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At least 811 records · Page 45Linked to original sources
PubMed2001

Neurometabolic changes during treatment with moderate hypothermia in a patient suffering from severe middle cerebral artery infarction.

Microdialysis is a means of measuring neurochemical changes in the extracellular space and has been applied in acute brain trauma, subarachnoid hemorrhage and stroke patients. In this study, we monitored neurochemical changes in the extracellular space using microdialysis in a patient with left-sided hemispheric infarction treated with moderate hypothermia (33 degrees C). Microdialysis probes were obtained from the infarcted and noninfarcted hemisphere during hypothermia and rewarming. Concentrations of extracellular substances in the infarcted hemisphere (glutamate, glycerine, lactate/pyruvate) decreased with hypothermia and remained stable (glutamate) or increased (glycerine, lactate/pyruvate) during rewarming. Concentrations of these substances in the noninfarcted hemisphere remained at normal levels. Microdialysis monitoring of therapeutic hypothermia in severe hemispheric infarction might be a useful additional monitoring tool to assess the status of the brain and to predict further deterioration.

Adult↗
PubMedDate not supplied

[The effect of adrenergic agents on the level of extracellular potassium normally and in myocardial ischemia (infarct)].

Adrenergic drugs exert effects on the processes of potassium ions transmembrane distribution between the intra- and extracellular spaces. Drug-induced hypokalemia is the result of beta (predominantly beta-2) adrenergic stimulation. Arrhythmias in myocardial ischemia occur at the combination of hypercatecholaminemia and rapid transmembrane distribution of potassium ions between the intra- and extracellular spaces. The distribution results in the association of the increased local extracellular potassium concentration in the myocardium and rapidly developing hypokalemia.

Animals↗
PubMed1986

A critical maturation period in neonatal-rat-lens development.

The transition of the immature lens to the mature lens was investigated in the Sprague-Dawley rat during the neonatal period which extends for 21 days after birth. The lens of the newborn rat consists of uniformly hydrated cortical and primary fiber cells while the mature lens is characterized by the presence of a nucleus which has a lower water content relative to the surrounding cortex. Our studies reveal that a critical maturation period occurs between days 12-16. In this investigation, the period is defined by the following physiological and anatomical alterations: A significant decline in the rate of lens wet weight growth occurs between days 12-16. However, the growth in dry weight is linear throughout the neonatal period. There is a significant decline in lens percentage water during this 12-16-day period. The loss in lens water is primarily from the intracellular compartment since the lens extracellular space is constant throughout the neonatal period. Lens anterior-posterior and equatorial dimensions exhibit a zero growth rate between days 14-16 and 12-14, respectively. The permeability of lens extracellular space declines significantly during the critical maturation period as determined by Procion Yellow, an extracellular marker. The significant decline in lens percentage water and the decline in the depth of penetration of Procion Yellow to the lens interior during the critical maturation period is related to the transition of an immature to a mature lens.

Animals↗
PubMed2004

C(a2+)-dependent glutamate release involves two classes of endoplasmic reticulum Ca(2+) stores in astrocytes.

Astrocytes can modulate synaptic transmission by releasing glutamate in a Ca(2+)-dependent manner. Although the internal Ca(2+) stores have been implicated as the predominant source of Ca(2+) necessary for this glutamate release, the contribution of different classes of these stores is still not well defined. To address this issue, we cultured purified solitary cortical astrocytes and monitored changes in their internal Ca(2+) levels and glutamate release into the extracellular space. Ca(2+) levels were monitored by using the Ca(2+) indicator fluo-3 and quantitative fluorescence microscopy. Glutamate release was monitored by an L-glutamate dehydrogenase-linked detection system. Astrocytes were mechanically stimulated with a glass pipette, which reliably caused an increase in internal Ca(2+) levels and glutamate release into the extracellular space. Although we find that the presence of extracellular Cd(2+), a Ca(2+) channel blocker, significantly reduces mechanically induced glutamate release from astrocytes, we confirm that internal Ca(2+) stores are the predominant source of Ca(2+) necessary for this glutamate release. To test the involvement of different classes of internal Ca(2+) stores, we used a pharmacological approach. We found that diphenylboric acid 2-aminoethyl ester, a cell-permeable inositol 1,4,5-trisphosphate (IP(3)) receptor antagonist, greatly reduced mechanically induced glutamate release. Additionally, the preincubation of astrocytes with caffeine or ryanodine also reduced glutamate release. Taken together, our data are consistent with dual IP(3)- and caffeine/ryanodine-sensitive Ca(2+) stores functioning in the control of glutamate release from astrocytes.

Aniline Compounds↗
PubMed2003

Oviduct cells express the cyclic AMP-adenosine pathway.

The extracellular cAMP-adenosine pathway refers to the local production of adenosine mediated by cAMP egress into the extracellular space, conversion of cAMP to AMP by ectophosphodiesterase (PDE), and the metabolism of AMP to adenosine by ecto-5'-nucleotidase. The goal of this study was to assess whether the cAMP-adenosine pathway is expressed in oviduct cells. Studies were conducted in cultured bovine oviduct cells (mixed cultures of fibroblasts and epithelial cells, 1:1 ratio). Confluent monolayers of oviduct cells were exposed to cAMP (0.01-100 micromol/L) in the presence and absence of 3-isobutyl-1-methylxanthine (IBMX, 1 mmol/L, an inhibitor of both extracellular and intracellular PDE activity), 1,3-dipropyl-8-p-sulfophenylxanthine (DPSPX, 100 micromol/L, a xanthine that can inhibit extracellular or ecto-PDE activity at high concentrations), or alpha,beta-methylene-adenosine-5'-diphosphate (AMPCP, 100 micromol/L, an ecto-5'-nucleotidase inhibitor) for 0-60 min. The medium was then sampled and assayed for AMP, adenosine, and inosine. Addition of exogenous cAMP to oviduct cells increased extracellular levels of AMP, adenosine, and inosine in a concentration- and time-dependent manner. This effect was attenuated by blockade of total (extracellular and intracellular) PDE activity (IBMX), ecto-PDE activity (DPSPX), or ecto-5'-nucleotidase (AMPCP). The functional relevance of the cAMP-adenosine pathway is supported by the findings that treatment with adenylyl cyclase stimulants (forskolin plus isoproterenol) resulted in the egress of cAMP (97% extracellular) into the extracellular space and its conversion into adenosine. The extracellular cAMP-adenosine pathway exists in oviduct cells and may play an important role in regulating the biology and physiology of the oviduct. This pathway also may play a critical role in regulating sperm function, fertilization, and early embryo development.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1985

23Na NMR studies of rat outer medullary kidney tubules.

Two reservations have previously made interpretation of biological 23Na NMR measurements difficult: the "size" of the extracellular space penetrated by the shift reagent and the possibility of a 60% reduction in the intensity of the NMR-visible 23Na signal due to quadrupolar interactions (Berendsen, H. J. C., and Edzes, H. T. (1973) Ann. N. Y. Acad. Sci. 204, 459-485; Civan, M. M., Degani, H., Margalit, Y., and Shporer, M. (1983) Am. J. Physiol. 245, C213-C219; Gupta, R. K., and Gupta, P. (1982) J. Magn. Reson. 47, 344-350). We have addressed both these issues using a suspension of rat outer medullary kidney tubules, nephron segments responsible for the fine control of total body volume and electrolyte balance. First, the extracellular space penetrated by the shift reagent dysprosium tripolyphosphate, as defined by the extracellular 23Na resonance, revealed a space similar to that which contained extracellular 35Cl- ions. Measurement of an extracellular 35Cl- space using 35Cl NMR was possible because the intracellular 35Cl- resonance was broadened beyond detection in the cells studied. Second, to characterize the reduction of the 23Na signal by quadrupolar interactions, the intracellular 23Na level was raised artificially by simultaneously inhibiting Na+ efflux and increasing the ion permeability of the plasma membrane. Under these conditions, NMR-observable intracellular Na+ reached a level which was approximately 81% of that in the medium, a level determined using chemical techniques. This observation would suggest that the resonance of the intracellular 23Na pool was not subject to a 60% reduction in signal intensity, as a result of nuclear quadrupolar interaction. The intracellular 23Na level measured, under basal conditions, was 23 +/- 2 mumol/ml of cell water (37 degrees C) (n = 3, S.D.) and was demonstrated to be responsive to a number of physiological stimuli. The level was temperature-sensitive. It was reduced by inhibitors of apical Na+ transport, furosemide and amiloride, and it was raised with (Na+ + K+)-ATPase inhibition. The furosemide and amiloride actions described would suggest that the Na+-transporting mechanisms sensitive to these agents (e.g. Na+/K+/Cl- cotransport system, Na+:H+ exchange system) contribute to the regulation of the intracellular Na+ level in the kidney tubular preparation studied.

Adrenalectomy↗
PubMed1975

[Expermental contribution on the genesis of arteriosclerosis caused by hypertension].

Autoradiographic tests carried out on rats with renal hypertension using 3H-proline resulted in an acclerated collagen synthesis by media cells of aorta and coronary arteries. Electronmicroscopically an increased content of collagen fibers and an enrichment of ruthenium-red-positive substances in the extracellular space were found. The 35S-sulfate-incorporation in aorta and coronary arteries of animals with hypertension is also increased. These changes in the extracellular space of the vascular wall have an atherosclerosis promoting effect, probably caused by a distrubance of the permeability.

Animals↗
PubMed2003

Taurine enhances volume regulation in hippocampal slices swollen osmotically.

Cell volume regulation has been studied in neuronal and glial cultures but little is known about volume regulation in brain tissue with an intact extracellular space. We investigated volume regulation in hippocampal slices maintained in an interface chamber and exposed to hypo-osmotic medium. Relative changes in intracellular and extracellular volume were measured respectively as changes in light transmittance and extracellular resistance. Slices exposed to hypo-osmotic medium (200-240 mOsm/L) showed a decrease in light transmittance, which occasionally was preceded by a brief transient increase. However, hypo-osmotic exposure was always accompanied by a monotonic increase in extracellular resistance. Peak changes in light transmittance and extracellular resistance occurred at 15-20 min following exposure to hypo-osmotic medium. Optical evidence of volume regulation (RVD) was observed in six of 12 slices and occurred over the next 60-90 min. We hypothesized that the relatively low incidence of RVD was related to depletion of taurine, an osmolyte known to play an important role in volume regulation, during preparation of the slices. Indeed, taurine levels in freshly prepared slices were <50% of those reported in intact hippocampus. Incubation of slices in 1 mM taurine restored taurine to levels observed in situ and increased both the likelihood and magnitude of RVD in hypo-osmotic medium. Inhibition of taurine flux with 100 microM 5-nitro-2-(3 phenylpropylamino) benzoic acid blocked both RVD and the transient undershoot of volume commonly associated with return of swollen slices to iso-osmotic medium. Taurine treatment had no effect on levels of several other amino acids but preserved slice potassium content. The results indicate a critical role for cellular taurine during hypo-osmotic volume regulation in hippocampal slices. Inconsistencies between optical measurements of cellular volume changes and electrical measurements of extracellular space are likely to result from the complex nature of light transmittance in the interface slice preparation.

Adenosine Triphosphate↗
PubMed1996

Inhibition of ATP-diphosphohydrolase(apyrase) of Torpedo electric organ by 5'-p-fluorosulfonylbenzoyladenosine.

It has been shown previously that ATP is released into extracellular space from pre- and postsynaptic sources in peripheral synapses. The extracellular metabolism of ATP is likely to affect nucleotide- and nucleoside-mediated regulation of neurotransmission. The enzymes responsible for ATP breakdown are nucleotidases whose active site faces the extracellular space. ATPase and ADPase Ca(2+)-dependent activities were characterized in presynaptic plasma membrane preparation from the electric organ of Torpedo. Features described were in accordance with the presence of an ATP-diphosphohydrolase (apyrase EC 3.6.1.5) in this fraction. Active site studies using the affinity label 5'-fluorosulfonylbenzoyladenosine were performed on Torpedo apyrase. ATPase and ADPase Ca(2+)-dependent activities were inhibited with 5'-fluorosulfonylbenzoyladenosine. From this study it is concluded: (1) 5'-fluorosulfonylbenzoyladenosine binds specifically to the active site of apyrase. (2) Divalent cations accelerate the apyrase inactivation rate. (3) Divalent cations are not required for the binding of either the substrate or the inhibitor to the active site. (4) The apyrase active site is more specific for highly phosphorylated nucleotides. The results presented may be extrapolated to apyrases from other sources. The importance of this enzyme and its regulation are discussed.

5'-Nucleotidase↗
PubMed1975

Cell contacts in human islets of Langerhans.

The freeze-fracturing technique was applied to fresh human islets of Langerhans. With this technique, the inside of cellular membranes was revealed, and specific membrane differentiations, hitherto unknown, were observed in the plasma membrane of the endocrine cells. The specific membrane differentiations represent two types of intercellular junctions, namely the tight junction, which determines a closure of the extracellular space and the gap junction which allows molecules and ions to diffuse from one cell to another (sharing the gap junction) without leaking in the extracellular space (intercellular coupling). The presence of such junctions may be important for the secretory behavior of the cells within the islet.

Adult↗
PubMed1978

The dynamics of K+ leakage and recovery in cerebral ischemia.

A combination of K+/DC surface electrode and a fiberoptic fluorometric probe are applied to measurements in brain during cerebral ischemia. The kinetics of the responses of extracellular K+ activity and intracellular NADH fluorescence in the gerbil cerebrum following reversible carotid ligation are measured. K+e shows a two-phase response to carotid occlusion and an extended recovery phase following recirculation. The length of the recovery phase is dependent on the duration and severity of the ischemic period. In the gerbil model the degree of communication in the anterior circulation is variable, whereas a bilateral carotid occlusion is presumed to give complete cerebral ischemia. Pyridine nucleotide fluorescence serves as an indicator of the degree of ischemia. Bilateral carotid occlusions of up to 35 minutes in duration were performed. K+e reaches 30--50 mEq/liter in the extracellular space within the first two minutes. This represents cell depolarization and equilibration of K+ activity levels. Recovery appears to be complete in terms of the ability of the system to clear raised levels of K+e from the extracellular space.

Animals↗
PubMedDate not supplied

Astroglia and glutamate in physiology and pathology: aspects on glutamate transport, glutamate-induced cell swelling and gap-junction communication.

Astroglia have the capacity to monitor extracellular glutamate (Glu) and maintain it at low levels, metabolize Glu, or release it back into the extracellular space. Glu can induce an increase in astroglial cell volume with a resulting decrease of the extracellular space, and thereby alter the concentration of extracellular substances. Many lines of evidence show that K(+) can be buffered within the astroglial gap-junction-coupled network, and recent results show that gap junctions are permeable for Glu. All these events occur dynamically: the astroglial network has the capacity to interfere actively with neurotransmission, thereby contributing to a high signal-to-noise ratio for the Glu transmission. High-quality neuronal messages during normal physiology can then be maintained. With the same mechanisms, astroglia might exert a neuroprotective function in situations of moderately increased extracellular Glu concentrations, i.e., corresponding to conditions of pathological hyper-excitability, or corresponding to early stages of an acute brain injury. If the astroglial functions are failing, neuronal dysfunction can be reinforced.

Animals↗
PubMed2002

Intrinsic optical imaging reveals regionally different manifestation of spreading depression in hippocampal and entorhinal structures in vitro.

The spatiotemporal features of spreading depression (SD) were analyzed in vitro by using combined hippocampal-entorhinal cortex slices. SDs were induced by microinjection of 1 M KCl in the stratum radiatum of the CA1 region of the hippocampus. Measurements of extracellular field potentials, extracellular space (ECS) volume changes and intrinsic optical signal changes were combined to study SD features in different regions of the slice. Each SD was associated with a pronounced shrinkage of the extracellular space (ECS) volume and a decrease in light transmittance. The beginning of the optical signal change occurred simultaneously with the electrographic onset as measured with extracellular microelectrodes but outlasted the dc shift for tens of seconds. The amplitude of the intrinsic optical signal change displayed marked regional variations with greatest changes of 12% in cortical regions. The signal amplitudes were considerably lower in hippocampal regions. The analysis of spread patterns revealed two types of waves: fully propagated waves spreading from CA1 all the way to the temporal neocortex and abortive waves that ceased earlier. The spread velocities displayed pronounced regional differences with highest velocities of 5.4 +/- 0.3 mm/min in the area CA3 of the hippocampal formation and lowest velocities of 2.7 +/- 0.1 mm/min in cortical regions.

Animals↗
PubMed2002

Functional consequences of morphological neuroglial changes in the magnocellular nuclei of the hypothalamus.

The supraoptic and paraventricular nuclei of the hypothalamus undergo reversible anatomical changes under conditions of intense neurohypophysial hormone secretion, such as lactation, parturition and chronic dehydration. This morphological remodelling includes a reduction in astrocytic coverage of neurones resulting in an increase in the number and extent of directly juxtaposed somatic and dendritic surfaces. There is a growing body of evidence indicating that such anatomical plasticity is of functional significance. Astrocytic-dependent clearance of electrolytes and neurotransmitters from the extracellular space appears to be altered under conditions where glial coverage of magnocellular neurones is reduced. Glutamate, for example, has been found to accumulate in the extracellular space in the supraoptic nucleus of lactating animals and cause a modulation of synaptic efficacy. On the other hand, the range of action of substances released from astrocytes and acting on adjacent magnocellular neurones is expected to be limited during such anatomical remodelling. It thus appears that the structural plasticity of the magnocellular nuclei does affect neuroglial interactions, inducing significant changes in signal transmission and processing.

Animals↗
PubMed1994

Evidence for amino acid concentration gradients between CSF and extracellular fluid.

A small volume in the extracellular space of the medulla in the anesthetized cat was perfused with cisternal cerebrospinal fluid (CSF) using a push-pull technique. The recovered perfusate was a mixture of pushed CSF and the extracellular fluid. HPLC-EC analysis showed that the concentration of some primary amino acids in recovered perfusate often differed from their concentrations in CSF. These results suggested that amino acid gradients existed between CSF and the extracellular space.

Amino Acids↗
PubMed1976

Uptake and transport of exogenous proteins by respiratory epithelium.

The tracer proteins, horseradish peroxidase and ferritin, placed in the trachea of guinea pigs were taken up by epithelial cells and transported to the extracellular space. The interval between the introduction of the tracer proteins into the lumen of the trachea and the morphologic demonstration of the porteins in the extracellular space or within the basal portion of the cells was between 30 and 60 minutes. The proteins were transported in vesicles and no penetration of the epithelial intercellular tight junctions was found. The intercellular tight junctions were made permeable to horseradish peroxidase by anesthetic ether and this permeable epithelium was compared to the vesicle type transport. Transepithelial transport of proteins is a possible mechanism for the introduction of antigenic material into the subepithelial lymphoid tissue and this transport may also be of importance in the late onset type of asthma.

Animals↗
PubMed1983

Revised pathophysiology on BBB damage: the edema as an ingeniously provided condition for cell motility and lesion repair.

Probably, the most important evidence concerning the breakdown of the BBB is a large inflow of hematogenous fluid into the extravascular spaces. Thus all parenchymal cell elements represent freely floating cells in this fluid medium called the edema fluid. These essential morphological alterations, such as extremely expanded extracellular space and freely floating cells within the fluid, were also observed in the developing normal fetal brain. Many neuroblasts were vigorously migrating in the fetal brain, as were the macrophages and reactive astrocytes in the edema fluid. Obviously, hematogenous cells and reactive astrocytes in the edematous lesion take part in its repair. Many astrocytes, GFAP positive, in the 3 or 4 day-old lesions, revealed mitosis. And in vitro, when we immersed these astrocytes in the protein and glucose rich medium, they demonstrated a remarkably changed morphology and were moved into the M and G1 phases, thus gaining the ability of cell motility. This was also true in the edema fluid. Brain edema is definitely a serious "pathological" condition. But it is also conceivable from a different biological aspect that as a result of BBB "opening", free extracellular space essential for cell motility and a source of their energy is ingeniously provided for these cells, and thus the lesion can be effectively repaired. The biological significance of the edema fluid was emphasized and stereotaxic morphology and cinematography, supporting the above evidence, have also been presented.

Animals↗