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Results for “Permeability”

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At least 19 recordsLinked to original sources

PubMed1991

Glycosylation is essential for efficient secretion but not for permeability-enhancing activity of vascular permeability factor (vascular endothelial growth factor).

The hyperpermeability of the microvasculature supplying solid tumors is largely attributable to a heterodimeric Mr 34,000-43,000 tumor-secreted protein, vascular permeability factor. Upon reduction, the vascular permeability factor secreted by line 10 tumor cells is resolved by SDS-PAGE into 3 discrete bands of Mr 24,000, 19,500, and 15,000. We demonstrate here that line 10 vascular permeability factor is an N-linked glycoprotein. Nonglycosylated vascular permeability factor migrates on reduced SDS-PAGE as two bands of Mr 20,000 and 15,000. Pulse-chase studies demonstrated that all three chains of native vascular permeability factor were secreted rapidly following synthesis and at equal rates, with a cellular half-retention time of approximately 37 min. When glycosylation was prevented by tunicamycin, individual bands of nonglycosylated vascular permeability factor were also secreted at equivalent rates, but much more slowly (approximately 60 min) than native glycoprotein. Both glycosylated and nonglycosylated forms of vascular permeability factor were equally potent at increasing dermal vessel permeability.

Animals↗

PubMed1985

The permeability of skin and oral mucosa to water and horseradish peroxidase as related to the thickness of the permeability barrier.

The permeability of porcine skin and keratinized and nonkeratinized oral mucosa to tritium-labeled water and horseradish peroxidase (HRPO) was determined using perfusion chambers. Small blocks from each tissue were also incubated with HRPO and the extent of penetration visualized microscopically; this enabled measurements to be made of the thickness of the permeability barrier to this water-soluble tracer. Results obtained after inverting the oral mucosa in the chambers or adding metabolic inhibitors indicated that both compounds diffuse across the tissue. The permeability constants derived directly in the study showed that skin was less permeable than oral mucosa and that the floor of the mouth was significantly more permeable than all other regions. When these constants were normalized in terms of a standard permeability barrier thickness and the different tissues compared, the values obtained for skin were again less than those of the oral regions but, of these, the buccal mucosa was significantly higher. The difference in permeability between epidermis and keratinized oral epithelium may be due to differences in the volume density of membrane-coating granules known to exist between the tissues; differences between the oral mucosal regions may reflect differences in the nature of the intercellular barrier material.

Animals↗

PubMed1986

Role of the altered transmural permeability in the pathomechanism of arteriosclerosis. History of arteriosclerosis theories. Role of the altered permeability in experimental arteriosclerosis models.

After presenting an overview on classification and history of arteriosclerosis theories, the physiological factors involved in the transmural permeability of the arteries are discussed in detail. The development and characteristic features of the altered transmural permeability were studied in various experimental models such as in rat's hypercholesterolemia, local aortic hypoxia, lymphedema of the vascular wall and in hypertension. Results appear to show that alterations in permeability invariably developed in all of the pathological conditions examined, they were transient in nature and preceded the onset of intimal proliferation(s). The disturbance of transmural permeability might be the common pathologic clue which initiates uniform vascular responses to injuries produced by a variety of noxious stimuli. The possible role of the altered transmural permeability in the induction of smooth muscle cell proliferation is also discussed and evidence is provided that after withdrawal of stimulus for vascular injury intimal proliferation will not develop despite the manifest disorders in permeability.

Animals↗

PubMed1992

Papaverine reduces the sodium permeability of the apical membrane and the potassium permeability of the basolateral membrane in isolated frog skin.

The effect of papaverine, an inhibitor of the phosphodiesterase responsible for breakdown of cAMP, on the transepithelial sodium transport across the isolated frog skin was investigated. Serosal addition of papaverine caused initially an increase in the short-circuit current (SCC), a doubling of the cellular cAMP content and a depolarization of the intracellular potential under SCC conditions (Vscc). The initial increase in the SCC was followed by a pronounced decrease both in the SCC and in the natriferic action of antidiuretic hormone (ADH), but papaverine had no inhibitory effect on the ability of ADH to increase the cellular cAMP content. As SCC declines, no hyperpolarization was observed. The I/V relationship across the apical membrane during the inhibitory phase, revealed that papaverine reduces the sodium permeability of the apical membrane (PNaa) as well as intracellular sodium concentration. These observations and the previously noted effect of papaverine on Vscc indicates that papaverine must have an effect on the cellular Cl or K permeability. The basolateral Na,K,2Cl cotransporter was blocked with bumetanide, which should bring the cellular chloride in equilibrium. Bumetanide had no effect on basal SCC and Vscc. When papaverine was added to skins preincubated with bumetanide, the effect of papaverine on SCC and Vscc was unchanged. Therefore, the depolarization of Vscc, observed during the papaverine-induced inhibition of the SCC, must be due to a reduction in the cellular K permeability. In conclusion, it is suggested that papaverine reduces the sodium permeability of the apical membrane and the potassium permeability of the basolateral membrane of the frog skin epithelium.

Animals↗

PubMed1977

Measurements of intestinal permeability using low molecular weight polyethylene glycols (PEG 400). II. Application to normal and abnormal permeability states in man and animals.

A new approach to the measurement of intestinal permeability using low molecular weight polyethylene glycols (PEG 400) has been applied to the study of normal and abnormal permeability states in man and animals. Successful assessments of gastric, jejunal, ileal, and colonic permeability suggest that the technique has application to any area of the gastrointestinal tract. The method has shown that bile acids alter mucosal permeability in the stomach and colon and that celiac sprue is associated with decreased intestinal permeability. These examples illustrate the potential of the technique for studying the function of diseases intestine in man.

Adult↗

PubMed1985

Passive cation permeability of turtle colon: evidence for a negative interaction between intracellular sodium and apical sodium permeability.

The role of intracellular sodium in the regulation of apical sodium permeability was investigated in an electrically "tight" epithelium, the turtle colon. In the presence of low mucosal sodium (3 mM) and serosal ouabain, an inhibitor of the basolateral sodium pump, the apical membrane retained a substantial amiloride-sensitive, sodium conductance and the basolateral membrane exhibited a barium-sensitive potassium conductance in parallel with a significant sodium (and lithium) conductance. In the presence of a high mucosal sodium concentration (114 mM), however, inhibition of active sodium absorption by ouabain led to a disappearance of the amiloride-sensitive, transepithelial conductance that was due, at least in part, to a virtual abolition of the apical sodium permeability. Two lines of evidence indicate that this permeability decrease was dependent upon an increase in intracellular sodium content. First, raising the mucosal sodium concentration from 3-114 mM in the presence of ouabain reversibly inhibited the amiloride-sensitive conductance. The time course of the decline in conductance paralleled the apparent intracellular accumulation of sodium in exchange for potassium, which was monitored as a transient deflection in the amiloride-sensitive, short-circuit current. Second, the inhibitory effect of mucosal sodium-addition was markedly attenuated by serosal barium, which prevented the accumulation of sodium by blocking the electrically coupled, basolateral potassium exit. These results support the notion of a "negative feedback" effect of intracellular sodium on the apical sodium permeability.

Amiloride↗

PubMed1989

The effect of ferricyanide with iodoacetate in calcium-free solution on passive cation permeability in human red blood cells: comparison with the Gardos-effect and with the influence of PCMBS on passive cation permeability.

Freshly prepared human red blood cells incubated with 5 mM ferricyanide, 0.2 mM iodoacetate and 2 mM adenosine in the presence of 5 mM EGTA demonstrate comparable increases in Na+ and K+ permeability (ferricyanide effect). This effect is unrelated to the Ca2+-activated K+ channel (Gardos effect) since influx of Ca2+ from outside the cell is excluded. Also this effect is different from the non-specific Na+ and K+ permeability change elicited by PCMBS. These differences become obvious by using various reagents. For example, A23187 and quinidine exert opposite effects in Gardos and ferricyanide experiments, where A23187 and atebrin react oppositely in the latter and in PCMBS experiments. The ferricyanide effect described here does not involve formation of nonspecific channels. The change in Na+ permeability separately from K+ permeability under certain circumstances suggests a more specific effect.

4-Chloromercuribenzenesulfonate↗

PubMed1978

A protease-like permeability factor in the guinea pig skin. 2. In vitro activation of the latent form permeability factor by weakly acidic phosphate buffer.

Conditions for the in vitro activation of the latent form of a protease-like permeability factor in the pseudoglobulin fraction from guinea pig skin were examined. (1) The factor was activated by dialysis against 67 mM phosphate buffer at pH 5.8--6.4, not at pH 7.0--8.0. (2) High salt concentration (200 mM or greater phosphate buffer or 67 mM phosphate buffer containing 200 mM or greater KCl or NaCl) prevented the activation at pH 6.2. (3) High osmotic pressure (sucrose at 1 M) did not affect activation at pH 6.2. (4) Reconversion of the activated permeability factor into an inactive form was not observed under high salt conditions, under which the latent permeability factor was stable in its own form. (5) The molecular size of the latent permeability factor was estimated as approx. 80 000 by Sephadex G-100 gel filtration at high salt concentration.

Animals↗

PubMed1989

Cl- permeability of human sweat duct cells monitored with fluorescence-digital imaging microscopy: evidence for reduced plasma membrane Cl- permeability in cystic fibrosis.

Salt reabsorption by the human sweat duct is markedly reduced in cystic fibrosis (CF). We used fluorescence-digital imaging microscopy in combination with a halide-specific fluorescent dye [6-methoxy-N-(3-sulfopropyl)quinolinium (SPQ)] to determine if this defective salt reabsorption is referable to a reduced plasma membrane Cl- permeability of the epithelial cells that line the sweat duct. Sweat duct cells were cultured from explants of normal and CF reabsorptive duct and loaded with SPQ, the fluorescence of which is specifically quenched by halide ions (Br- greater than Cl-) and provides a relative index of intracellular halide concentration. Two lines of evidence indicate that normal sweat duct cells exhibit a substantial permeability to Cl- and Br-. First, the replacement of extracellular Cl- with an impermeant anion (i.e., gluconate) resulted in a rapid and reversible increase in the intracellular fluorescence, as expected if the cells rapidly lost Cl- to the extracellular media. Second, the replacement of extracellular Cl- with Br- resulted in a rapid and reversible quenching of the intracellular fluorescence, as expected if the cells accumulated Br- (a more effective quencher of SPQ fluorescence) in exchange for Cl-. The rate of fluorescence change that was induced by either maneuver was inhibited by the Cl- channel blocker, diphenylamine-2-carboxylate (10 microM). Moreover, CF cells exhibited markedly reduced rates of fluorescence change in response to either maneuver. Our results document the utility of this imaging strategy for assessing the Cl- permeabilities of individual epithelial cells that are affected in cystic fibrosis and indicate that the defective salt reabsorption by the CF sweat duct is referable, at least in part, to a reduced plasma membrane Cl- permeability of sweat duct cells.

Adolescent↗

PubMed1978

Effect of propranolol on ricinoleic acid- and deoxycholic acid-induced changes of intestinal electrolyte movement and mucosal permeability. Evidence against the importance of altered permeability in the production of fluid and electrolyte accumulation.

Hydroxy fatty acids and bile acids produce both intestinal fluid and electrolyte accumulation and increases in inulin clearance, a parameter of mucosal permeability. The relationship of the changes in mucosal permeability to the production of fluid and electrolyte accumulation is uncertain. These experiments were designed to determine whether the alterations of mucosal permeability produced by ricinoleic acid and deoxycholic acid were related to production of hydroxy fatty acid- and bile acid-induced fluid and electrolyte accumulation in the rat colon. Propranolol (1 mg per 100 g of body weight) administered daily for 3 days inhibited ricinoleic acid- and deoxycholic acid-induced Na and water accumulation. In contrast, propranolol did not affect either the increase in inulin clearance or the decrease in electrical potential difference produced by ricinoleic acid and deoxycholic acid. Further, amphotericin B increased inulin clearance by the colon and also increased water and Na absorption. These studies suggest that changes in mucosal permeability are not primarily responsible for hydroxy fatty acid- and bile acid-induced fluid and Na accumulation.

Amphotericin B↗

PubMed1976

[Permeability-increasing effect of punctates. 3. Inhibition of the permeability-increasing activity by contrykal].

The punctate of the pleural cavity of a patient was examined which very much increased the permeability of the membrane in the animal experiment. Proteases is ascribed the effect increasing permeability, which are adsorbed to macromolecules. The increase of permeability could be inhibited by contrycal. An increase of permeability by proteolytic enzymes is discussed as one of the possible pathomechanisms for the development of exudations.

Animals↗

PubMed1977

Ion permeability and strength of cell contacts: ion permeability and mechanical properties of cell contacts in small intestine epithelium.

The effects of several simple parameters (pH, concentration of bivalent cations, osmotic pressure, and temperature) on the ion permeability and mechanical properties of cell contacts have been investigated. It has been shown that the mechanical properties of a cell contact make it possible to describe it as a viscoelastic system. The main contribution to cell adhesion is made by the tight junction. Two populations of acidic centers have been identified on the cell membrane surface. One population interacts with bivalent cations to assure cell adhesion. The other population of weaker acidic centers regulating ion permeation is involved in the cell membrane's interaction of the repulsion type. An intimate correlation has been established between changes in passive transepithelial ion permeability and cell adhesion in response to changes in pH and in bivalent cation concentration. Such a correlation is possible if the tight junction is the principal contributor to the passive ion permeability and mechanical strength of the cell contacts.

Animals↗

PubMed1989

Densitometric measurement of increased endothelial permeability in arteriosclerotic plaques and inhibition of permeability under the influence of two calcium antagonists.

A densitometric technique was established to investigate quantitative changes in endothelial permeability for horseradish peroxidase (HRP), mol. wt. 40,000 daltons, in rabbit carotid artery. Repeated weak electrical stimulations of rabbit carotid arterial walls with implanted electrodes lead to fibromuscular plaques mainly beneath the anode. It could be demonstrated that there exists a typical growth curve of the plaques dependent on the number of days of electrostimulation, with a fast proliferation rate of smooth muscle cells in the first 2 weeks of electrostimulation, and an increasing retardation of proliferation during the next 4 weeks. Endothelial permeability for HRP increases in close relation to the plaque development. Intravenous applications of single doses of the calcium entry blockers flunarizine or nimodipine are able to inhibit the increased permeability of the endothelial lining covering arteriosclerotic plaques. The intensity of the inhibitory action of these calcium antagonists correlates with the size of the arteriosclerotic plaques in inverse proportion, but nevertheless in large plaques an inhibitory effect is seen.

Animals↗

PubMed1986

Corneal permeability of aldose reductase inhibitor, M79175. I. In vitro study using corneal permeability apparatus.

Transcorneal permeability of M79175, aldose reductase inhibitor (Eisai), and various factors influencing it were examined using excised rabbit cornea mounted on the methacrylate apparatus. High permeability was exhibited and this was independent of the concentration of M79175. Cornea hydrated by exposure to the eye drop solution of high concentration of benzalkonium chloride, which had an enhancing effect on the permeability of M79175. Corneal hydration was also caused by the solution of low pH. These findings will show the basic conditions for this eye drop solution to be an artificial tear fluid.

Aldehyde Reductase↗

PubMed1992

[Estimation of pulmonary vascular permeability by indocyanine green in permeability pulmonary edema].

In this study we attempted to estimate pulmonary vascular permeability by indocyanine green (ICG). Permeability pulmonary edema was produced in 9 adult dogs by injecting 0.08 ml/kg oleic acid. We injected 50 mg ICG intravenously in 18 dogs (9 dogs with pulmonary edema and 9 control dogs). We measured the time course of ICG concentrations in pulmonary arterial blood, ICG concentration of peripheral lung tissue, tissue/serum ICG concentration ratios, and wet/dry lung weight ratios. The following results were obtained. The time course of ICG concentration in pulmonary arterial blood showed peak values at 2 minutes and became constant at 5 or 10 minutes after injection. The ICG concentration in peripheral lung tissue, tissue/serum ICG concentration ratios, and wet/dry lung weight ratios in the pulmonary edema group were significantly higher than those in the normal group. There was a strong linear correlation between wet/dry lung weight ratio and ICG concentration in peripheral lung tissue, with correlation coefficients of r = 0.936 (p < 0.01) in the right lung and r = 0.901 (p < 0.01) in the left lung. From these results, we conclude that estimation of pulmonary vascular permeability by ICG is a useful method.

Animals↗

PubMed1977

Permeability studies on taeniid metacestodes: II. Antibody-mediated effects on membrane permeability in larvae of Taenia taeniaeformis and Taenia crassiceps.

Incubation in immune rat serum (IRS) was shown to increase the rate of absorption of 125I RNase-A but not 125I BSA by larvae of Taenia taeniaeformis and T. crassiceps. This effect required a heat labile factor in serum, and partial activity could be restored in heat-treated IRS by adding normal rat serum (NRS) as a source of complement. In addition, the effectiveness of IRS in altering permeability was shown to be dependent on the concentration of functional complement. Both live and dead larvae incubated in NRS rapidly depleted hemolytic complement levels in the surrounding medium. Immunoglobulin fractions from IRS separated by anion exchange chromatography and and gel filtration were tested in the presence of excess complement for their ability to affect uptake of 125I RNase-A. Enhanced permeability was observed in larvae incubated in each fraction. The results show that antibodies in conjunction with complement are capable of disrupting larval permeability control in vitro. The observation that larvae were able to restore normal control as complement levels declined suggests that the parasites may overcome this immunologic effector mechanism by interfering with complement function.

Animals↗

PubMed1986

Defining the lower limits of blood-brain barrier permeability: factors affecting the magnitude and interpretation of permeability-area products.

Experimental alteration in the restricted permeability of the blood-brain barrier to polar, blood-borne molecules is often quantitated in the rat with use of 14C-sucrose or 3H-mannitol delivered as a test substance into the circulation. The underlying principle is to relate the quantity of saccharide that has permeated into brain parenchyma, after an arbitrary time period, to some index of the circulating tracer level. This study indicates that to correct the radioactivity level in the brain tissue for intravascular tracer, it is an erroneous practice to estimate the latter as the product of tissue blood volume and the tracer concentration measured in a systematic blood sample. Dissected brain tissue was found to have a lower hematocrit and thereby larger plasma/tracer compartment per unit blood volume than femoral arterial blood. It is further shown that, although commercially supplied stocks of 14C-sucrose or 3H-mannitol may contain only small quantities of radioactive impurities, their inclusion in injectates and preferential uptake into brain may cause significant overestimation of permeability to the parent tracer. It is also confirmed that magnitude of permeability-area (PA) products for permeation of purified sucrose or mannitol into brain varies inversely with the length of time allotted for tracer circulation in the bloodstream. This finding is at variance with the assumptions of a two-compartment (plasma/brain) diffusion model underlying such measurements and supports a recently published model for blood-to-brain transfer based on multiple uptake compartments in brain parenchyma. The factors compromising PA measurement identified in this study may partly underlie variations in PA values published from several laboratories that had been attributed to genetic differences in laboratory rats.

Animals↗

PubMed1988

Regulation of membrane permeability by vasopressin; activation of the water permeability pathway in toad urinary bladder by N-ethyl-maleimide.

1. Vasopressin induces a rapid increase in water permeability and stimulates net sodium transport in responsive epithelia through the mediation of cAMP. 2. In amphibian urinary bladder, the increase in water permeability is dependent on an intact cytoskeleton and is associated with the exocytotic insertion of tubular vesicles containing particle aggregates (the putative water channels) into the apical membrane of the granular epithelial cells. 3. In the toad bladder, mucosal addition of NEM, 0.1 mM, elicits a slow and irreversible increase in transepithelial water flow, whilst decreasing net sodium transport. 4. The hydrosmotic response to mucosal NEM is inhibited by cellular acidification, by pretreatment with cytoskeleton-disruptive drugs, and by agents that increase cytosolic calcium. 5. Mucosal NEM potentiates the hydrosmotic response to a submaximal, but not a maximal, dose of vasopressin. 6. Mucosal NEM, like vasopressin, induces both vesicle fusion and the appearance of particle aggregates at the granular cell apical surface. 7. NEM, unlike vasopressin, does not increase cellular cAMP content. 8. Mucosal NEM appears to increase transcellular water flow by activating cellular processes normally triggered by vasopressin, at a step beyond cAMP.

Animals↗