Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Permeability”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 577 records · Page 32Linked to original sources
PubMed1998

Effect of diuretics on sodium and chloride permeability in the rat papillary collecting duct.

While in vivo data suggests that diuretics such as furosemide and hydrochlorothiazide alter inner medulla collecting duct (IMCD) cell electrolyte transport, this has not been confirmed by in vivo studies nor have the mechanisms been evaluated. This study evaluated the direct effect of these diuretics as well as amiloride on sodium and chloride unidirectional permeability in the isolated perfused rat IMCD. In the absence of diuretics, the permeability of sodium was lower than that of chloride (0.63 +/- 0.05 compared with 0.83 +/- 0.08 micrometer/s), although both were relatively impermeable when compared to water. Furosemide (10(-4)) and hydrochlorothiazide (10(-3)) both increased the diffusional permeability of chloride by approximately 30% (0.80 +/- 0.06 to 1.04 +/- 0.09 micrometer/s, p < 0.01, and 0.74 +/- 0.09 to 0.98 +/- 0.10 micrometer/s, p < 0.02, respectively). However, sodium permeability was unaltered. Inhibition of Na+, K+-ATPase by ouabain or cooling (4 degrees C) inhibited basal sodium but not chloride permeability while a maximal antidiuretic AVP concentration did not alter sodium or chloride permeability. However, increasing the lumen and bath sodium chloride concentration from 150 to 300 and 600 mM significantly increased both sodium and particularly chloride conductance. In contrast, amiloride (10(-4)) significantly reduced both sodium and chloride permeability. These studies support a direct effect of furosemide and hydrochlorothiazide on the IMCD and suggest that their in vivo effect is primarily mediated by facilitating the passive movement of chloride into the lumen via a favourable electrochemical gradient. These results also demonstrate that amiloride inhibits both sodium and chloride unidirectional permeability by mechanisms separate to that of the sulphonamide-related diuretics.

Amiloride↗
PubMed1996

Do intestinal hyperpermeability and the related food antigens play a role in the progression of IgA nephropathy? I. Study of intestinal permeability.

Intestinal permeability was investigated by using 51Cr-EDTA as a probe molecule in 29 patients with immunoglobulin A nephropathy (IgA NP) and 20 healthy controls in 1990. Intestinal permeability was significantly higher in the IgA NP patients than in the controls (IgA NP, 3.86 +/- 0.29%; controls, 2.72 +/- 0.23%, p < 0.005). There was a significant relation between the manifestations of the disease (proteinuria and/or microhematuria) and the increased intestinal permeability (p < 0.05). By 1994, after an interval of 4 years, average intestinal permeability in the 21 patients available for study had not changed (3.80 +/- 0.36 vs. 4.57 +/- 0.63%) and was significantly higher than in the controls (p < 0.02). In patients with elevated serum IgA levels (serum IgA > 3.2 g/l; n = 15) there was a significant correlation between serum IgA levels and the degree of intestinal permeability (p < 0.02). During the 4-year period, the patients' kidney function deteriorated (n = 25; creatinine clearance in 1990, 92.4 +/- 6.1 ml/min; in 1994, 73.9 +/- 7.6 ml/min; p < 0.0002), the deterioration being greater in patients with increased intestinal permeability. There was no relation between the histologic grade of the biopsy specimen, hypertension and intestinal permeability. These data collected over a 4-year period suggest that in IgA NP increased intestinal permeability may play a role in the pathogenesis of the disease and adversely influence its progression.

Adult↗
PubMed1986

Studies on vascular permeability increasing factors involved in 48-hour homologous PCA in the mouse ear.

Several attempts were made to elucidate the possible role of histamine, serotonin, leukotrienes C4 (LTC4) and D4 (LTD4), and prostaglandin E1 (PGE1) as vascular permeability increasing factors involved in 48-hour homologous passive cutaneous anaphylaxis (PCA) in the mouse ear. Increased vascular permeability in the mouse ear caused by the mediator injection or PCA was assessed quantitatively by measuring the amount of extravasated dye. In skin reactions, all of the mediators used in the present study significantly increased vascular permeability. The most potent mediator was serotonin, which increased the vascular permeability from a concentration of 10(-8) g/ml, and the activity was about 100 times higher than that of histamine on a weight basis. Vascular permeability increasing activity of LTC4 was about 10 times higher than that of histamine, and LTD4 and PGE1 were also more potent than histamine. Increases of vascular permeability caused by histamine, serotonin, LTC4 and LTD4 were significantly potentiated by injecting 10(-6) g/ml of PGE1 simultaneously. Histamine-, serotonin- and LTC4-induced skin reactions in the mouse ear were suppressed significantly by the administrations of chlorpheniramine, methysergide and FPL 55712, respectively. In contrast, though chlorpheniramine and methysergide suppressed also mouse ear PCA (about 50 and 40%, respectively), neither FPL 55712, indomethacin nor BW 755C suppressed it. These results strongly suggest that the most important mediator involved in mouse ear PCA is histamine and that serotonin also plays an important role in the increase of vascular permeability caused by PCA. Despite their potent vascular permeability increasing activity LTC4, LTD4 and PGE1 do not seem to play an important role in mouse ear PCA.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed2005

Alterations in internal elastic lamina permeability as a function of age and anatomical site precede lesion development in apolipoprotein E-null mice.

Early atherosclerosis is characterized by the accumulation of plasma-borne macromolecules (eg, low-density lipoproteins) in the arterial intima, which is bordered by endothelial cells (EC) and the internal elastic lamina (IEL). This accumulation is believed to be secondary to increased EC permeability. We hypothesized that a decrease in IEL permeability may precede lesion development and contribute to macromolecular accumulation. To test this hypothesis, we quantified EC and IEL permeability in lesion-free areas of the thoracic and abdominal aortas of chow-fed C57BL/6 control and atherosclerotic-prone apolipoprotein E (apoE)-null mice at 3 and 5 months of age. Between 3 and 5 months of age, apoE-null mice begin to develop atherosclerotic lesions in the thoracic aorta. No significant differences in EC and IEL permeability were observed at either time in C57BL/6 control mice. In contrast, 78% and 19% decreases in IEL permeability of the thoracic aorta and abdominal aorta, respectively, were observed between 3 to 5 months of age in apoE-null mice (thoracic: 2.05+/-1.33 and 0.44+/-0.15 microm/min, P<0.001; abdominal: 1.13+/-0.58 and 0.93+/-0.44 microm/min, P<0.05). To further determine whether decreased IEL permeability is linked with atherosclerotic lesion development, we quantified IEL permeability in the greater and lesser curvature of the aortic arch. In apoE-null mice, the lesser curvature of the aortic arch develops lesions before the greater curvature. We found a significant and sustained decrease (59%) in IEL permeability in the lesser curvature of the aortic arch compared with the greater curvature. These data suggest that atherogenesis involves the pathological remodeling of the IEL, not the endothelium before lesion development. This remodeling may be attributable to local responses of the endothelium and smooth muscle cells to hyperlipidemia.

Age Factors↗
PubMed1998

Lipopolysaccharide-induced alveolar epithelial permeability: the role of nitric oxide.

Intratracheal instillation of lipopolysaccharide (LPS) in the rat has been used as a model of acute lung inflammation. Among the early events in this process is a transient increase in airspace epithelial permeability which peaks 4 h after intratracheal instillation of LPS. The increased epithelial permeability is concomitant with the influx of neutrophils into the airspaces, peaking 8 h postinstillation. We have investigated the mechanism of this LPS-induced increase in epithelial permeability. The role of the neutrophil in LPS-induced epithelial permeability was assessed by pretreatment with neutrophil antibody to abolish neutrophil influx, which did not affect the increase in epithelial permeability. Because LPS instillation also induced increased tumor necrosis factor alpha (TNF-alpha) activity in bronchoalveolar lavage (BAL) fluid, and its release by cultured BAL leukocytes from treated animals, TNF-alpha antibody was coinstilled intratracheally with LPS in rats. TNF-alpha antibody eliminated TNF-alpha activity in BAL fluid, but had no effect on LPS-induced increased epithelial permeability. Increased levels of nitric oxide (NO), measured as nitrite, were also present in BAL fluid from LPS-treated rat lungs and LPS-elicited BAL leukocytes produced increased NO in culture. Treatment of rats with the specific NO synthase inhibitor L-NMMA significantly diminished the LPS-induced increased epithelial permeability. These data suggest that NO is involved in LPS-induced changes in epithelial integrity. However, other mechanisms should be evoked in addition to NO to explain completely the increased epithelial permeability produced by LPS.

Animals↗
PubMed1989

Macrophages activated by fibrin increase albumin permeability across pulmonary artery endothelial monolayers.

We have examined the effects of alveolar macrophages (AM) obtained after challenge with alpha-thrombin on 125I-labeled albumin permeability across ovine pulmonary artery endothelial monolayers. AM were obtained by bronchoalveolar lavage before and after challenging the sheep with alpha-thrombin (80 U/kg). Post-thrombin AM increased 125I-labeled albumin transendothelial permeability, whereas resting AM had no effect (82.7 +/- 7.9% increase versus 17.2 +/- 1.6% increase at the AM:endothelial cell ratio of 1:1; p less than 0.001). The permeability increase was also seen at AM:endothelial cell ratios of 0.2:1 and 5:1. Endothelial permeability to 125I-labeled albumin did not increase after in vitro incubation of macrophages with 10(-8) M thrombin, suggesting that AM are activated as a result of thrombin-induced fibrin microembolism rather than by the alpha-thrombin per se. The increase in permeability was not due to endothelial lysis since macrophages did not cause release of endothelial lactate dehydrogenase. Adherence of AM to the endothelium did not correlate with the ability of AM to increase endothelial permeability. Superoxide anion production was increased when post-thrombin AM were exposed to the endothelial monolayers (30.6 +/- 4.2 nmol/10(6) cells/10 min) compared with production by post-thrombin AM in the absence of endothelial cells (2.5 +/- 0.5 nmol/10(6) cells/10 min). The addition of superoxide dismutase (SOD) blunted the permeability increase induced by AM (32.3 +/- 3.9% increase with SOD versus 84.1 +/- 7.1% increase without SOD; p less than 0.001), indicating that superoxide anion is an important mediator of the macrophage-induced increase in endothelial monolayer permeability.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Permeability of retinal pigment epithelium: effects of permeant molecular weight and lipophilicity.

PURPOSE: To determine the effects of solute molecular weight and lipophilicity on the permeability of a retinal pigment epithelium (RPE)-choroid preparation. METHODS: Fresh RPE-choroid specimens from bovine eyes were placed in diffusion chambers for permeability experiments with carboxyfluorescein, fluorescein isothiocyanate (FITC)-labeled dextrans with molecular masses from 4 to 80 kDa, and beta-blockers exhibiting a wide range of lipophilicity (atenolol, nadolol, pindolol, timolol, metoprolol, and betaxolol). Permeability experiments were performed both in the choroid-to-retina (inward) direction and in the retina-to-choroid (outward) direction. Carboxyfluorescein and FITC-dextrans were determined by fluorometry, and beta-blockers by HPLC. The transepithelial electrical resistance and potential difference were monitored during the experiments. RESULTS: Permeability of the fluorescent FITC-dextran probes through RPE-choroid decreased significantly with the increasing size of the probe. RPE-choroid was 35 times more permeable to carboxyfluorescein (376 Da) than to FITC-dextran 80 kDa. The permeabilities of lipophilic beta-blockers were up to 8 and 20 times higher than that of hydrophilic atenolol and carboxyfluorescein, respectively. The lag time of solute flux across the RPE-choroid increased with the molecular weight and lipophilicity. Compared with published data on isolated sclera, bovine RPE-choroid was 10 to 100 times less permeable to hydrophilic compounds and macromolecules. The permeability of lipophilic molecules in RPE-choroid was in the same range as in the sclera. CONCLUSIONS: RPE is a major barrier and may be the rate-limiting factor in the retinal delivery of hydrophilic drugs and macromolecules through the transscleral route. For lipophilic molecules, RPE-choroid, and sclera are approximately equal barriers.

Adrenergic beta-Antagonists↗
PubMed1987

Urea permeability of mammalian inner medullary collecting duct system and papillary surface epithelium.

To compare passive urea transport across the inner medullary collecting ducts (IMCDs) and the papillary surface epithelium (PSE) of the kidney, two determinants of passive transport were measured, namely permeability coefficient and surface area. Urea permeability was measured in isolated perfused IMCDs dissected from carefully localized sites along the inner medullas of rats and rabbits. Mean permeability coefficients (X 10(-5) cm/s) in rat IMCDs were: outer third of inner medulla (IMCD1), 1.6 +/- 0.5; middle third (IMCD2), 46.6 +/- 10.5; and inner third (IMCD3), 39.1 +/- 3.6. Mean permeability coefficients in rabbit IMCDs were: IMCD1, 1.2 +/- 0.1; IMCD2, 11.6 +/- 2.8; and IMCD3, 13.1 +/- 1.8. The rabbit PSE was dissected free from the underlying renal inner medulla and was mounted in a specially designed chamber to measure its permeability to urea. The mean value was 1 X 10(-5) cm/s both in the absence and presence of vasopressin (10 nM). Morphometry of renal papillary cross sections revealed that the total surface area of IMCDs exceeds the total area of the PSE by 10-fold in the rat and threefold in the rabbit. We conclude: the IMCD displays axial heterogeneity with respect to urea permeability, with a high permeability only in its distal two-thirds; and because the urea permeability and surface area of the PSE are relatively small, passive transport across it is unlikely to be a major source of urea to the inner medullary interstitium.

Animals↗
PubMed1996

Intestinal permeability in exocrine pancreatic insufficiency due to cystic fibrosis or chronic pancreatitis.

Disturbances of the intestinal integrity, reflected by an increased intestinal permeability, are reported in cystic fibrosis (CF). Controversy exists whether the increased intestinal permeability is due to CF itself or a consequence of the concomitant exocrine pancreatic insufficiency (PI). We measured intestinal permeability by the sugar absorption test in 32 PI patients: 20 CF-PI, 12 nonCF-PI with chronic pancreatitis, and 50 controls. In the sugar absorption test, the lactulose/mannitol ratio is measured in 5-h urine samples after oral ingestion of a solution of lactulose and mannitol, hyperosmolar by the addition of sucrose. The lactulose/mannitol ratio was increased in both CF-PI and nonCF-PI versus controls (p < 0.0001). In CF, the L/M ratio and permeability for lactulose and mannitol did not change by increasing pancreatic enzyme supplementation by 30-50% for 2 wk (p = 0.74, p = 0.97, p = 0.74, respectively) nor by decreasing the osmolarity of the test solution by 75% (p = 0.24, p = 0.10, p = 0.39, respectively). We conclude that an increased intestinal permeability in CF is probably a consequence of PI and is not related to the dose of pancreatic enzyme supplementation nor the osmolarity of the test solution. The increase is due to an increased permeability for lactulose which might point toward a defect in the tight junctions of the villi and/or crypts. The cause of the increased intestinal permeability in the presence of PI is still unclear. An increased intestinal permeability points toward an impaired functional integrity of the small bowel, which may contribute to gastrointestinal dysfunction in CF.

Adolescent↗
PubMed2000

Role of nitric oxide and cyclic guanosine 3',5'-monophosphate in the estrogen regulation of cervical epithelial permeability.

Treatment of cultured human cervical epithelia on filters with 17beta-estradiol increases paracellular permeability in a time- and dose-related manner (EC50, 1.1 nM). The objective of the present study was to understand the molecular mechanisms of estrogen action. In cultured human cervical epithelial cells the nitric oxide (NO) donors sodium nitroprusside (SNP) and N-[ethoxycarbonyl]-3-[4-morpholinyl]sydnoneimine (SIN-I) and the cell-permeable cGMP analog 8-bromo-cGMP (8-Br-cGMP) increased paracellular permeability. In estrogen-treated cells SNP and 8-Br-cGMP increased permeability to a lesser degree than in estrogen-deprived cells, suggesting that NO and cGMP mediate the effect of estrogen on permeability. Tamoxifen blocked the estrogen-induced increase in permeability, but it had no effect on increases in permeability that were induced by SNP or by 8-Br-cGMP. LY-83583 (blocker of guanylate cyclase) attenuated the effect of SNP, whereas KT-5823 (blocker of cGMP-dependent protein kinase) abrogated the effects of both SNP and 8-Br-cGMP. Treatment with 17beta-estradiol increased NO release and cellular cGMP in a dose-related manner (EC50, approximately 1 nM), and the effects were inhibited by tamoxifen. Treatment with SNP increased cGMP maximally, even in estrogen-deficient cells. LY-83583 blocked the estrogen-induced increase in cGMP, but neither LY-83583 nor KT-5823 had a significant effect on the estrogen-induced increases in NO release and cellular cGMP. The NO synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester decreased NO release, and pretreatment of cells with L-arginine reversed the effect. Cultured human cervical epithelial cells express messenger RNA for the NOS isoforms endothelial NOS (ecNOS), brain NOS, and inducible NOS. 17beta-Estradiol up-regulated ecNOS messenger RNA, and tamoxifen blocked the effect. Based on these results we suggest that the effect of estradiol on permeability involves four signaling steps: 1) activation of estrogen receptors, 2) increase in ecNOS transcription and up-regulation of NO activity, 3) NO activation of guanylate cyclase and increase in cGMP, and 4) cGMP activation of cGMP-dependent protein kinase.

Alkaloids↗
PubMed1998

A quantitative analysis of connexin-specific permeability differences of gap junctions expressed in HeLa transfectants and Xenopus oocytes.

Gap junctions provide direct intercellular communication by linking adjacent cells with aqueous pores permeable to molecules up to 1 kDa in molecular mass and 8-14 A in diameter. The identification of over a dozen connexins in the mammalian gap junction family has stimulated interest in the functional significance of this diversity, including the possibility of selectivity for permeants as seen in other channel classes. Here we present a quantitative comparison of channel permeabilities of different connexins expressed in both HeLa transfectants (rat Cx26, rat Cx32 and mouse Cx45) and Xenopus oocytes (rat Cx26 and rat Cx32). In HeLa cells, we examined permeability to two fluorescent molecules: Lucifer Yellow (LY: anionic, MW 457) and 4',6-diamidino-2-phenylindole, dihydrochloride (DAPI, cationic, MW 350). A comparison of the kinetics of fluorescent dye transfer showed Cx32, Cx26 and Cx45 to have progressively decreasing permeabilities to LY, but increasing permeabilities to DAPI. This pattern was inconsistent with selection based on physical size of the probe, nor could it be accounted for by the differences between clones in the electrical conductance of the monolayers. In Xenopus oocytes, where electrical and dye coupling could be assessed in the same cells, Cx32 coupled oocytes showed an estimated 6-fold greater permeability to LY than those coupled by Cx26, a comparable result to that seen in HeLa cells, where an approximately 9-fold difference was seen. The oocyte system also allowed an examination of Cx32/Cx26 heterotypic gap junction that proved to have a permeability intermediate between the two homotypic forms. Thus, independent of the expression system, it appears that connexins show differential permeabilities that cannot be predicted based on size considerations, but must depend on other features of the probe, such as charge.

Animals↗
PubMed1984

Studies on rabbit corneal permeability of local anesthetics (I).

To elucidate the pharmacokinetics of local anesthetics with respect to corneal permeability in the rabbit, we examined the relationship between the corneal permeability velocities of three agents, cocaine X HCl, procaine X HCl and tetracaine X HCl and corneal hydration. The corneal permeability velocity constants (k) of these three ester-type local anesthetics were approximately 0.5-6.0 X 10(-6) cm/sec and the membrane permeability constants of these agents were approximately 0.5-4.0 X 10(-7) cm2/sec, whereas the rabbit corneal hydration values were 3.2-4.2. Tetracaine X HCl with the strongest topical anesthetic action showed the greatest corneal hydration and the smallest corneal permeability velocity constant among these local anesthetics. Rabbit corneal permeability decreased with increasing molecular length of the agents. Permeability of these local anesthetics in the rabbit cornea appears to result from passive transport. As corneal hydration values and the corneal permeability constant increased with greater topical anesthetic activity, it appears that the degree of inhibition of Na+-K+ ATPase activity is associated with the order of topical anesthetic activity in a similar manner as general anesthetics.

Anesthetics, Local↗
PubMed2004

Plasma oxygen permeability may be a factor in atherosclerosis.

Plasma oxygen permeability measures how easily oxygen dissolves in and diffuses through blood plasma. There has long been evidence that artery wall hypoxia plays a role in atherogenesis. This paper reviews the influence that plasma oxygen permeability has on artery wall oxygenation and presents experimental evidence for a relationship between plasma oxygen permeability and clinically significant obstructive coronary artery disease. Thirty-eight inpatients referred for diagnostic cardiac catheterization were scored for active coronary artery disease, and their plasma oxygen permeabilities were measured. There was a statistically significant (p = 0.04) correlation between active coronary artery disease and plasma oxygen permeability. There were also statistically significant differences in mean plasma oxygen permeability both between patients who did and did not have actively progressing coronary artery disease (p = 0.01) and between patients who did and did not have clinically significant obstructive coronary artery disease, whether it was actively progressing or not (p = 0.02). These findings suggest that a decline in plasma oxygen permeability may be one of the many factors associated with progression of atherosclerosis and that substances which increase oxygen permeability might offer a useful adjunct to current therapeutic measures.

Adult↗
PubMed1999

Dentin permeability after toothbrushing with different toothpastes.

PURPOSE: To evaluate the interaction of smear layer produced during brushing and dentifrice particles. MATERIALS AND METHODS: Dentin disks were obtained from extracted human third molars. Dentin permeability was evaluated using a hydraulic pressure apparatus working at 1 psi of pressure. After preparation, each sample was connected to the hydraulic pressure apparatus to evaluate the permeability of dentin with the smear layer produced during specimen preparation. After 5 min of measurements dentin was etched with 37% phosphoric acid gel for 2 min, washed and gently dried with cotton to measure the permeability after smear layer removal. This was done to measure the maximum permeability of each specimen (expressed as 100%). Then a second smear layer was produced using a #400 carbide paper under water for 1 min. Dentin permeability of the smear layer covered dentin was then measured, and expressed as a percent of the maximum permeability of that specimen, permitting each specimen to serve as its own control. The three toothpastes used (Merfluan powder, Merfluan paste and Fluorigard) were applied on dentin surfaces using a small sponge to completely cover the dentin surface. After 5 s, each sample was connected to a mechanical device and brushed under water for 3 min with constant pressure of 250 gr using a Colgate medium toothbrush. After this treatment, each sample was gently washed with tap water, gently air dried for 3-5 s and connected with the pressure apparatus to remeasure the permeability after brushing. For SEM examination of dentin before and after treatment with toothpaste and brushing, each dentin and enamel sample was fixed in 2% buffered glutaraldehyde. RESULTS: Dentin permeability proved unaffected by dentifrice treatments. SEM observations demonstrated the presence of dentifrice particles on dentin surface and inside dentin tubules. Smear plugs produced during dentin brushing were not removed by dentifrices.

Dentin↗
PubMed2000

Limitations of cyclosporin A inhibition of the permeability transition in CNS mitochondria.

Activation of the mitochondrial permeability transition may contribute to excitotoxic neuronal death (Ankarcrona et al., 1996; Dubinsky and Levi, 1998). However, cyclosporin A (CsA), a potent inhibitor of the permeability transition in liver mitochondria, only protects against neuronal injury by limited doses of glutamate and selected ischemic paradigms. The lack of consistent CsA inhibition of the mitochondrial permeability transition was analyzed with the use of isolated brain mitochondria. Changes in the permeability of the inner mitochondrial membrane were evaluated by monitoring mitochondrial membrane potential (Deltapsi), using the distribution of tetraphenylphosphonium, and by monitoring mitochondrial swelling, using light absorbance measurements. Metabolic impairments, large Ca(2+) loads, omission of external Mg(2+), or low doses of palmitic acid or the protonophore FCCP exacerbated Ca(2+)-induced sustained depolarizations and swelling and eliminated CsA inhibition. BSA restored CsA inhibition in mitochondria challenged with 50 microm Ca(2+), but not with 100 microm Ca(2+). CsA failed to prevent Ca(2+)-induced depolarization or to repolarize mitochondria when mitochondria were depolarized excessively. Similarly, CsA failed to prevent mitochondrial swelling or PEG-induced shrinkage after swelling when the Ca(2+) challenge produced a strong, sustained depolarization. Thus in brain mitochondria CsA may be effective only as an inhibitor of the permeability transition and the Ca(2+)-activated low permeability state under conditions of partial depolarization. In contrast, ADP plus oligomycin inhibited both permeabilities under all of the conditions that were tested. In situ, the neuroprotective action of CsA may be limited to glutamate challenges sufficiently toxic to induce the permeability transition but not so severe that mitochondrial depolarization exceeds threshold.

Adenosine Diphosphate↗
PubMed2001

Increased human scleral permeability with prostaglandin exposure.

PURPOSE: To investigate the effect of prostaglandins (PGs) on the permeability of human sclera in vitro. METHODS: Twenty-three pairs of human eye bank eyes were studied. Circular pieces of sclera were cultured in low-serum DMEM/F-12 media. Scleral hydration was assessed by measuring wet and dry weight of scleral cultures incubated with medium for 3 days and with Hanks' buffered saline solution (HBSS) for 4 hours. To assess scleral permeability, organ-cultured scleral tissues were exposed to 100 to 500 nM PGF(2alpha), 17-phenyltrinor PGF(2alpha), or PhXA85 (the active form of latanoprost) for 1, 2, and 3 days. Scleral permeability was measured using a two-chamber Ussing apparatus and rhodamine-dextran polymers dissolved in HBSS (MW = 10,000, 40,000, and 70,000). The movement of each rhodamine-dextran across the cultured sclera was measured using a spectrofluorometer. To understand the biological basis of the permeability change, the media were collected from the treated cultures, and the concentration of MMP-1, 2, and 3 was measured using an enzyme-linked immunosorbent assay. RESULTS: There was no difference in scleral hydration among fresh sclera and sclera incubated with medium for 3 days, with HBSS for 4 hours, or with medium for 3 days followed by HBSS for 4 hours. Compared to tracer movement across untreated scleral cultures (1.5 x 10(-6) cm/sec for 10 kDa dextran, 0.7 x 10(-6) cm/sec for 40 kDa dextran, and 0.4 x 10(-6) cm/sec for 70 kDa dextran), exposure to PGF(2alpha), 17-phenyltrinor PGF(2alpha), or PhXA85 each increased scleral permeability in a dose- and time-dependent manner. Increases in permeability were greater with the10 kDa dextran than with the 40 or 70 kDa dextran. The magnitude of these effects was greatest with exposure to PhXA85 and similar with exposure to PGF(2alpha) or 17-phenyltrinor-PGF(2alpha). MMP expression also was significantly increased after PG exposure. These increases were generally time and dose dependent and greater with MMP-2 and -3 than with MMP-1. CONCLUSIONS: There is increased permeability of human sclera exposed to various PGs in organ culture. This increased permeability is accompanied by increased expression of MMPS:

Aged↗
PubMed1994

Permeability of membranes to amino acids and modified amino acids: mechanisms involved in translocation.

The amino acid permeability of membranes is of interest because they are one of the key solutes involved in cell function. Membrane permeability coefficients (P) for amino acid classes, including neutral, polar, hydrophobic, and charged species, have been measured and compared using a variety of techniques. Decreasing lipid chain length increased permeability slightly (5-fold), while variations in pH had only minor effects on the permeability coefficients of the amino acids tested in liposomes. Increasing the membrane surface charge increased the permeability of amino acids of the opposite charge, while increasing the cholesterol content decreased membrane permeability. The permeability coefficients for most amino acids tested were surprisingly similar to those previously measured for monovalent cations such as sodium and potassium (approximately 10(-12)-10(-13) cm s-1). This observation suggests that the permeation rates for the neutral, polar and charged amino acids are controlled by bilayer fluctuations and transient defects, rather than partition coefficients and Born energy barriers. Hydrophobic amino acids were 10(2) more permeable than the hydrophilic forms, reflecting their increased partition coefficient values. External pH had dramatic effects on the permeation rates for the modified amino acid lysine methyl ester in response to transmembrane pH gradients. It was established that lysine methyl ester and other modified short peptides permeate rapidly (P = 10(-2) cm s-1) as neutral (deprotonated) molecules. It was also shown that charge distributions dramatically alter permeation rates for modified di-peptides. These results may relate to the movement of peptides through membranes during protein translocation and to the origin of cellular membrane transport on the early Earth.

Amino Acids↗
PubMedDate not supplied

Variations of permeability and pore size distribution of porous media with pressure.

Porosity and permeability of porous and fractured geological media decrease with the exploitation of formation fluids such as petroleum, natural gas, or ground water. This may result in ground subsidence and a decrease of recovery of petroleum, natural gas, or ground water. Therefore, an evaluation of the behavior of permeability and porosity under formation fluid pressure changes is important to petroleum and ground water industries. This study for the first time establishes a method, which allows for the measurement of permeability, porosity, and pore size distribution of cores simultaneously. From the observation of the pore size distribution by low-field nuclear magnetic resonance (NMR) relaxation time spectrometry the mechanisms of pressure-dependent porosity and permeability change can be derived. This information cannot be obtained by traditional methods. As the large-size pores or fractures contribute significantly to the permeability, their change consequently leads to a large permeability change. The contribution of fractures to permeability is even larger than that of pores. Thus, the permeability of the cores with fractures decreased more than that of cores without fractures during formation pressure decrease. Furthermore, it did not recover during formation pressure increase. It can be concluded that in fractures, mainly plastic deformation takes place, while matrix pores mainly show elastic deformation. Therefore, it is very important to keep an appropriate formation fluid pressure during the exploitation of ground water and petroleum in a fractured formation.

Environmental Monitoring↗