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PubMed2003

Native and minimally oxidized low density lipoprotein depress smooth muscle matrix metalloproteinase levels.

Vascular lesion development is associated with an accumulation of extracellular matrix proteins within the vessel wall. Matrix metalloproteinases (MMPs) degrade these proteins. Conversely, oxidized low density lipoprotein (LDL) is implicated in atherogenesis through, amongst other cellular effects, a stimulation of the deposition of collagen within the vascular lesion. The present study investigated the potential for an interaction between oxidized LDL and MMP levels. Within the vessel wall fibroblasts, smooth muscle, endothelial and infiltrating cells have been reported to secrete MMPs into the extracellular space to effect remodeling of the extracellular matrix. A consequence of angioplasty and atherosclerotic disease is the loss of endothelial cells or endothelial function, respectively. We have investigated the effects of chronic incubation of cultured vascular smooth muscle cells from rabbit thoracic aorta with oxidized LDL and its influence on MMP levels in the extracellular space. Our data indicate that a low concentration of minimally oxidized LDL (0.005 mg/mL) significantly depressed the levels of MMP-2 and MMP-9 present in the culture medium. Native LDL exerted the same effect but exhibited reduced potency. The effects were not attributable to cytotoxicity exerted by the oxidized LDL. The reduction in MMP secretion into the extracellular medium was a result of decreased enzyme synthesis within the smooth muscle cell. Our results demonstrate that an important atherogenic moiety, oxidized LDL, can reduce MMP activity and hence has the potential to increase the deposition of extracellular matrix proteins within SMC-rich vascular lesions.

Animals↗
PubMed1996

X-irradiation-induced changes in the diffusion parameters of the developing rat brain.

Three diffusion parameters of brain tissue, extracellular space volume fraction (alpha), tortuosity (lambda) and non-specific uptake (kappa') of tetramethylammonium were studied in the somatosensory neocortex and subcortical white matter of the rat during postnatal development (postnatal days 2-21) after X-irradiation at postnatal days 0-1. The diffusion parameters were determined from extracellular concentration-time profiles of tetramethylammonium. The tetramethylammonium concentration was measured in vivo with ion-selective microelectrodes positioned 130-200 microns from an iontophoretic source. X-irradiation with a single dose of 40 Gy resulted in typical early morphological changes in the tissue, namely cell death, DNA fragmentation, extensive neuronal loss, blood-brain barrier damage, activated macrophages, astrogliosis, increase in extracellular fibronectin and concomitant changes in all three diffusion parameters. The changes were observed as early as 48 h post-irradiation (at postnatal days 2-3) and still persisted at postnatal day 21. On the other hand, X-irradiation with a single dose of 20 Gy resulted in relatively light neuronal damage and loss, while blood-brain barrier damage, astrogliosis and changes in diffusion parameters were not significantly different from those found with 40 Gy. It is known that the volume fraction of the extracellular space in the non-irradiated cortex is large in newborn rats and diminishes with age [Lehmenkühler A. et al. (1993) Neuroscience 55, 339-351]. X-irradiation with a single dose of 40 or 20 Gy blocked the normal pattern of volume fraction decrease during postnatal development, and in fact brought about a significant increase. At postnatal days 4-5, alpha increased to 0.49 +/- 0.036 in layer III, 0.51 +/- 0.042 in layer IV, 0.48 +/- 0.02 in layer V, 0.48 +/- 0.028 in layer VI and 0.48 +/- 0.025 in the white matter. The large increase in alpha persisted three weeks after X-irradiation. Tortuosity and non-specific uptake decreased significantly at postnatal days 2-5; at days 8-9 they were not significantly different from those of control animals, while they increased significantly at days 10-21. Less pronounced but significant changes in all three diffusion parameters were also found in areas in the ipsilateral hemisphere adjacent to directly X-irradiated cortex. Compared to the control animals [Lehmenkühler A. et al. (1993) Neuroscience 55, 339-351], a significant decrease of alpha, lambda and kappa' was found in the contralateral hemisphere 48-72 h after X-irradiation. Later, alpha values were not significantly different from those in control animals. The decrease in lambda persisted at postnatal days 4-5. A significant increase in lambda and kappa' was found at postnatal days 18-21. We conclude that X-irradiation of the brain in the early postnatal period, even when it results in only relatively light damage, still produces changes in all three diffusion parameters, particularly a large increase in extracellular space volume fraction in all cortical layers, and in the subcortical white matter. Such changes in extracellular volume fraction of the brain can contribute to impairment of signal transmission, e.g. by diluting ions and neuroactive substances released from cells, and can play an important role in functional deficits, as well as in the impairment of developmental processes. Moreover, the increase in tortuosity (inferred from the decrease in apparent diffusion coefficient) in the X-irradiated cortex, as well as in the contralateral hemisphere, suggests that, even when extracellular volume is large, the diffusion of the substances is substantially hindered.

Animals↗
PubMed1986

Immunoultrastructural demonstration of prostatic acid phosphatase isoenzyme 2 in prostatic carcinoma.

Human prostatic acid phosphatase isoenzyme 2 (HPAcP-2) was isolated from semen. This purified enzyme was immunized to rabbit to produce polyclonal antibodies. The specificity of the antibodies was tested by Western blot transfer method. Rabbit IgG-peroxidase conjugate was prepared from the antiserum and used to localize HPAcP-2 in prostatic carcinoma. It was found that in the tumor glandular acinus the normal basal cells were replaced by tumor cells containing reaction product. In the tumor cells, the reaction product was seen in the cisternae of rough endoplasmic reticulum (ER) and Golgi apparatus. The secretory vesicles which contained reaction product-stained granules and some amorphous material were seen to fuse with the apical plasma membrane and discharged their content into the glandular lumen. On the other hand, some secretory vesicles in the tumor cells facing to the basement membrane also discharged their similar content into the extracellular spaces. Reaction product-stained granules were found in the interstitial spaces surrounding the tumor cells. These findings suggest that HPAcP-2 is synthesized on the bound ribosomes and discharged into the cisternae of rough ER. The molecules are transported to the Golgi cisternae. After concentration and packaging, HPAcP-2 molecules are then transferred to the secretory vesicles, and discharged into the glandular lumen and to the extracellular spaces. The isoenzyme released in the extracellular space may reach the blood stream through the interstitial spaces or the lymphatic system, resulting in the elevation of serum HPAcPase level in some prostatic cancer patients.

Acid Phosphatase↗
PubMed1996

Tyrosine kinase is involved in angiotensin II-stimulated phospholipase D activation in aortic smooth muscle cells: function of Ca2+ influx.

In the present study, we examined the effect of angiotensin II (Ang II) on phosphatidylcholine-hydrolyzing phospholipase D activity in subcultured rat aortic smooth muscle cells (SMC). Ang II dose-dependently stimulated the formation of choline and inositol phosphates. The effect of Ang II on the formation of inositol phosphates (EC50 was 0.249 +/- 0.091 nM) was more potent than that on the formation of choline (EC50 was 2.39 +/- 1.29 nM). A combination of Ang II and 12-O-tetradecanoylphorbol-13-acetate (TPA), an activator of protein kinase C, additively stimulated the formation of choline. Staurosporine, an inhibitor of protein kinases, inhibited the TPA-induced formation of choline, but had little effect on the Ang II-induced choline formation. Ang II stimulated Ca2+ influx from extracellular space time- and dose-dependently. The depletion of extracellular Ca2+ by (ethylenebis(oxyethylenenitrilo)) tetraacetic acid (EGTA) significantly reduced the Ang II-induced formation of choline. Genistein and tyrphostin, protein tyrosine kinase inhibitors, significantly suppressed the Ang II-induced Ca2+ influx. Genistein and tyrphostin also suppressed the Ang II-induced formation of choline. These results suggest that Ang II stimulates phosphatidylcholine-hydrolyzing phospholipase D due to Ca2+ influx from the extracellular space in rat aortic SMC, and that protein tyrosine kinase is involved in the Ang II-induced Ca2+ influx, resulting in the promotion of phosphatidylcholine hydrolysis.

Alkaloids↗
PubMed2001

Cadmium toxicity in synaptic neurotransmission in the brain.

Chronic exposure to cadmium causes central nervous system disorders, e.g. olfactory dysfunction. To clarify cadmium toxicity in synaptic neurotransmission in the brain, the movement of cadmium in the synapses was examined using in vivo microdialysis. One and 24 h after injection of (109)CdCl(2) into the amygdala of rats, (109)Cd release into the extracellular space was facilitated by stimulation with high K(+), suggesting that cadmium taken up by amygdalar neurons is released into the synaptic clefts in a calcium- and impulse-dependent manner. Moreover, to examine the action of cadmium in the synapses, the amygdala was perfused with artificial cerebrospinal fluid containing 10-30 microM CdCl(2). The release of excitatory neurotransmitters, i.e. glutamate and aspartate, into the extracellular space was decreased during perfusion with cadmium, while the release of inhibitory neurotransmitters, i.e. glycine and gamma-amino butyric acid (GABA), into the extracellular space was increased during the period. These results suggest that cadmium released from the amygdalar neuron terminals affect the degree and balance of excitation-inhibition in synaptic neurotransmission.

Amygdala↗
PubMed1980

Fate of horseradish peroxidase in the secretion zone of the rat incisor enamel organ.

Adult CDF albino rats were killed from 10 min to 6 hr after a single intravenous dose of HRP. Experimental and control tissues were reacted for peroxidase activity and processed for light and electron microscopy. At 10 min, all extracellular spaces of the secretion zone showed reaction product. A reaction was also seen around Tomes' processes and in a layer of enamel spaces in the region of thin enamel. At later times intervals, reactions around Tomes' processes were also seen in regions of thicker enamel. Tracer was located preferentially at the growth fronts of rod and interrod enamel, and also diffused for some distance into enamel. From 2 to 6 hr, the enamel over the transition zone became heavily labeled. The tracer penetrated for more than 90 micrometer into the enamel and was localized mainly in the interrod enamel. Droplets of dense stippled material in the extracellular spaces between Tomes' processes did not mix with tracer, but sites which contain a light stippled material in the controls (extracellular spaces, vesicles within ameloblasts) showed a reaction. It is concluded that (1) the basal terminal bars of secretory ameloblasts do not impede the flow of large molecules, (2) the apical terminal bars are permeable in early secretion, become increasingly tight as secretion progresses, and are again permeable in the transition zone, (3) ameloblasts can shuttle large extracellular molecules towards the enamel growth fronts, (4) large molecules can diffuse into enamel; rod and interrod enamel differ with regard to the diffusion of large molecules, (5) ameloblasts phagocytose significant amounts of light stippled material. The possibility is considered that extracellular enamel precursor molecules move preferentially towards the enamel growth fronts, perhaps by a mechanism involving membrane flow, and diffuse through enamel in similar fashion as HRP.

Ameloblasts↗
PubMed2003

Changes in dialysate concentrations of glutamate and GABA in the brain: an index of volume transmission mediated actions?

Brain microdialysis has become a frequently used method to study the extracellular concentrations of neurotransmitters in specific areas of the brain. For years, and this is still the case today, dialysate concentrations and hence extracellular concentrations of neurotransmitters have been interpreted as a direct index of the neuronal release of these specific neurotransmitter systems. Although this seems to be the case for neurotransmitters such as dopamine, serotonin and acetylcholine, the extracellular concentrations of glutamate and GABA do not provide a reliable index of their synaptic exocytotic release. However, many microdialysis studies show changes in extracellular concentrations of glutamate and GABA under specific pharmacological and behavioural stimuli that could be interpreted as a consequence of the activation of specific neurochemical circuits. Despite this, we still do not know the origin and physiological significance of these changes of glutamate and GABA in the extracellular space. Here we propose that the changes in dialysate concentrations of these two neurotransmitters found under specific treatments could be an expression of the activity of the neurone-astrocyte unit in specific circuits of the brain. It is further proposed that dialysate changes of glutamate and GABA could be used as an index of volume transmission mediated actions of these two neurotransmitters in the brain. This hypothesis is based firstly on the assumption that the activity of neurones is functionally linked to the activity of astrocytes, which can release glutamate and GABA to the extracellular space; secondly, on the existence of extrasynaptic glutamate and GABA receptors with functional properties different from those of GABA receptors located at the synapse; and thirdly, on the experimental evidence reporting specific electrophysiological and neurochemical effects of glutamate and GABA when their levels are increased in the extracellular space. According to this concept, glutamate and GABA, once released into the extracellular compartment, could diffuse and have long-lasting effects modulating glutamatergic and/or GABAergic neurone-astrocytic networks and their interactions with other neurotransmitter neurone networks in the same areas of the brain.

Animals↗
PubMed2001

Prion protein expression in senile plaques in Alzheimer's disease.

Prion protein (PrPC) is a glycolipid-anchored cell membrane sialoglycoprotein that localises in presynaptic membranes. Since synapses are vulnerable to Alzheimer's disease (AD), the present study examines PrPC expression in senile plaques, one of the major structural abnormalities in AD, by single- and double-labelling immunohistochemistry. Punctate PrPC immunoreactivity is found in diffuse plaques, whereas isolated large coarse PrPC-positive granules reminiscent of dystrophic neurites are observed in neuritic plaques. Finally, PrPC deposition also occurs as dense filamentous and amorphous precipitates in amyloid cores of senile plaques, but not in the walls of blood vessels with amyloid angiopathy. In contrast to PrPC, betaA4-amyloid immunoreactivity is preserved and even enhanced following incubation of the tissue sections with proteinase K prior to immunohistochemistry, thus indicating no PrPC and betaA4-amyloid cross-reactivity in dense amyloid cores of senile plaques. Punctate PrPC deposition in diffuse plaques is similar to that of synaptophysin, a synaptic vesicle-associated protein, as already reported in other studies. Immunoprecipitation, electrophoresis and Western blot studies have shown that synaptophysin, amyloid precursor protein (APP) and betaA4 do not co-precipitate with PrP. These results suggest that synaptophysin, APP and betaA4 are likely not bound to PrP. PrPC accumulation in betaA4-amyloid dense cores may be the consequence of the release of PrP into the extracellular space. Whether PrPC accumulation in the extracellular space is the result of impaired endocytosis and subsequent hydrolysis in the endosomal compartment, in contrast to normal degradation of PrPC, resulting from or occurring in parallel to abnormal APP degradation, deserves further study.

Aged↗
PubMed1987

Autoantibodies--a mechanism of microdebridement.

Antibodies to foreign debris are generally beneficial because they speed inflammation and debridement of tissue. Intracellular components are debris if they reach extracellular space. If not rapidly debrided from extracellular space, intracellular components stimulate autoantibody production. If not debrided, cellular constituents like other foreign material can initiate a chronic tissue response. Antibodies will speed removal of debris if an effective microdebridement mechanism is present. This is their general biologic significance. If the patient has a defective microdebridement system as in lupus erythematosus or rheumatoid arthritis, the autoantibodies occur to large numbers of intracellular substances and accumulate and contribute to tissue damage. Tissue damage occurs and autoantibodies accumulate in lupus erythematosus and rheumatoid arthritis because of inadequate microdebridement. This should not detract from the fact that autoantibodies are a common secondary phenomenon which plays an important part in maintaining tissue microdebridement.

Aging↗
PubMed1996

Comparison of PAF- and fMLP-induced [Ca2+]i transients in human polymorphonuclear leukocytes.

Changes of [Ca2+]i in human polymorphonuclear leukocytes (PMNL) were studied. PMNL suspension was activated three times every 5 min with 10(-7) M PAF and fMLP. Both PAF and fMLP, induced three consecutive [Ca2+]i transients in PMNL suspended in medium with 1 mM Ca2+. The first Ca2+ response was a result of Ca2+ release from internal stores and the extracellular Ca2+ influx, while the second and third responses were completely dependent on Ca2+ influx from extracellular space. The contribution of Ca2+ from intracellular stores to the first PAF-induced Ca2+ response was about 1.4-fold lower in comparison with the first fMLP induced Ca2+ response (27 +/- 1 vs 37 +/- 6% (p < 0.05). Previous addition of PAF enhanced 3-fold (p < 0.001) the PMNL response to fMLP while cells pretreated with fMLP failed to increase their [Ca2+]i after challenge with PAF. PMNL from 40% of donors did not respond to PAF in the presence of 100 nM Ca2+. However, the cells responding to PAF as the cells treated with fMLP or cyclopiazonic acid released almost the entire Ca2+ from intracellular stores after challenge. Subtraction of mean [Ca2+]i transients in the presence of 100 nM Ca2+ from that obtained in medium with 1 mM Ca2+ showed that, in PMNL stimulated with PAF in contrast to the cells treated with fMLP, the onset of Ca2+ influx from extracellular space precedes Ca2+ release from intracellular stores. These results suggest that PAF-induced Ca2+ influx from extracellular space is at least partly independent of Ca2+ release from intracellular stores.

Blood Coagulation Factors↗
PubMed1981

A study of pace-maker potential in rabbit sino-atrial node: measurement of potassium activity under voltage-clamp conditions.

1. A single sucrose-gap voltage-clamp technique was used to control the membrane potential and to measure current in rabbit sino-atrial (SA) strips. K+ activity in the extracellular space was simultaneously measured using K+-selective micro-electrodes. 2. Using double-barrelled K+ selective micro-electrodes it was possible to measure the time course of accumulation or depletion of K+ accompanying a single action potential without complications arising from mechanical or electrical artifacts. 3. K+ activity in the extracellular space increased during the action potential and then decreased to base-line levels during the diastolic depolarization phase. Single beat accumulations of 0.1-0.4 M could be measured. 4. The magnitude of accumulation or depletion of K+ depended upon the membrane potential such that K+ accumulated at potentials positive to -50 mV (K+ efflux greater than K+ uptake) and was depleted from the extracellular space at potentials negative to -50 mV (K+ efflux less than K+ uptake). 5. The rate of K+ depletion was fairly constant during the time course of a clamp step within the range of diastolic depolarization (-55 to -75 mV) even though the accompanying membrane current showed marked time-dependent kinetics. 6. The total membrane conductance measured during the time course of the diastolic depolarization or during the time course of activation of time-dependent 'pace-maker' current remained fairly constant or increased. 7. No reversal potential for the time-dependent 'pace-maker' current could be measured at EK in solutions containing 2.7, 5.4 and 8.1 mM-K+. 8. These results do not support the turn-off a K+ conductance as the primary mechanisms for the generation of the pace-maker potential in SA nodal tissue; rather the results are more consistent with the idea that activation of an inward current, with large positive equilibrium potential, is responsible for pace-making activity.

Animals↗
PubMed1986

Dual peroxidase and colloidal gold-labeling study of angiotensin converting enzyme and angiotensin-like immunoreactivity in the rat subfornical organ.

The cellular relationships between angiotensin converting enzyme (ACE) (EC 3.4.14.1) and angiotensin-like immunoreactivity (AGLI) were examined in the subfornical organ (SFO). Brains from adult rats were fixed by vascular perfusion with 3.75% acrolein and 2% paraformaldehyde. The region containing the SFO was then sectioned on a vibrating microtome. Partially permeabilized sections were immunocytochemically labeled using the peroxidase-antiperoxidase (PAP) or combined PAP and immunogold methods. Goat antiserum to ACE was localized to both non-neuronal and neuronal cells within the SFO. Intense peroxidase immunoreactivity for ACE was associated with the ventricular and basal surface of ependymal cells, the luminal surface of the vascular endothelium, portions of glial membranes exposed to extracellular spaces, and membranous organelles within neuronal processes. Two antisera raised in rabbits against angiotensin II showed peroxidase immunoreactivity within the extracellular spaces and throughout the cytoplasm of numerous axon terminals and a few perikarya and dendrites in the SFO. Axon terminals and dendrites also showed aggregates of AGLI in smooth membranes and vesicles near the plasmalemma. Gold labeling for AGLI was evident in only 6% of the axon terminals and in a smaller number of dendrites containing peroxidase immunoreactivity for ACE. The low incidence of terminals containing both markers appeared to at least partially reflect limited penetration of the 10 nm gold particles. These results provide the first ultrastructural evidence that ACE is associated with the plasmalemma and membranous organelles strategically located for interaction with precursors of angiotensin II or other peptides within the cerebrospinal fluid, extracellular spaces and neurons of the SFO.

Angiotensin I↗
PubMed2005

Oxidized galectin-1 is an essential factor for peripheral nerve regeneration.

Although many factors have been implicated in the regenerative response of peripheral axons to nerve injury, the signals that prompt neurons to extend processes in peripheral nerves after axotomy are not well-understood. As shown in the first chapter, oxidized recombinant human galectin-1 (rhGAL-1/Ox), which lacks lectin activity, promotes initial axonal growth in an in vitro peripheral nerve regeneration model at low concentrations (pg/ml). At a similarly low concentration, rhGAL-1/Ox has also been shown to be effective in enhancing axonal regeneration using in vivo experiments. Moreover, the application of functional anti-rhGAL-1 antibody strongly inhibited axonal regeneration in vivo as well as in vitro. Since galectin-1 (GAL-1) is expressed in the regenerating sciatic nerves as well as in both sensory and motoneurons, these results indicate that GAL-1, which is secreted into the extracellular space, is subsequently oxidized and then may regulate initial repair after axotomy. This possibility was confirmed by Western blot analysis, which revealed that both reduced and oxidized forms of GAL-1 are present in culture media of DRG neurons and immortalized adult mouse Schwann cells (IMS32). Externalized GAL-1/Ox has been found to stimulate macrophages to secrete an axonal regeneration-promoting factor. From these results, we propose that axonal regeneration occurs in axotomized peripheral nerves as a result of cytosolic reduced GAL-1 being released from Schwann cells and injured axons, which then becomes oxidized in the extracellular space. GAL-1/Ox in the extracellular space stimulates macrophages to secrete a factor that promotes axonal growth and Schwann cell migration, thus enhancing peripheral nerve regeneration and functional recovery. These results suggest that rhGAL-1/Ox may be a novel factor for functional restoration of injured peripheral nerves.

Animals↗
PubMed2000

Macromolecule uptake in human melanoma xenografts. relationships to blood supply, vascular density, microvessel permeability and extracellular volume fraction.

The uptake of albumin-Evans blue in human melanoma xenografts was studied and related to blood supply, vascular density, microvessel permeability and extracellular volume fraction in an attempt to identify transport barriers limiting the delivery of macromolecular therapeutic agents to tumours. Three melanoma lines (A-07, R-18, U-25) were included in the study. Tissue concentrations of albumin-Evans blue were determined by spectrophotometry. The [86Rb] uptake method was used to measure tumour blood supply. Vascular density was determined by stereological analysis of histological sections. Microvessel permeability was measured by using the indicator diffusion method. Contrast-enhanced magnetic resonance imaging was used to measure tumour extracellular volume fraction. The fractional volume of the extracellular space governed the uptake of albumin-Evans blue in the tumours. The uptake of albumin-Evans blue in the extracellular space was primarily limited by transport in the vasculature and not by transport across the microvascular wall or the transport through the interstitium. Our study thus suggests that novel strategies for improving the delivery of macromolecular therapeutic agents to tumours should focus on enhancing the tumour blood supply, increasing the half-life of the therapeutic agent in the blood plasma and/or enhancing the volume of the extracellular space available to macromolecules rather than on increasing the permeability of the microvascular wall or improving diffusion conditions in the tumour interstitium.

Albumins↗
PubMed1994

Mechanism of intraocular pressure decrease after contact transscleral continuous-wave Nd:YAG laser cyclophotocoagulation.

Twenty-two eyes of 11 cynomolgus monkeys were subjected to contact transscleral cyclophotocoagulation with a continuous-wave Nd:YAG laser. The right eye of each monkey was coagulated at the pars plicata region by the contact probe placed 1.0 mm from the limbus, while the left eye of each monkey was coagulated at the pars plana region by the contact probe placed 3.0 mm from the limbus. Physiological and morphological studies were carried out up to 6 months after the treatment. The postoperative intraocular pressure showed a significant decrease within 1 week, corresponding to the inflammation of the anterior chamber. A gradual increase of the intraocular pressure occurred from the 2nd week on and returned to the preoperative value 8 weeks after pars plicata coagulation. The pars plana coagulation group maintained the intraocular pressure lower than the preoperative value until the end of the observation period. Histopathological examinations were carried out by the use of tracer particle perfusion into the anterior chamber. The pathologic features of pars plicata coagulation were necrosis, followed by atrophy of the ciliary process. The tracer particles accumulated at the anterior portion of the space between the bundles of ciliary muscle. The pathologic features of pars plana coagulation were necrosis followed by extension of proliferative tissue into the vitreous. The surrounding extracellular space of the stroma was enlarged, and the ciliary muscles were separated from the sclera. The tracer particles accumulated at the enlarged extracellular space of the stroma and the opened suprachoroidal space. These results suggest that the decrease of the intraocular pressure after pars plicata cyclocoagulation resulted from the reduction of aqueous secretion, whereas that after pars plana cyclocoagulation resulted from enhancement of the uveoscleral outflow through the enlarged extracellular space from the anterior chamber into the suprachoroidal space.

Animals↗
PubMed1990

Electron microscopic study of perivascular structure associated with experimentally induced brain edema in cats.

The fine structural features and water content of white matter associated with the resolution process of brain edema were sequentially investigated in the model produced by infusion of autoserum, mock CSF, or ferritin into the centrum semiovale of cats. The correlation between water content and morphological features was good. Mock CSF-infused edema disappeared within 3 days, serum infused edema within 6 days. In a fine structural study of serum-infused white matter, the distended extracellular spaces were found to be occupied with electron-dense materials, active phagocytosis of the dense materials being observed in the macrophages. Around the postcapillary venules, edematous changes were characterized by wide expansion of the perivascular spaces between endothelial cells and astrocytic endfeet. In some instances, the dense materials in the cytoplasm or in the membrane-bound vacuoles of the astrocytic endfeet were continuous with those in the perivascular space, through the hiatuses of the perivascular astrocytic endfeet being separated at their margins. At 3 days after infusion, wide distension of the extracellular space persisted, but the dense materials had markedly diminished. These results strongly suggest that water clearance of vasogenic brain edema does not commence until proteinaceous macromolecules are degraded and removed from the extracellular space. Perivascular channels around the postcapillary venules might also have some role on the movement of edematous fluid.

Animals↗