscures intracellular detail in the STEM image. The irradiation required for an EDXS analysis, approximately 50 nanoCoulomb (50 nanoAmpere seconds), need not produce intolerable radiation damage when spread over an area 200 nm or more in diameter. Finer structure, for example mitochondria and regions of rough or smooth endoplasmic reticulum, can be identified and analysed in frozen-dried cryosections cut approximately 100 nm thick. Recently such features have been visualized in 100 nm frozen-hydrated sections where the water is vitreous. This opens the prospect of analysing material where elemental distributions have been preserved on a very fine scale, since one might avoid even the ionic shifts from aqueous solution to supramolecular structures which must occur on freeze-drying. But radiation damage may be prohibitive when an irradiation of 50 nanoCoulomb is concentrated into a hydrated area less than 200 nm in diameter.

Animals↗
PubMed1994

Expression of transforming growth factor-beta 1 and its relation to endomysial fibrosis in progressive muscular dystrophy.

Progressive muscular dystrophy is characterized by muscle fiber necrosis, regeneration, and endomysial fibrosis. Although absence of dystrophin has been known as the cause of muscle fiber degeneration, pathogenesis of interstitial fibrosis is still unknown. Transforming growth factor-beta 1 (TGF-beta 1) induces accumulation of extracellular matrix in various diseases, such as liver cirrhosis and interstitial pneumonitis. To investigate its function on the pathogenesis of progressive muscular dystrophy, it was necessary to determine the degree of TGF-beta 1 expression and the site of TGF-beta 1 immunoreactivity. In Duchenne muscular dystrophy and most of Becker muscular dystrophy, high TGF-beta 1 immunoreactivity expressed on muscle fibers and extracellular space. In other myopathies with endomysial fibrosis, however, TGF-beta 1 was seldom observed. We also examined the immunoreactivity of the latent TGF-beta binding protein, which is bound to the TGF-beta precursors. In all Duchenne muscular dystrophy and half of Becker muscular dystrophy cases, high latent TGF-beta 1 binding protein immunoreactivity was seen, but in other myopathies its immunoreactivity was seldom seen on muscle fibers or extracellular space. Therefore TGF-beta 1 may play an important role in synthesis and accumulation of extracellular matrix in progressive muscular dystrophy.

Animals↗
PubMed1995

On the use of 133Cs as an NMR active probe of intracellular space in vivo.

Data are presented from 133Cs NMR studies on both excised and in situ tissues from rats fed a regular diet and administered i.p. CsCI in aqueous solution for 6 to 14 days. Cesium is an NMR-active potassium analog which accumulates in the intracellular spaces of tissues [Davies et al., Biochemistry 27, 3547 (1988); Shehan, B.P. et al., Magn. Reson. Med. 30,573 (1993)]. Chemical shifts, relaxation properties, sensitivity and detectability of cesium in tissues were investigated. Consistent with previous reports, two resonances (representing intra- and extracellular cesium) were detected in blood. Only one resonance was detected in brain, kidney, and muscle tissue. Efforts to resolve intra- and extracellular components by T1 and T2 relaxation discrimination were not successful. Following i.p. administration, cesium accumulates intracellularly with a brain-to-cerebrospinal fluid concentration (mumol/g) ratio of 9:1 and a thigh muscle-to-plasma concentration ratio of 40:1. Considering the small extracellular volume in these tissues (ca 18% and 10%, respectively), the net content differences between intra- and extracellular cesium are approximately 40-fold in brain and 360-fold in muscle. The concentration ratio of cesium in brain to cesium in cerebrosinal fluid decreased to 3:1 1 h after death, indicating a relatively slow rate of leakage of cesium from the intra- to extracellular space in the face of bioenergetic failure. These data suggest that the cesium signal is dominated by the intracellularly located cesium and, thus, cesium may be useful as a probe of the intracellular environment despite an inability to resolve and directly observe distinct resonances from intra- and extracellular spaces.

Animals↗
PubMed1995

Delayed elevation of platelet activating factor in ischemic hippocampus.

We used in vivo microdialysis to define the chronological relationship between release of thromboxane and platelet activating factor (PAF) into the extracellular space of ischemic hippocampus. The thromboxane level peaked after 20 min of postischemic reperfusion, followed by a delayed PAF response 120 min later. We conclude that cerebral ischemia causes delayed elevation of PAF in the extracellular space, long after the immediate synthesis and release of thromboxane metabolites.

Analysis of Variance↗