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PubMed1984

Comparative physiologic performance of polymethyl methacrylate and gas-permeable contact lenses.

A short-term study of the physiologic response of the cornea to polymethyl methacrylate (PMMA) contact lenses and hard, gas-permeable contact lenses of different materials (polycon and Menicon 02), thicknesses, and fittings, was carried out on nine unadapted subjects using one eye as the experimental eye and the other as the control eye (no lens). Changes in corneal thickness were monitored at seven locations across the cornea using an electronic micropachymeter. It was found that gas-permeable lenses produced less corneal swelling than the PMMA lenses. However, lens thickness and the fit of the lens were still important control variables with these gas-permeable lenses. The thin gas-permeable lens produced less swelling than thicker lenses, and the flatter fitting gas-permeable lenses produced less swelling than the steeper fitting lenses. The swelling with all the hard lenses studied was confined primarily to the central 6 mm of the cornea.

Adult↗
PubMed1988

Prostaglandin-independent inhibition of ocular vascular permeability by a platelet-activating factor antagonist.

Platelet-activating factor (PAF), a lipid mediator of inflammation, may markedly increase vascular permeability. We assessed the ability of the PAF antagonist SRI 63-441 to inhibit ocular vascular permeability induced by the intravenous injection of endotoxin or anterior chamber paracentesis. The PAF antagonist SRI 63-441 significantly blocked ocular vascular permeability following either intravenous endotoxin or anterior chamber paracentesis as determined by the reduction in accumulation of 70,000-molecular-weight fluorescein isothiocyanate-conjugated dextran or serum proteins into the anterior chamber. SRI 63-441 did not reduce increases in aqueous humor prostaglandin E2 levels. The efficacy of the PAF antagonist was additive in combination with either topical indomethacin or topical corticosteroid. Combined therapy almost completely prevented increases in ocular vascular permeability. These data support the conclusion that multiple mediators contribute to ocular vascular permeability and that combinations of pharmacologic agents may be superior to a single drug.

Animals↗
PubMed1988

Changes of the permeability of round window membrane in otitis media.

The effects of endotoxin, exotoxin, and otitis media on the permeability of the round window membrane (RWM) in chinchillas was investigated by detecting tetraethylammonium chloride, applied to the RWM, using a potassium-selective microelectrode in the scala tympani. The RWM, 48 hours following the application of endotoxin or exotoxin, became significantly more permeable to tetraethylammonium chloride than the normal RWM. Two weeks after the obstruction of the eustachian tube, the permeability of the RWM was decreased. These results suggest that bacterial toxins and the consequential migration of chemical inflammatory mediators act as promotive factors of RWM permeability, and that a pathologic thickness of the RWM and the presence of effusion induced by the obstruction of the eustachian tube acts as an inhibitory factor. In the clinical role of RWM permeability in human otitis media, these two factors must be taken into consideration.

Animals↗
PubMed1990

Permeability of the round window membrane to middle-sized molecules in purulent otitis media.

The effect of pneumococcal otitis media on the permeability of the round window membrane was evaluated using tetraethylammonium ions as a tracer. Round window membrane permeability is reduced significantly at resolved stages of purulent otitis media. In contrast, measurements of round window membrane permeability indicate that acute purulent otitis media has a tendency to facilitate such permeability. Moreover, histologic observations of the round window membrane following bacterial inoculation further support the evidence of functional changes in round window membrane permeability. These findings indicate that the round window membrane in resolved stages of purulent otitis media plays a protective role in preventing the penetration of harmful substances into the inner ear.

Animals↗
PubMed1988

Increased intestinal permeability associated with infection in burn patients.

Thermal injury may be associated with disruption of normal gut barrier integrity. To test this hypothesis, we assessed intestinal permeability with the nonmetabolizable, poorly absorbed disaccharide lactulose, which is efficiently excluded by the normal intestinal mucosa. Permeability studies were performed in 15 burned patients (aged 18 to 67 years; mean burn size, 40%) and 11 healthy controls. Lactulose, 10 g, was administered enterally, together with 5 g of mannitol as a control, and urinary excretion rates were determined. Lactulose excretion and the lactulose/mannitol excretion ratio increased threefold (160 +/- 30 vs 57 +/- 7 mumol and 0.113 +/- 0.033 vs 0.035 +/- 0.005) in the infected patients (sepsis score, 10 +/- 2; burn size, 38% +/- 6%). In contrast, noninfected burn patients (sepsis score, 0) had permeability values similar to those of controls (66 +/- 10 mumol and 0.036 +/- 0.007). Permeability increased as the severity of infection increased. Infection in burn patients is associated with increased bowel permeability. The intestine may be a primary source of sepsis. Alternatively, the systemic response to infection may alter gut barrier function, which could facilitate translocation of bacteria and absorption of endotoxin.

Adolescent↗
PubMed1993

Intestinal permeability after severe trauma and hemorrhagic shock is increased without relation to septic complications.

After thermal injury, alterations in intestinal permeability have been demonstrated and have correlated with subsequent infections. We measured intestinal permeability on the second day after severe trauma and hemorrhagic shock (ruptured abdominal aneurysm). The mean (+/- SD) lactulose-mannitol (L/M) excretion ratio was 0.012 +/- 0.005 in seven healthy control subjects, 0.069 +/- 0.034 in 11 severely traumatized patients, and 0.098 +/- 0.093 in eight patients with aneurysm, indicating a significant increase of intestinal permeability in both patient groups. No significant correlation was found between L/M ratios and age, severity of injury or shock, lactate levels on admission, APACHE (acute physiology and chronic health evaluation) II score, daily pulmonary gas exchange parameters, or mean multiple organ failure scores. No difference in intestinal permeability between patients with and without subsequent infections could be demonstrated. In 11 patients we looked for endotoxin in the systemic circulation. In six patients endotoxemia was present immediately after admission and before the L/M test. However, during the L/M test and 1 day afterward no circulating endotoxin was observed. The present data provide evidence for the hypothesis that increased intestinal permeability and subsequent infectious complications are independent phenomena, frequently seen in patients after severe trauma or hemorrhagic shock.

Adolescent↗
PubMed1997

Proteinase-free myeloperoxidase increases airway epithelial permeability in a whole trachea model.

In cystic fibrosis the bronchiectatic conducting airways have large numbers of neutrophils in their walls and in their luminal contents. The neutrophil's primary granule enzyme activities of elastase and peroxidase are increased in the sputum of these patients. It has been postulated that these enzymes--together or individually--act to damage the airway epithelium. However, only peroxidase activity has consistently correlated with the degree of structural and functional airway disease in these patients with leakage of plasma protein into the airway lumen (Regelmann et al., Pediatr Pulmonol, 1995; 19:1-9). The present study was designed to test whether human neutrophil-derived myeloperoxidase can independently produce bronchial epithelial damage without the presence of proteases, as measured by increased permeability of the airway epithelium. Human peripheral blood neutrophils were purified, their primary granules isolated, and their peroxidase purified using affinity and ion exchange column chromatography. Activity of the proteinase-free peroxidase was measured using a chromogenic substrate. The effect of this peroxidase on the permeability of excised rat tracheas was measured using radioactive and fluorescent-labeled non-ionic molecules of varying molecular weight. Rat tracheas exposed to 15 minute treatments with either 130 U of peroxidase or hydrogen peroxide (10(-5) M) did not show a significant increase in the permeability of the epithelium to [3H]inulin, [14C]sucrose, and fluorescein isothiocyanate dextran 20 compared with control tracheas. However, those tracheas exposed to 130 U peroxidase followed by 10(-5) M hydrogen peroxide showed an increased permeability to each of the three test solutes. We conclude that proteinase-free myeloperoxidase, in the presence of non-toxic concentrations of its substrates, hydrogen peroxide and halide, produced increases in permeability to non-ionic molecules in the rat trachea within 15 minutes.

Animals↗
PubMed2000

Evaluation of an accelerated Caco-2 cell permeability model.

An accelerated 3-7-day Caco-2 cell permeability model was examined and compared to the traditional 21-25-day model. Caco-2 cell permeability coefficients (P(Caco-2)) of 33 structurally diverse small molecular weight compounds from apical to basolateral (AP-->BL) direction in the accelerated model were approximately twice those in the traditional model. As observed with microscopy and transepithelial electrical resistance measurements, this difference was attributed to less confluent and differentiated Caco-2 cell monolayers in the accelerated model. However, there were no significant differences in rank ordering of the compounds. The expression of P-glycoprotein in the accelerated model was shown to be significantly less than that in the traditional model. This resulted in lower permeability directional ratios defined as the ratio between permeability coefficients from BL-->AP and from AP-->BL for compounds that were cellular efflux pump substrates. The accelerated model may not be suitable for studying cellular efflux pumps such as P-glycoproteins. However, it is a feasible alternative to the traditional model for rank ordering of compounds in the process of drug discovery and development by significantly improving the turnover time and labor efficiency. This makes it an excellent Caco-2 cell permeability model for high throughput screening.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2001

Inhibition of renal permeability towards albumin: a new function of apolipoproteins with possible pathogenetic relevance in focal glomerulosclerosis.

Focal segmental glomerulosclerosis (FSGS) is a degenerative renal disease characterized by the accumulation of extracellular matrix and lipids within the glomerular tuft. It has been proposed that an abnormal renal permeabilization towards proteins induced by a putative plasma factor is, in some way, involved in the pathogenesis of the disease. In this paper, we measured the plasma permeability activity (Palb) in several sera of patients with FSGS and found a mean activity of 0.82+/-0.03 which means a marked increase compared to a mean Palb of 0.16+/-0.03 in normal controls. Coincubation of FSGS and normal serum reduced the permeability activity within the normal range; normal serum added to the incubation medium after the glomeruli had already been exposed to the FSGS serum had no effect, suggesting the presence of inhibitory substances with a direct effect on a circulating substrate. Finally, the antipermeability activity was retained when heated to 60 degrees C but not to 100 degrees C. By serial fractionations of normal serum and reported activity measurements at each step, five natural occurring inhibitors of albumin permeabilization were purified and characterized by matrix assisted laser desorption/ionization-mass spectrometry (MALDI-MS), as components of apolipoproteins (apo) (apo E2 and E4, apo L, the high Mr apo J and a 28 kDa fragment of apo A-IV). Coincubation of each apolipoprotein with FSGS serum inhibited permeability, but only apo J and apo E2 and E4 were found to be crucial for the process. In conclusion, we have purified from normal serum five inhibitors of permeability induced by FSGS serum, all corresponding to apolipoproteins. An imbalance between permeability factors and apolipoproteins may play a pathogenetic role in FSGS.

Amino Acid Sequence↗
PubMed1986

Opening the blood-brain and blood-tumor barriers in experimental rat brain tumors: the effect of intracarotid hyperosmolar mannitol on capillary permeability and blood flow.

Using quantitative autoradiography, we investigated the effect of intracarotid infusions of hyperosmolar mannitol solutions on capillary permeability and blood flow. Capillary permeability, expressed in terms of a blood-to-tissue transfer constant (K), was determined in two rat brain tumor models by measuring the entry of 14C-alpha aminoisobutyric acid into brain tumor, into brain tissue adjacent to tumor, and into cortex. Cerebral blood flow was determined by measuring the uptake of 14C-iodoantipyrine in one rat brain tumor model. Blood flow was examined in the same regions as K, as well as in the corpus callosum. Before mannitol administration, K values in both Walker 256 (W256) carcinosarcoma and C6 gliomas were much higher than those in cortex. C6 gliomas were about three times more permeable than were W256 tumors. There was a direct correlation between tumor size and increased capillary permeability. Mannitol at a concentration of 1.37 M did not increase the K values for either tumor or adjacent tissue. At 1.6 M, mannitol increased the K values for both tumors (1.7-fold in C6 glioma and 13-fold in W256) as well as for adjacent tissue. At both concentrations, mannitol markedly increased cortical K values in all groups: by 48- to 72-fold at 1.37 M and by 90- to 105-fold at 1.6 M. The net effect of the mannitol was to reverse the tumor-to-cortex permeability relationship. Cortical blood flow increased modestly after intracarotid mannitol administration on both sides of the brain. These data provide little justification for using intracarotid mannitol during chemotherapy of human brain tumors.

Animals↗
PubMed2005

Monitoring myeloablative therapy-induced small bowel toxicity by serum citrulline concentration: a comparison with sugar permeability tests.

BACKGROUND: Intestinal mucositis is an important cause of cancer treatment-related morbidity and mortality, carrying a serious economic burden. Currently, objective parameters are lacking that would enable the monitoring of gut damage in routine clinical practice, thus hindering the development of clinical studies designed to investigate potential new strategies aimed at reducing or preventing this side effect. The authors investigated the characteristics of serum citrulline concentration compared with sugar permeability tests with respect to its use as a marker for cancer treatment-induced small bowel injury. METHODS: In this prospective study, 10 patients with hematologic malignancies who were receiving myeloablative therapy had gut toxicity assessed with sugar permeability tests. Serum citrulline concentrations also were determined using archival serum samples. The association between both parameters and their respective characteristics were analyzed and compared with data from the literature. RESULTS: Sensitivity and specificity were better for the citrulline assay compared with sugar permeability tests. Maximum gut damage assessed with the citrulline assay was observed 1-2 weeks earlier compared with the sugar permeability test. Similarly, citrulline indicated recovery of gut damage at 3 weeks after transplantation, whereas most sugar permeability tests remained abnormal. CONCLUSIONS: The simplicity of the method, the low costs, and the lack of drawbacks to the method make the citrulline assay the first choice for measuring and monitoring treatment-related gut damage and provides an objective parameter for cancer treatment-related gut toxicity.

Adult↗
PubMedDate not supplied

Increased retinal endothelial cell monolayer permeability induced by the diabetic milieu: role of advanced non-enzymatic glycation and polyol pathway activation.

BACKGROUND: Increased vascular permeability could be involved in the pathogenesis of diabetic retinopathy. The present study was aimed at assessing whether high glucose concentrations can impair retinal endothelial cell barrier function directly, irrespective of changes in other determinants of permeability, and the role of non-enzymatic glycation and polyol pathway activation in these alterations. METHODS: Bovine retinal endothelial cells (BREC) were exposed for various periods to high glucose vs iso-osmolar mannitol and normal glucose containing media+/-agents mimicking or inhibiting advanced glycation end product (AGE) formation and polyol pathway activation. Monolayer permeability was assessed by measuring the transendothelial passage of (125)I-labeled proteins. RESULTS: Permeability increased significantly (up to +70%) in BREC exposed to high glucose, but not to mannitol, for 1-30 days, vs normal glucose control cells. Exposure to AGE-modified bovine serum albumin (BSA) (> or = 90%) and, to a lesser extent, sorbitol (+28%) mimicked the high glucose effect. The AGE formation and nitric oxide synthase (NOS) inhibitor aminoguanidine significantly reduced (by 60%) changes induced by 30-day exposure to high glucose, whereas methylguanidine, which inhibits only NOS activity, did not affect permeability. Aldose reductase or sorbitol dehydrogenase inhibitors decreased (by approximately 40%) the enhanced leakage produced by 1-day, but not 30-day, incubation in high glucose. CONCLUSIONS: The present results indicate that high glucose is capable of impairing retinal endothelial cell barrier function directly and that non-enzymatic glycation and polyol pathway activation may mediate these changes, with AGEs participating in the long-term alterations and increased flux through the sorbitol pathway in the short-term effect.

Animals↗
PubMed2005

Mechanisms of tumor vascular shutdown induced by 5,6-dimethylxanthenone-4-acetic acid (DMXAA): Increased tumor vascular permeability.

The novel vascular targeting agent 5,6-dimethylxanthenone-4-acetic acid (DMXAA) has completed phase 1 clinical trial and has shown tumor antivascular activity in both mice and humans. We have investigated its ability to change tumor vascular permeability, relating it to tumor vascular perfusion and other responses. The murine colon 38 adenocarcinoma was grown in C57Bl wild-type mice and mice lacking expression of either tumor necrosis factor receptor-1 (TNFR1(-/-)) or TNF (TNF-/-). Tumor vascular permeability, as measured by extravasation of albumin-Evans Blue complexes 4 hr after DMXAA treatment, was significantly increased in tumor tissue in C57Bl, TNFR1-/- and TNF-/- mice but not in normal (skin) tissue. Significant linear relationships were found between increased tumor vascular permeability, decreased functioning tumor blood vessels (measured by Hoechst 33342 staining at 4 hr), increased plasma 5-hydroxyindole-3-acetic acid concentrations (as a measure of serotonin release by platelets) and the degree of induced tumor hemorrhagic necrosis. The results support the hypothesis that DMXAA increases tumor vascular permeability both directly and through the induction of other vasoactive mediators, including TNF. DMXAA might be useful clinically to potentiate the vascular permeability of other anticancer modalities such as cytotoxic drugs, antibodies, drug conjugates and gene therapy.

Adenocarcinoma↗
PubMed1994

Voltage-dependent calcium-permeable channels in the plasma membrane of a higher plant cell.

Numerous biological assays and pharmacological studies on various higher plant tissues have led to the suggestion that voltage-dependent plasma membrane Ca2+ channels play prominent roles in initiating signal transduction processes during plant growth and development. However, to date no direct evidence has been obtained for the existence of such depolarization-activated Ca2+ channels in the plasma membrane of higher plant cells. Carrot suspension cells (Daucus carota L.) provide a well-suited system to determine whether voltage-dependent Ca2+ channels are present in the plasma membrane of higher plants and to characterize the properties of putative Ca2+ channels. It is known that both depolarization, caused by raising extracellular K+, and exposure to fungal toxins or oligogalacturonides induce Ca2+ influx into carrot cells. By direct application of patch-clamp techniques to isolated carrot protoplasts, we show here that depolarization of the plasma membrane positive to -135 mV activates Ca(2+)-permeable channels. These voltage-dependent ion channels were more permeable to Ca2+ than K+, while displaying large permeabilities to Ba2+ and Mg2+ ions. Ca(2+)-permeable channels showed slow and reversible inactivation. The single-channel conductance was 13 pS in 40 mM CaCl2. These data provide direct evidence for the existence of voltage-dependent Ca2+ channels in the plasma membrane of a higher plant cell and point to physiological mechanisms for plant Ca2+ channel regulation. The depolarization-activated Ca(2+)-permeable channels identified here could constitute a regulated pathway for Ca2+ influx in response to physiologically occurring stimulus-induced depolarizations in higher plant cells.

Calcium Channels↗
PubMed2005

Permeability of adhesive resin films.

The purpose of this study was to quantify the permeability of adhesive resin films to water by measuring convective flow across thin films. Cured resin films were prepared with the use of five commercially available adhesive resins and an experimental resin. Two types of resin films were prepared from solvated comonomer blends within each product; resin films made before or after evaporation of solvent (10 s of drying with air-syringe). The permeability of the resin films was measured 30 min or 24 h after polymerization by placing the films in a split-chamber device. Fluid filtration rate through the resin films was measured with the use of 20 cm of water pressure. Osmotically induced water movement was measured by applying hypertonic aqueous solutions of CaCl2 or HEMA to the resin films. The results showed that evaporation of solvent before polymerization reduced the permeability of adhesive resin films, compared to permeabilities obtained without solvent evaporation. The cured adhesive resin films were all permeable to water, but to varying degrees.

Adhesives↗
PubMed1982

Occluding junctions in MDCK cells: modulation of transepithelial permeability by the cytoskeleton.

In MDCK cell monolayers the opening and resealing of occluding junctions can be induced by removal and restoration of calcium to the external medium. The overall changes in permeability of the occluding junctions in the monolayer can be monitored by the drop and recovery of the total transepithelial electrical resistance. We have investigated the effects of cytochalasin B (CB) on this process. When CB is added to sealed monolayers there is a gradual drop in the electrical resistance across the monolayer. This drop is accompanied by a slow disorganization of the microfilament pattern of these cells, including a disturbance of a ring of cortical microfilaments that is normally associated with the junctions. Cells in open monolayers treated with CB will not reseal and have an altered filament distribution. These cells do not have a continuous cortical ring. We have used a voltage scanning technique that uses a microelectrode to measure the resistance at selected points along the junction which surrounds a single cell. In untreated, closed monolayers, the junction is heterogeneous with alternating points of high and low conductance. In closed monolayers treated with CB, although there are low conductance points, we have observed an increased frequency of high conductance points that correlates with the change in the overall conductance. The frequency of high conductance points along the junction and the overall conductance both increase with time of exposure to CB. In an effort to understand the molecular basis for the permeability changes induced by EGTA and CB, we have looked for differences in the protein components of the cell membranes of open, closed, and CB-treated MDCK monolayers. This was done by radioiodinating the surface membrane proteins under control and experimental conditions that bring about permeability changes. No significant differences in the labeled protein patterns were found under these conditions. These results suggest that the permeability changes involve only a structural rearrangement of membrane components. In additions we have observed that about 36% of the surface label remains bound to the insoluble cytoskeletons obtained from cells in control and experimental conditions that alter the permeability of the tight junctions. The iodinated proteins attached to the CS include polypeptides with Mr of greater than or equal to 120K daltons as well as peptides with Mr = 56K, 50K, 36K, and 18K daltons.

Animals↗
PubMed2007

Vascular permeability induced by VEGF family members in vivo: role of endogenous PAF and NO synthesis.

We previously reported that vascular endothelial growth factor (VEGF) increases vascular permeability through the synthesis of endothelial platelet-activating factor (PAF), while others reported the contribution of nitric oxide (NO). Herein, we addressed the contribution of VEGF receptors and the role played by PAF and NO in VEGF-induced plasma protein extravasation. Using a modified Miles assay, intradermal injection in mice ears of VEGF-A(165), VEGF-A(121), and VEGF-C (1 microM) which activate VEGFR-2 (Flk-1) receptor increased vascular permeability, whereas a treatment with VEGFR-1 (Flt-1) analogs; PlGF and VEGF-B (1 microM) had no such effect. Pretreatment of mice with PAF receptor antagonist (LAU8080) or endothelial nitric oxide synthase (eNOS) inhibitor (L-NAME) abrogated protein extravasation mediated by VEGF-A(165). As opposed to PAF (0.01-1 microM), treatment with acetylcholine (ACh; up to 100 microM; inducer of NO synthesis) or sodium nitroprusside (SNP; up to 1 microM; NO donor) did not induce protein leakage. Simultaneous pretreatment of mice with eNOS and protein kinase A (PKA) inhibitors restored VEGF-A(165) vascular hyperpermeability suggesting that endogenous NO synthesis leads to PKA inhibition, which support maintenance of vascular integrity. Our data demonstrate that VEGF analogs increase vascular permeability through VEGFR-2 activation, and that both endogenous PAF and NO synthesis contribute to VEGF-A(165)-mediated vascular permeability. However, PAF but not NO directly increases vascular permeability per se, thereby, suggesting that PAF is a direct inflammatory mediator, whereas NO serves as a cofactor in VEGF-A(165) proinflammatory activities.

Animals↗
PubMed1977

Decreased membrane potassium permeability and transport in human chronic leukemic and tonsillar lymphocytes.

Human blood T-lymphocytes increase their potassium (K+) permeability and active K+ transport following lectin or antigen stimulation. We have studied the permeability and active transport of K+ by lymphocytes in chronic lymphocytic leukemia (CLL) to determine if their membrane K+ transport was similar to resting or lectin-stimulated normal blood lymphocytes. K+ transport was assessed both by the rate of isotopic 42K+ uptake and by the rate of change in cell K+ concentration after inhibition of the K+ transport system with ouabain. CLL lymphocytes had a marked decrease in membrane K+ permeability and active transport of K+ when compared to blood T lymphocytes. K+ transport in five subjects with CLL (10 mmol.1 cell water-1.h-1) was half that in normal blood T-lymphocytes (20 mmol.1 cell water-1 h-1). Phytohemagglutinin (PHA) treatment of CLL lymphocytes did not increase significantly their active K+ transport, whereas K+ transport by normal T-lymphocytes increased by 100%. Since there were 73% T-lymphocytes in normal blood and 14% in CLL blood, the difference in membrane K+ turnover could be related either to neoplasia or to the proposed B-lymphocyte origin of CLL. We studied human tonsillar lymphocytes which contained a mean of 34% T-cells. In five studies of tonsils, K+ transport was 14 mmol.1 cell water-1.h-1 and treatment with PHA increased K+ transport only 30%. The intermediate values of basal K+ transport and K+ transport in response to PHA in tonsillar lymphocytes were consistent with the proportion of T-lymphocytes present. These data suggest that B-lymphocytes have reduced membrane permeability and active transport of K+. Thus the marked decrease in CLL lymphocyte membrane K+ permeability and transport may be a reflection of its presumed B-cell origin, rather than a membrane alteration related to malignant transformation.

B-Lymphocytes↗