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At least 847 records · Page 47Linked to original sources
PubMed1998

Human body-fluid distribution during exercise in hot, temperate and cool environments.

Using a simultaneous-dilution technique, we investigated body-fluid volume changes during exercise in seven males, during 50 min of cycling (50% maximal work rate) in hot (36.2 degrees C), temperate (22.0 degrees C) and cool conditions (14.4 degrees C). Total body water (TBW), extracellular fluid (ECFV), plasma (PV) and erythrocyte volumes (RCV) were measured, while blood volume (BV), interstitial fluid volume (IFV), extracellular water (ECW) and intracellular water volumes (ICW) were derived. During the initial 10 min of cycling, BV decreased in all environments (P .01), primarily because of a PV reduction (P = 0.01), while IFV, ECFV and ICW were not significantly changed. By 30 min, BV recovered in the temperate and cool conditions, despite mass losses of 563 and 520 mL (respectively), but remained depleted in the hot condition (P = 0.01). The 50-min volume changes revealed that, throughout exercise, body-fluid losses appeared to be drawn primarily from the extracellular space, regardless of air temperature. In the hot condition, the PV change represented 63% of the TBW loss, with the ICW contributing 23%. It was concluded that, during cycling, progressive dehydration mainly affected the extracellular space, with the intravascular and intracellular spaces being defended in less stressful conditions.

Adult↗
PubMed1976

The subdural neurothelium of the cranial meninges in man.

The neurothelium obtained from human biopsy specimens is a very thin cellular layer located between the dura mater and the arachnoidea. It is a pluri-stratified squamous layer which has some epithelial features (desmosomes and tonofilaments), and lacks connective tissue fibers in the extracellular spaces. Usually there is increased nuclear and cytoplasmic density and enlarged extracellular spaces from the deepest to the most superficial layer. Since neurothelium is fragile and easily torn apart, it probably occupies the position considered to be the subdural space.

Adolescent↗
PubMed1976

[Ultramicroscopic studies on the drainage system of the human corpus luteum].

The granulosa lutein cells of the human corpus luteum have a specialized system of drainage with a particularly formed extracellular space, by which the steroids pass into the capillary vessels. The extracellular space consists of two partial systems: First one finds, similar to the bile capillaries of the liver, lacune-like widnings of the intercellular space, where numerous microvilli of the lining cells are to be found and which are lined by desmosomes and invaginations of the cell membrane. Second there exist relatively wide canals limited by a granular membrane forming a network of their own among the lutein cells. Both systems contact without direct communication. We believe that first the steroids pass into the intracellular lacunes by diffusion or active transport from where they reach the membrane-lined canals by help of the network they pass on to the pericapillar space from where they diffuse into the blood vessels.

Adult↗
PubMed1994

Calciotropic hormones in salt-sensitive essential hypertension: 1,25-dihydroxyvitamin D and parathyroid hypertensive factor.

HYPOTHESIS: Some, but not all, men and women display a pressor response to increases in dietary salt intake. The mechanism(s) underlying this salt-sensitive hypertension remains poorly defined. We have developed a hypothesis that all hypertension arises from an imbalance between mechanisms of cytosolic calcium accumulation from the extracellular space versus calcium release into the cytoplasm from intracellular storage sites. Extracellular calcium-dependent hypertension predominates in salt-sensitive subjects, while excess angiotensin II mediates the excess intracellular calcium release that is characteristic of renin-dependent salt-insensitive forms of hypertension. Studies on pressor hormones: We investigated potential etiologic factors mediating the cellular calcium accumulation in salt-sensitive hypertensive human subjects, and focused on two calcium-related circulating hormonal substances, 1,25-dihydroxyvitamin D and the recently described parathyroid hypertensive factor. Both of these substances directly facilitate calcium transport from the extracellular space in the cell. Furthermore, levels of these hormones are greatest in black normotensive and low-renin essential hypertensive subjects, both groups associated with salt-related hypertensive disease. Lastly, dietary salt loading elevates 1,25-dihydroxyvitamin D and parathyroid hypertensive factor levels, and the greater the level of either hormone, the greater the pressor response to salt. CONCLUSIONS: It is reasonable to consider that these salt-induced cellular ionophoric actions of 1,25-dihydroxyvitamin D and parathyroid hypertensive factor contribute, at least in part, to the mechanism of salt-sensitive hypertension in man.

Biological Factors↗
PubMed1993

Increased water self-diffusion in chronic plaques and in apparently normal white matter in patients with multiple sclerosis.

A new method for measurement of water self-diffusion compensating for zeroth and first order movements was used to study the apparent diffusion coefficient (ADC) in 15 patients with chronic multiple sclerosis (MS) and in two patients with acute MS. Ten healthy volunteers served as controls. A significantly higher ADC was found within chronic plaques compared to the apparently normal white matter of the chronic patients. The ADC was higher in the acute plaques compared to the chronic plaques. The ADC in apparently normal white matter of the chronic patients were significantly higher than in white matter of healthy volunteers. We hypothesize that an increase of the ADC in plaques may be related to an increase in the extracellular space due to oedema and demyelination. The increased ADC in apparently normal white matter suggests that there may be a change in the composition of the white matter of chronic MS patients, perhaps related to oedema and expanded extracellular space.

Adult↗
PubMed2000

[Intercellular integration in the central nervous system].

A humoral mechanism of the intercellular communication in the CNS based on diffusion of neuroactive compounds within the brain extracellular space, was studied. The leading role of the volume transmission was shown in the early stage of ontogeny. Structural basis of this mechanism was studied in adult mammals, and the data on extrasynaptic receptors and release of classical neurotransmitters into the extracellular space was reviewed.

Animals↗
PubMed1981

Surface capacity of electrically syncytial tissues.

An exact geometry-independent formula is derived that gives the total surface membrane capacity of an electrical syncytium in terms of its input resistance (RIN) and the phase angle (phi) of its complex admittance. The formula strips off the effects of resistance in the extracellular space and exposes the true capacity of the external surface of preparations such as skeletal muscle fibers, cardiac Purkinje fibers, or spherical cardiac aggregates. The shape, extent, and resistivity of the extracellular space may be arbitrary and need not be measured. The medium in this space may have an arbitrary and nonuniform resistivity. It is assumed that the tissue is impaled with current and voltage electrodes, so that the intracellular resistance between the electrodes and membranes is negligible or can de dealth with by theoretical calculations. Under these circumstances the total surface membrane capacity at high frequency is determined exactly by RIN and a frequency domain integral over phi. The method is tested with synthetic data for RIN and phi generated by the "disk" model of skeletal muscle fibers and the "pie" model of cardiac Purkinje fibers. The formula allows the "inversion" of these data and the deduction of the correct value of the total surface membrane capacity.

Cell Aggregation↗
PubMedDate not supplied

gamma-Aminobutyric acid levels in the intercellular space in the nucleus accumbens of the rat brain during a nociceptive conditioned response.

Studies on Lister rats, using intracerebral dialysis in behaving animals combined with high-performance liquid chromatography with electrochemical detection, showed that the development and realization of an emotional conditioned response were accompanied by increases in the gamma-aminobutyric acid (GABA) levels in the extracellular space of the medial part of the nucleus accumbens. Regression analysis demonstrated that measures of investigative behavior (horizontal movements, rearings, and sniffing and grooming times) during quenching of the emotional conditioned response (but not on presentation of the experimental chamber to control rats) correlated with individual changes in the extracellular GABA levels in the nucleus accumbens. Thus, this is the first report of in vivo recording of changes in GABA levels in the extracellular space of the brain during realization of normal behavior.

Animals↗
PubMed1975

The distribution of sodium in aortic walls from spontaneously hypertensive and normotensive rats.

The contents of exchangeable sodium, bound sodium and total water and the extracellular space of thoracic aortas from normotensive and spontaneously hypertensive rats were measured. The aortas from the hypertensive rats contained more sodium than those from the normotensive animals while the total water content and extracellular space in the two groups were the same. The capacity to bind sodium in an osmotically inactive form was greater in the aortas from the hypertensives than in those from the normotensives. The difference in binding capacity was of the same order of magnitude as the difference in sodium content, indicating that the excess sodium in the thoracic aortas from the hypertensive rats was osmotically inactive and thus unable to cause water logging.

Animals↗
PubMed2006

Regional differences in spontaneous Ca2+ spark activity and regulation in cat atrial myocytes.

Calcium sparks result from the concerted opening of a small number of Ca2+ release channels (ryanodine receptors, RyRs) organized in clusters in the membrane of the sarcoplasmic reticulum (SR). Calcium sparks represent the elementary events of SR Ca2+ release in cardiac myocytes, and their spatial and temporal summation results in whole-cell [Ca2+]i transients observed during excitation-contraction coupling (ECC). Atrial myocytes generally lack transverse tubules; however, during ECC Ca2+ release is initiated from junctional SR (j-SR) in the cell periphery from where activation propagates inwardly through Ca(2+)-induced Ca2+ release (CICR) from non-junctional SR (nj-SR). Despite the structural differences in the microdomains of RyRs of j-SR and nj-SR, spontaneous Ca2+ sparks are observed from both types of SR, albeit at different frequencies. In cells that showed spontaneous Ca2+ sparks from j-SR and nj-SR, subsarcolemmal (SS) Ca2+ sparks from the j-SR were 3-4 times more frequent than central (CTR) Ca2+ sparks occurring from nj-SR. Subsarcolemmal Ca2+ sparks had a slightly higher amplitude, but were essentially identical in their spatial spread and duration when compared to CTR Ca2+ sparks. Sensitization of RyRs with a low concentration (0.1 mM) of caffeine led to a 107% increase in the frequency of CTR Ca2+ sparks, whereas the SS Ca2+ spark frequency increased by only 58%, suggesting that the nj-SR is capable of much higher Ca2+ spark activity than observed normally in unstimulated cells. The L-type Ca2+ channel blocker verapamil reduced SS Ca2+ spark frequency to 38% of control values, whereas Ca2+ spark activity from nj-SR was reduced by only 19%, suggesting that SS Ca2+ sparks are under the control of Ca2+ influx from the extracellular space. Removal of extracellular Ca2+ eliminated SS Ca2+ sparks completely, whereas Ca2+ sparks from the nj-SR continued, albeit at a lower frequency. In membrane-permeabilized (saponin-treated) atrial myocytes, where [Ca2+] can be experimentally controlled throughout the entire myocyte, j-SR and nj-SR Ca2+ spark frequencies were identical, and Ca2+ sparks could be observed spaced at sarcomeric distances throughout the entire cell, suggesting that all release sites of the nj-SR can become active. Measurement of SR Ca2+ load (10 mM caffeine) revealed no difference between j-SR and nj-SR. The data suggest that in atrial myocytes, which lack a t-tubular system, the nj-SR is fully equipped with a three-dimensional array of functional SR Ca2+ release sites; however, in intact cells under resting conditions, peripheral RyR clusters have a higher probability of activation owing to their association with surface membrane Ca2+ channels, leading to higher spontaneous Ca2+ spark activity. In conclusion, Ca2+ sparks originating from both j-SR and nj-SR are rather stereotypical and show little differences in their spatiotemporal properties. In intact cells, however, the higher frequency of spontaneous SS Ca2+ sparks arises from the structural arrangement of sarcolemma and j-SR membrane and thus from the difference in the trigger mechanism.

Animals↗
PubMed1980

[Cerebral edema (author's transl)].

Edema of vascular origin, which occurs most frequently of all, is usually due to extensive lesions or traumata. It is the result of a change in vascular permeability and requires treatment with corticosteroids. Edema of cellular origin is characterized by swelling of the glia cells, the neurones and endothelial cells with subsequent reduction of the extracellular space. It is associated with hypo-osmolarity and hypoxia and essentially requires the treatment of the causal damage but also the principal general measures of osmotherapy. Interstitial edema is characterized by an increase in the fluid content in the periventricular extracellular space and is due to obstructive hydrocephalus. This form eventually requires neurosurgical treatment.

Brain Edema↗
PubMed1993

Metabolic depression and Na+/K+ gradients in the aestivating Australian goldfields frog, Neobatrachus wilsmorei.

During aestivation the metabolic rate of the Australian goldfields frog Neobatrachus wilsmorei was reduced by 80% from its standard metabolic rate. The in vitro rate of oxygen consumption of isolated muscle and skin from aestivating frogs was up to 50% lower than that of the non-aestivating frogs. This in vitro rate of oxygen consumption was maintained for 6-12 h, indicating an intrinsic metabolic depression of tissues during aestivation. Frogs became dehydrated during aestivation. Muscle, skin and liver also became dehydrated during aestivation, but brain and kidney did not. Na+ and K+ contents and extracellular space measurement for muscle indicated that ion gradients were maintained across the muscle cell membrane during aestivation. Increases in plasma concentrations of Na+ and K+ were matched with similar increases in muscle intracellular ion concentrations. Extracellular space measurements were unsuccessful in the other tissues, but K+ content in all tissues (per dry weight) was maintained during aestivation, and the concentration of plasma K+ did not increase above that which can be accounted for by dehydration, indicating that K+ gradients were maintained.

Animals↗
PubMed1999

Cesium induces spontaneous epileptiform activity without changing extracellular potassium regulation in rat hippocampus.

Cesium has been widely used to study the roles of the hyperpolarization-activated (I(h)) and inwardly rectifying potassium (K(IR)) channels in many neuronal and nonneuronal cell types. Recently, extracellular application of cesium has been shown to produce epileptiform activity in brain slices, but the mechanisms for this are not known. It has been proposed that cesium blocks the K(IR) in glia, resulting in an abnormal accumulation of potassium in the extracellular space and inducing epileptiform activity. This hypothesis has been tested in hippocampal slices and cultured hippocampal neurons using potassium-sensitive microelectrodes. In the present study, application of cesium produced spontaneous epileptiform discharges at physiological extracellular potassium concentration ([K(+)](o)) in the CA1 and CA3 regions of hippocampal slices. This epileptiform activity was not mimicked by increasing the [K(+)](o). The epileptiform discharges induced by cesium were not blocked by the N-methyl-D- aspartate (NMDA) receptor antagonist AP-5, but were blocked by the non-NMDA receptor antagonist CNQX. In the dentate gyrus, cesium induced the appearance of spontaneous nonsynaptic field bursts in 0 added calcium and 3 mM potassium. Moreover, cesium increased the frequency of field bursts already present. In contrast, ZD-7288, a specific I(h) blocker, did not cause spontaneous epileptiform activity in CA1 and CA3, nor did it affect the field bursts in the dentate gyrus, suggesting that cesium induced epileptiform activity is not directly related to blockade of the I(h). When potassium-sensitive microelectrodes were used to measure [K(+)](o), there was no significant increase in [K(+)](o) in CA1 and CA3 after cesium application. In the dentate gyrus, cesium did not change the baseline level of [K(+)](o) or the rate of [K(+)](o) clearance after the field bursts. In cultured hippocampal neurons, which have a large and relatively unrestricted extracellular space, cesium also produced cellular burst activity without significantly changing the resting membrane potential, which might indicate an increase in [K(+)](o). Our results suggest that cesium causes epileptiform activity by a mechanism unrelated to an alteration in [K(+)](o) regulation.

2-Amino-5-phosphonovalerate↗
PubMed1989

The effect of gadolinium DTPA on tissue water compartments in slow- and fast-twitch rabbit muscles.

Proton T2 relaxation and its biexponential components have been determined in rabbit skeletal muscle in the presence and absence of GdDTPA. The effect of GdDTPA, which distributes only in the extracellular space, was greatest in the longer-relaxing T2 component (T22). A 27% reduction in T22 was measured for slow-twitch (red) muscle and 17% for fast-twitch (white) muscle, consistent with the larger extracellular space of the former. Magnetic resonance images demonstrated apparent contrast between red and white rabbit muscles. This contrast was instantaneously enhanced by administration of GdDTPA and returned to near normal levels after approximately 30 min. These functional changes in tissue contrast are consistent with differences in blood perfusion and biological water compartmentation between fast- and slow-twitch skeletal muscles.

Animals↗
PubMedDate not supplied

Is there a zone of vascular vulnerability in the fetal brain stem?

The pattern of malformations in congenital anomalies such as Möbius syndrome and following prenatal cocaine exposure suggests that there is a zone of vascular vulnerability or ischemic sensitivity in the paramedian region of the developing brain stem. In the present study, postmortem examination of the brain of an infant with Möbius syndrome revealed mineralized foci concentrated in paramedian wedge-shaped areas of the pontine and medullary tegmentum. We also examined the development of brain stem vasculature in the rat at the light and ultrastructural level to determine whether anatomical features of the paramedian brain stem region could contribute to elevated incidence of vascular accidents in that zone. Several observations of relevance to the question of vascular vulnerability of the midline were made. Firstly, and as previously noted by other authors, the brain stem midline remains avascular for protracted periods during fetal life. We propose that the inability of vessels in the paramedian region to anastomose across the avascular midline gives rise to paramedian watershed zones that could be vulnerable to ischaemia in the event of hypoperfusion due to teratogenic action. Secondly, we studied the development of cytochrome oxidase activity in the fetal brain stem and noted high oxidative metabolic activity of the somatic efferent nuclei in the paramedian region, which could render their constituent neurons particularly susceptible to hypoxia. Thirdly, our ultrastructural examination revealed large amounts of extracellular space surrounding paramedian pontine vessels in comparison to laterally placed vessels, although there was no significant difference between the vessels of the two regions in tight junction length and endothelial thickness. We propose that the greater proportion of unoccupied extracellular space surrounding medial vessels may contribute to poorer support of these vessels in ischemic/reperfusion episodes. This poor support could in turn give rise to an increased risk of hemorrhage.

Animals↗
PubMed1980

Extracellular shedding of photoreceptor membrane in the open rhabdom of a tipulid fly.

The compound eyes of the Australia tipulid fly, Ptilogyna, shed the bulk of their rhabdomeral membrane to extracellular space during turnover. The rhabdomeres of the retinulae lie in a common extracellular space (ECS), which is subdivided in the proximal retina. Before dawn, a distal region of the microvilli in each rhabdomere differentiates and becomes less electron-dense after conventional fixation. The differentiated region then dilates and develops an irregular profile. A few hours after dawn, the transformed tips break off and form a detritus in the ECS. The degraded membrane is internalised back into the retinula cells by mass endocytosis. Retinulae develop pseudopodia at sites bordering the ECS and engulf the membrane detritus, which comes to lie first of all in vacuoles within the receptor cells and then forms very large multivesicular bodies. The latter transform to multilamellar and residual bodies and are, presumably, lysed. Surrounding these secondary lysosomes are rough endoplasmic reticulum and smooth tubular systems, tentatively considered on comparative grounds to provide hydrolases. The literature concerning the ultrastructure of compound eyes offers a small number of instances where extracellular shedding can be suspected for morphological reasons. Attention is drawn to analogies with the shedding of photoreceptor membranes in vertebrate retinae.

Animals↗
PubMed1978

[The role of the glial cells in the maintenance of the ionic environment of the photoreceptors of the retina of the drone (author's transl)].

A double-barrelled potassium sensitive microelectrode was used to record electrical potentials and K+ activities in the retina of the drone Apis Mellifera during stimulation with trains of flashes, 1 per sec, intense enough to produce receptor potentials of near maximal amplitude. During the stimulation photoreceptors lose about 25% of their intracellular potassium concentration. During stimulation the potassium activity in the extracellular space increased transitorily up to 20 mM and then fell to a plateau. By this time the potassium concentration increased by about 20% in the glial cells. These results suggest that the glial cells may participate in the regulation of K+ activity in the extracellular space. The increase of potassium activity in the glial cells may be a stimulus for activation of cellular metabolism.

Animals↗
PubMed1994

Accelerated in vitro apoptosis of lymphocytes from patients with systemic lupus erythematosus.

SLE is a disease characterized by the generation of an immune response to intact nuclear Ags, especially components of the nucleosome, histones and DNA. The process of programmed cell death, or apoptosis, is characterized by cleavage of chromatin into oligonucleosomes and release of these nucleosomes into the extracellular space. To address the question of whether altered apoptosis might provide a source of extracellular nuclear Ags in SLE, we have examined apoptosis of lymphocytes isolated from patients with SLE, patients with rheumatoid arthritis (RA), and normal controls. Apoptosis was measured by three independent methods and confirmed by gel electrophoresis. Freshly isolated lymphocytes (t0) showed low levels of apoptosis. However, lymphocytes from SLE patients demonstrated a significant increase in the number of apoptotic cells at t0 compared with normal controls and RA patients. In tissue culture, lymphocytes from all patient groups underwent apoptosis, but the rate of apoptosis of lymphocytes derived from SLE patients was 2.35-fold faster than apoptosis of lymphocytes from normal controls or RA patients. The increased rate of apoptosis could not be accounted for by corticosteroid or cytotoxic medication. There was a significant correlation between SLE disease activity as measured by the systemic lupus activity measure and rate of apoptosis in vitro. The release of intact nucleosomes during apoptosis was measured by ELISA; lymphocytes from SLE patients released increased amounts of nucleosomal material into the extracellular space in direct proportion to the rate of apoptosis. Abnormal apoptosis of lymphocytes in SLE may provide a source of extracellular nuclear Ag to drive the immune response and to allow the formation of immune complexes. The demonstration of altered in vitro apoptosis of lymphocytes derived from SLE patients raises the possibility that abnormalities of apoptosis may contribute to the pathogenesis of SLE.

Adult↗