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PubMed1996

Permeability properties of the intact mammalian bladder epithelium.

Because the mammalian bladder must store urine of composition which differs markedly from that of plasma for prolonged periods, the bladder permeability barrier must maintain extremely low permeabilities to substances which normally cross membranes relatively rapidly, such as water, protons, and small nonelectrolytes like urea and ammonia. In the present studies, permeabilities of the apical membrane of dissected rabbit bladder epithelium to water, urea, ammonia, and protons were measured in Ussing chambers and averaged (in cm/s) for water, 5.15 +/- 0.43 x 10(-5); for urea, 4.51 +/- 0.67 x 10(-6); for ammonia, 5.14 +/- 0.62 x 10(-4); and for protons, 2.98 +/- 1.87 x 10(-3), respectively. These permeability values are exceptionally low and are expected to result in minimal to no leakage of these normally permeable substances across the epithelium. Water permeabilities in intact whole rabbit bladders were indistinguishable from those obtained in the dissected epithelial preparation. Moreover, addition of nystatin to the apical solution of dissected epithelia rapidly increased water permeability in conjunction with loss of epithelial resistance. These results confirm that the apical membrane of the bladder epithelial cells represents the bladder permeability barrier. In addition, they establish a model system that will permit examination of how membrane structure reduces permeability and how epithelial injury compromises barrier function.

Ammonia↗
PubMed1989

Calcium dependence of the thrombin-induced increase in endothelial albumin permeability.

We examined whether the increase in endothelial albumin permeability induced by alpha-thrombin is dependent on extracellular Ca2+ influx. Permeability of 125I-albumin across confluent monolayers of cultured bovine pulmonary artery endothelial cells was measured before and after the addition of 0.1 microM alpha-thrombin. In the presence of normal extracellular Ca2+ concentration ([Ca2+]o, 1000 microM), alpha-thrombin produced a 175 +/- 10% increase in 125I-albumin permeability. At lower [Ca2+]o (100, 10, 1, or less than 1 microM), alpha-thrombin caused a 140% increase in permeability (P less than 0.005). LaCl3 (1 mM), which competes for Ca2+ entry, blunted 38% of the increase in permeability. Preloading endothelial monolayers with quin2 to buffer cytosolic Ca2+ (Cai2+) produced a dose-dependent inhibition of the increase in 125I-albumin permeability. Preincubation with nifedipine or verapamil was ineffective in reducing the thrombin-induced permeability increase. A 60 mM K+ isosmotic solution did not alter base-line endothelial permeability. alpha-Thrombin increased [Ca2+]i in a dose-dependent manner and the 45Ca2+ influx rate. Extracellular medium containing 60 mM K+ did not increase 45Ca2+ influx, and nifedipine did not block the rise in 45Ca2+ influx caused by alpha-thrombin. Ca2+ flux into endothelial cells induced by alpha-thrombin does not occur through voltage-sensitive channels but may involve receptor-operated channels. In conclusion, the increase in endothelial albumin permeability caused by alpha-thrombin is dependent on Ca2+ influx and intracellular Ca2+ mobilization.

Animals↗
PubMed1994

Permeability of ferret trachea in vitro to 99mTc-DTPA and [14C]antipyrine.

Platelet-activating factor (PAF) and vasoactive drugs were tested on permeability of ferret trachea in vitro by measuring fluxes of 99mTc-diethylenetriamine pentaacetic acid (99mTc-DTPA; hydrophilic) and [14C]antipyrine ([14C]AP; lipophilic) across the tracheal wall. Tracheae were bathed on both sides with Krebs-Henseleit buffer, with luminal buffer containing either 99mTc-DTPA or [14C]AP. Luminal and abluminal radioactivities, potential difference, and tracheal smooth muscle tone were measured. Baseline 99mTc-DTPA and [14C]AP permeability coefficients were -4.7 +/- 0.6 (SE) x 10(-7) and -2.2 +/- 0.1 x 10(-5) cm/s, respectively. PAF (10 microM) increased permeability to 99mTc-DTPA to -35.3 +/- 7.6 x 10(-7) cm/s (P < 0.05), but permeability to [14C]AP did not change, suggesting that paracellular but not transcellular transport was affected. Abluminal and luminal applications of methacholine (MCh, 20 microM), phenylephrine (PE, 100 microM), and albuterol (Alb, 100 microM) caused no change in permeability to 99mTc-DTPA before or after exposure to luminal PAF, but abluminal histamine (Hist, 10 microM) significantly increased permeability. Abluminal Hist decreased permeability to [14C]AP before and after exposure to PAF. MCh, PE, and Hist increased smooth muscle tone; Alb and PAF had no effect. Thus, only PAF and Hist altered permeability to 99mTc-DTPA, and MCh, PE, and Hist changed smooth muscle tone. Tracheal permeability changes were greater for the hydrophilic than for the lipophilic agent.

Animals↗
PubMed1997

Effect of running intensity on intestinal permeability.

Enhanced intestinal permeability has been associated with gastrointestinal disorders in long-distance runners. The primary purpose of this study was to evaluate the effect of running intensity on small intestinal permeability by using the lactulose and rhamnose differential urinary excretion test. Secondary purposes included assessing the relationship between small intestinal permeability and gastrointestinal symptoms and evaluating gastric damage by using sucrose as a probe. Six healthy volunteers [5 men, 1 woman; age = 30 +/- 2 yr; peak O2 uptake (VO2peak) = 57.7 +/- 2.1 ml.kg-1.min-1] rested or performed treadmill exercise at 40, 60, or 80% VO2peak for 60 min in a moderate environment (22 degrees C, 50% relative humidity). At 30 min into rest or exercise, the permeability test solution (5 g sucrose, 5 g lactulose, 2 g rhamnose in 50 ml water, approximately 800 mosM) was ingested. Urinary excretion rates (6 h) of the lactulose-to-rhamnose ratio were used to assess small intestinal permeability, and concentrations of each probe were determined by using high-performance liquid chromatography. Running at 80% VO2peak increased (P < 0.05) small intestinal permeability compared with rest, 40, and 60% VO2peak with mean values expressed as percent recovery of ingested dose of 0.107 +/- 0.021 (SE), 0.048 +/- 0.009, 0.056 +/- 0.005, and 0.064 +/- 0.010%, respectively. Increases in small intestinal permeability did not result in a higher prevalence of gastrointestinal symptoms, and urinary recovery of sucrose did not reflect increased gastric permeability. The significance and mechanisms involved in increased small intestinal permeability after high-intensity running merit further investigation.

Adult↗
PubMedDate not supplied

Changes in gastrointestinal permeability in celiac disease.

Increased gastrointestinal permeability was found in celiac disease already 20 years ago. Originally a genetical defect was supposed leading to elevated permeability and later to celiac disease. However, patients under long-term gluten-free diet normalized their permeability tests. On the other side, unaffected relatives of patients with celiac disease showed high permeability but not different from patients with irritable bowel syndrome and with a tendency for normalization during follow-up. In active symptomatic celiac disease, permeability is elevated in the gastroduodenum - measured by sucrose test - as well as in the small intestine - measured by lactulose/mannitol ratio. The sensitivity in active celiac disease is high (near 100%), the specificity is low due to high permeability in many intestinal diseases as in acute infectious gastroenteritis, Crohn's disease, nonsteroidal anti-inflammatory drug treatment, etc. In contrast, lactulose/mannitol test permeability is much less sensitive in silent celiac disease without diarrhea (74%). The real importance of permeability disease is established by its use for follow-up of celiac patients under gluten-free diet whereas it is correlated to the degree of mucosal atrophy. In vitro tests also show increased lactulose mucosal to serosal flux in celiac disease, but not correlated to oral permeability test. In conclusion, lactulose/mannitol test is the only noninvasive functional test in celiac disease which has essential importance in active celiac disease and in follow-up under diet.

Celiac Disease↗
PubMed1990

Low density lipoprotein transport across a microvascular endothelial barrier after permeability is increased.

We investigated the pathways for low density lipoprotein (LDL) transport across an endothelial barrier in individually perfused microvessels before and after an increase in permeability. The divalent cation ionophore A23187 (5 microM) was used to increase microvessel permeability. LDL permeability coefficients (PsLDL) were measured using quantitative fluorescence microscopy. In the control state, PsLDL measured after 10-23 minutes of accumulation of fluorescent-labeled LDL outside the microvessel wall was 4.8 x 10(-8) cm/sec. The transvascular vesicular exchange of approximately 50 vesicles/sec would account for the measured flux. The flux of LDL across the microvessel wall increased as much as 170-fold at the peak of the permeability increase (2-4 minutes after ionophore infusion). Permeability returned toward control values 10 minutes after ionophore infusion but remained elevated for as long as ionophore was present in the perfusate. The effective PsLDL was similar in magnitude to the Ps for fluorescent-labeled dextran (MW 20,000) when permeability was increased. To investigate the nature of pathways for LDL in the high-permeability state, PsLDL was measured at a series of microvessel pressures. LDL transport increased as microvessel pressure increased, demonstrating coupling of LDL flux to transvascular water flow. Solvent drag accounted for more than 95% of the increased flux of LDL in the period 2-10 minutes after permeability increased. Our results conform to the hypothesis that porous pathways between adjacent endothelial cells contribute to LDL transport across an endothelial barrier when permeability is increased.

Animals↗
PubMed1991

Role of protein kinase C in bradykinin-induced increases in microvascular permeability.

The goal of this study was to determine whether protein kinase C mediates bradykinin-induced increases in microvascular permeability. Permeability of the hamster cheek pouch was evaluated using intravital fluorescent microscopy and fluorescein isothiocyanate (FITC)-dextran (MW 70,000). We examined effects of sphingosine, a protein kinase C inhibitor, on bradykinin-induced increases in permeability. Increases in permeability were quantitated by counting the number of leaky sites and calculating the clearance of FITC-dextran. During bradykinin (10(-6) M), leaky sites increased from 0 to 40 +/- 4 (mean +/- SEM) sites/0.11 cm2, and clearance increased from 1.7 +/- 1.0 to 22 +/- 9 ml/sec x 10(-6). The bradykinin type-2 receptor antagonist D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin virtually abolished formation of leaky sites in response to bradykinin. To determine whether changes in microvascular pressure contribute to the increase in leaky sites, venular pressure was measured using a micropipette and survo-null device. Increases in cheek pouch venular pressure were similar during application of bradykinin and adenosine, which increased permeability, and isoproterenol, which did not increase permeability in the cheek pouch. Thus, increases in permeability were not linked to changes in microvascular pressure. The protein kinase C inhibitor, sphingosine (10(-6) M), markedly attenuated responses to bradykinin. Leaky sites increased from 0 to only 2 +/- 1 sites/0.11 cm2, and clearance increased from 3.9 +/- 1.4 to only 6.7 +/- 2.2 ml/sec x 10(-6). To test the specificity of sphingosine, we examined effects of adenosine (10(-6) M). Sphingosine did not significantly alter increases in microvascular permeability in responses to adenosine. We also examined effects of 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), another protein kinase C inhibitor, on responses to bradykinin and adenosine. H-7 greatly attenuated formation of leaky sites during stimulation with bradykinin and did not alter the number of leaky sites produced during adenosine. The findings suggest that protein kinase C may mediate increases in vascular permeability in response to bradykinin.

Adenosine↗
PubMed1997

High glucose concentrations increase endothelial cell permeability via activation of protein kinase C alpha.

Endothelial cell permeability is impaired in diabetes mellitus and may be increased by high extracellular glucose concentrations. High glucose activates protein kinase C (PKC), a family of kinases vital to intracellular signaling. We tested the hypothesis that high glucose concentration activates PKC in endothelial cells and leads to an increase in endothelial cell permeability via distinct PKC isoforms. Porcine aortic endothelial cells were used, and the PKC isoforms alpha, delta, epsilon, zeta, and theta were identified in these cells. Glucose caused a rapid dose-dependent increase in endothelial cell permeability, with an EC50 of 17.5 mmol/L. Phorbol 12-myristate 13-acetate (TPA) induced an increase in permeability very similar to that elicited by glucose. The effect of glucose and TPA was totally reversed by preincubating the cells with the PKC inhibitors staurosporine (10(-8) mol/L) and Goe 6976 (10(-8) mol/L). Downregulation of PKC by preincubation with TPA for 24 hours also abolished the effect of glucose and TPA on endothelial cell permeability. High glucose (20 mmol/L) caused an increase in PKC activity at 2, 10, and 30 minutes. Cell fractionation and Western blot analysis showed a glucose-induced translocation of PKC alpha and PKC epsilon. Confocal microscopy confirmed the translocation and showed an association of PKC alpha and PKC epsilon with nuclear structures and the cell membrane. Specific antisense oligodesoxynucleotides (ODNs) against PKC alpha reduced the expression of the isoform, abolished the effects of glucose on endothelial cell permeability completely, and reduced the TPA effect significantly. In contrast, specific antisense ODNs against PKC epsilon had no effect on glucose-induced permeability and only a minor effect on the TPA-induced increase in permeability. We conclude that an increase in extracellular glucose leads to a rapid dose-dependent increase in endothelial cell permeability via the activiation of PKC and that this effect is mediated by the PKC isoform alpha.

Animals↗
PubMed1980

Permeability into aortic intima and atherosclerotic plaque.

For the purpose of examining the interrelation between the permeability of the plasma constituents and the site of the atherosclerosis. We have perfused the solution of a dye into human aorta and observed permeability into aortic intima with aging and into atherosclerotic plaque. In addition, the deposition of bilirubin and fibrin into atherosclerotic plaque was also investigated. When the extent of the permeability was expressed as the ratio of the depth of permeability/thickness of intima, it was found that the ratio for the thoracic aorta decreased with advancing age. Permeability of the abdominal aorta occurred to show that the value of the ratio was up to 3.0 in the subject with age from 0 to 19 years and then the ratio slightly decreased with advancing age, followed by a further one step down in the seventies. Permeability into the atheromatous plaque showed diffuse pattern in the young adult but the permeability became shallower with advancing age. Regional difference of permeability around the plaque was studied. The greatest permeability was seen on the lower side of the plaque. Bilirubin and fibrin deposition into plaque was also similar to its permeability pattern.

Adolescent↗
PubMed2004

Permeability classification of representative fluoroquinolones by a cell culture method.

This study was undertaken to categorize representative fluoroquinolone drug substance permeability based on the methods outlined in the Food and Drug Administration's biopharmaceutic classification system (BCS) Guidance for Industry. The permeability of ciprofloxacin, levofloxacin, lomefloxacin, and ofloxacin was measured in an in vitro Caco-2 assay with previously demonstrated method suitability. The permeability class and efflux potential were ascertained by comparing test drug results with standard compounds (metoprolol, atenolol, labetalol, and rhodamine-123). All 4 quinolones drugs demonstrated concentration-dependent permeability, indicating active drug transport. In comparing absorptive versus secretive in vitro transport, the tested fluoroquinolones were found to be subject to efflux in varying degrees (ciprofloxacin > lomefloxacin > rhodamine 123 > levofloxacin > ofloxacin). Based on comparison to labetalol, the high permeability internal standard, ciprofloxacin was classified as a low permeability drug, whereas lomefloxacin, levofloxacin, and ofloxacin were classified as high permeability drugs. The in vitro permeability results matched human in vivo data based on absolute bioavailabilities. This laboratory exercise demonstrated the applicability of an in vitro permeability method for classifying drugs as outlined in the BCS Guidance.

Caco-2 Cells↗
PubMed2002

Comparison of permeability in high-grade and low-grade brain tumors using dynamic susceptibility contrast MR imaging.

OBJECTIVE: The purpose of this study was to compare permeability measurements in high-grade and low-grade glial neoplasms using a T2(*)-weighted method. Our hypothesis was that permeability measurements using a T2(*)-weighted technique would show permeability in high-grade neoplasms to be higher than that in low-grade neoplasms. MATERIALS AND METHODS: Twelve patients with biopsy-proven high-grade neoplasms and 10 patients with biopsy-proven low-grade neoplasms underwent dynamic susceptibility contrast MR perfusion imaging (TR/TE, 1500/80) after bolus infusion of 0.2 mmol/kg of MR contrast material. Color-coded permeability-weighted maps were created using a model that weights relative contributions to signal intensity from intravascular T2(*) effects and extravascular T1 effects from blood-brain barrier permeability. Two measures of permeability were performed: mean value of highest permeability found on three images through the tumor (mean regional value) and highest value found at any region of interest in the tumor (single area of maximum permeability). Depending on the normality of the data sets, we used the Wilcoxon's rank sum test or the two-tailed Student's t test for statistical analysis. RESULTS: For low-grade tumors, the range was 0.006-0.041, and the median of the mean regional value for each image was 0.017. For high-grade tumors, the range was 0.005-0.092, and the median of the mean regional value was 0.035 (p = 0.025). For low-grade tumors, the range was 0.008-0.045, and the mean of the single area of maximum values was 0.02. For high-grade tumors, the range was 0.007-0.136, and the mean of the single area of maximum values was 0.054 (p = 0.018). CONCLUSION: Permeability values for high-grade tumors obtained using a T2(*)-weighted method were significantly greater than those for low-grade tumors and are consistent with previous studies reporting results using T1-weighted methods.

Adult↗
PubMed1995

Neoplastic and pharmacological influence on the permeability of an in vitro blood-brain barrier.

The authors investigated the effects of glioma cells and pharmacological agents on the permeability of an in vitro blood-brain barrier (BBB) to determine the following: 1) whether malignant glia increase endothelial cell permeability; 2) how glucocorticoids affect endothelial cell permeability in the presence and absence of malignant glia; and 3) whether inhibiting phospholipase A2, the enzyme that releases arachidonic acid from membrane phospholipids, would reduce any malignant glioma-induced increase in endothelial cell permeability. Primary cultures of rat brain capillary endothelium were grown on porous membranes; below the membrane, C6, 9L rat glioma. T98G human glioblastoma, or no cells (control) were cocultured. Dexamethasone (0.1 microM), bromophenacyl bromide (1.0 microM), a phospholipase A2 inhibitor, or nothing was added to culture media 72 hours prior to assaying the rat brain capillary endothelium permeability. Permeability was measured as the flux of radiolabeled sucrose across the rat brain capillary endothelium monolayer and then calculated as an effective permeability coefficient (Pe). When neither dexamethasone nor bromophenacyl bromide was present, C6 cells reduced the Pe significantly (p < 0.05), whereas 9L and T98G cells increased Pe significantly (p < 0.05) relative to rat brain capillary endothelium only (control). Dexamethasone reduced Pe significantly for all cell preparations (p < 0.05). The 9L and T98G cell preparations coincubated with dexamethasone had the lowest Pe of all cell preparations. The Pe was not affected in any cell preparation by coincubation with bromophenacyl bromide (p > 0.45). These in vitro BBB experiments showed that: 1) malignant glia, such as 9L and T98G cells, increase Pe whereas C6 cells probably provide an astrocytic influence by reducing Pe; 2) dexamethasone provided significant BBB "tightening" effects both in the presence and absence of glioma cells; 3) the in vivo BBB is actively made more permeable by malignant glia and not simply because of a lack of astrocytic induction; 4) tumor or endothelial phospholipase A2 activity is probably not responsible for glioma-induced increased in BBB permeability; and 5) this model is useful for testing potential agents for BBB protection and for studying the pathophysiology of tumor-induced BBB disruption.

Acetophenones↗
PubMed2001

Radioisotope albumin flux measurement of microvascular lung permeability: an independent parameter in acute respiratory failure?

AIM: To evaluate the extent to which single measurements of microvascular lung permeability may be relevant as an additional parameter in a heterogenous clinical patient collective with Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS). METHODS: In 36 patients with pneumonia (13), non pneumogenic sepsis (9) or trauma (14) meeting the consensus conference criteria of ALI or ARDS double-isotope protein flux measurements (51Cr erythrocytes as intravascular tracer, Tc-99m human albumin as diffusible tracer) of microvascular lung permeability were performed using the Normalized Slope Index (NSI). The examination was to determine whether there is a relationship between the clinical diagnosis of ALI/ARDS, impaired permeability and clinical parameters, that is the underlying disease, oxygenation, duration of mechanical ventilation and mean pulmonary-artery pressure (PAP). RESULTS: At the time of study, 25 patients presented with increased permeability (NSI > 1 x 10(-3) min-1) indicating on exudative stage of disease, and 11 patients with normal permeability. The permeability impairment correlated with the underlying disease (p > 0.05). With respect to survival, there was a negative correlation to PAP (p < 0.01). Apart from that no correlations between the individual parameters were found. Especially no correlation was found between permeability impairment and oxygenation, duration of disease or PAP. CONCLUSION: In ALI and ARDS, pulmonary capillary permeability is a diagnostic parameter which is independent from clinical variables. Permeability measurement makes a stage classification (exudative versus non exudative phase) of ALI/ARDS possible based on a measurable pathophysiological correlate.

Adult↗
PubMed1990

Neurogenic inflammation, vascular permeability, and mast cells. II. Additional evidence indicating that mast cells are not involved in neurogenic inflammation.

Activation of cutaneous sensory nerves induces vasodilatation and vascular permeability, i.e., neurogenic inflammation. We examined the histology and possible mast cell involvement in cutaneous neurogenic inflammation induced by electrical nerve stimulation (ENS). Three lines of evidence indicated that mast cells were not involved in rodent cutaneous neurogenic inflammation induced by electrical stimulation of the saphenous nerve. 1) Most mast cells (86.5% of all mast cells in the dorsal skin of the paw) were found in the deep dermis, whereas vessels developing increased vascular permeability after nerve stimulation (visualized with the supravital dye Monastral blue B, a macro-molecular tracer) were localized predominantly in the superficial dermis. By contrast, i.v. substance P, which also causes increased cutaneous vascular permeability, predominantly caused deeper vessels to leak. As analyzed by electron microscopy, the vessels that developed permeability in response to nerve stimulation, and were thereby stained with Monastral blue B, were found to be exclusively postcapillary venules. 2) Disodium cromoglycate (DSCG), a mast cell stabilizing compound, inhibited the cutaneous vascular permeability induced by intradermal injections of anti-IgE in a dose-dependent manner. By contrast, vascular permeability induced by ENS was not influenced by disodium cromoglycate treatment. 3) ENS and i.v. substance P both induced cutaneous vascular permeability in mast cell-deficient W/Wv mice, despite the fact that their skin contained only 4.7% of the mast cells present in their normal +/+ litter mates. The magnitude of ENS-induced vascular permeability responses in W/Wv mice were similar to control +/+ and BALB/c mice. This study supports our earlier observations suggesting that mast cell activation is not essential for the initial, vascular permeability phase of neurogenic inflammation in rodent skin.

Animals↗
PubMed2006

Early estimation of high peritoneal permeability can predict poor prognosis for technique survival in patients on peritoneal dialysis.

At the beginning of continuous ambulatory peritoneal dialysis (CAPD), different patients exhibit large differences in peritoneal permeability. To determine if early estimation of peritoneal permeability can predict the prognosis of CAPD, we used data from a personal dialysis capacity (PDC) study group in Japan to investigate patient and technique survival rates. Based on the data from a previously reported, prospective multicenter study encompassing eight dialysis centers in Japan (Am J Kidney Dis 2002; 40:1045-54), we recalculated patient and technique survival data. We reviewed the records of 139 patients newly initiated on CAPD from January 1995 to December 1999. Peritoneal permeability was estimated by PDC test within the first year after initiation. We divided the patients into paired groups according to several peritoneal permeability variables as calculated by the PDC test (area, plasma loss, and peritoneal creatinine clearance), and we compared patient and technique survival rate between the groups. The mean age of the patients was 49.6 years +/- 14.9 years (standard deviation). The mean pore area of peritoneum was 19,936 +/- 8383 cm/1.73 m2. Estimation of patient survival by the Kaplan-Meier method showed 94.2%, 88.4%, 84.1%, and 79.7% at 1, 2, 3, and 5 years respectively. Estimated technique survival (including death as an endpoint) by the Kaplan-Meier method showed 90.6%, 76.8%, 67.4%, and 54.3% at 1, 2, 3, and 5 years respectively. In the high peritoneal permeability group (high area and high plasma loss), the technique survival at 5 years was significantly lower than in the low peritoneal permeability group [area: 55.9% (high) vs. 72.7% (low), p = 0.0459; plasma loss: 43.3% (high) vs. 62.8% (low), p = 0.0197). We observed no significant difference in patient survival between the high and low peritoneal permeability patients. In the high peritoneal creatinine clearance group, patient and technique survival were both significantly lower than in the high peritoneal creatinine clearance group. Patients with high peritoneal permeability as calculated by the PDC test at the start of PD had a poor prognosis for technique and patient survival on CAPD. We conclude that early estimation of high peritoneal permeability can predict poor outcome for patients on CAPD.

Creatinine↗
PubMed1990

Cutaneous thermal injury alters macromolecular permeability of rat small intestine.

The intestinal epithelium normally provides a barrier function that prevents absorption of potentially harmful materials from the intestinal lumen. It has been postulated but never demonstrated that a cutaneous thermal injury will result in increased small-intestinal permeability. In a standardized 20% body surface area full-thickness scald injury, with polyethylene glycol 3350 and horseradish peroxidase used as permeability probes, small-intestinal permeability was examined regionally in an everted intestinal sac model. In the normal animals, the upper (proximal) and lower (distal) small intestine were less permeable to these probes than the middle segment. Within 6 hours after the injury, an increase in the mucosal uptake and transmural permeability was seen in all three small-intestinal segments; the most dramatic increase in permeability occurred in the ileum, p less than 0.01. The maximum increase in permeability was seen at 18 hours, and permeability was normal by 72 hours after the injury. This increase in intestinal permeability may represent a transient failure of the intestinal barrier function and may allow absorption of potentially toxic macromolecules from the intestinal lumen into the portal circulation early after thermal injury. Absorption of these macromolecules, such as endotoxin, may be potentially harmful by direct toxic actions or potentially helpful by activation of the immune system.

Animals↗
PubMed1989

Paracellular permeability of corneal and conjunctival epithelia.

The paracellular permeability of normal rabbit cornea and conjunctiva was studied in vivo and in vitro. After intravenous administration, horseradish peroxidase was found to percolate to the intercellular space of conjunctival epithelia and was restricted by the tight junctions of the superficial epithelium. Only minimal tracer was present in the limbus and cornea. The difference between corneal and conjunctival paracellular pathways was further compared in vitro by tissue perfusion studies using various tracers from subepithelial space to apical surface. The intact full-thickness cornea was permeable to mannitol (MW 182) but not to inulin or dextran. The conjunctiva was permeable to mannitol, inulin and FITC-dextran (MW 20,000). The quantitative permeability to 3H-mannitol (X10(-8) cm/sec) of adult rabbit cornea was 0.12 +/- 0.02, which is about 55-fold and 50-fold lower than that of conjunctiva (6.78 +/- 0.21) and peritoneum (6.12 +/- 0.63), respectively. Removal of the corneal epithelium increased the permeability 40-fold; however, removal of the endothelium had little effect on the solute permeation. When both corneal epithelium and endothelium were debrided, the bare stroma became edematous and the permeability increased 70-fold. The permeability of 1-week-old rabbit cornea was 1.32 +/- 0.18, which decreased to 0.46 +/- 0.06 in 2-week-old rabbits, and became similar to the adult level at 4 weeks of age. When Tenon's capsule was included in the perfusion, the conjunctival permeability decreased 2.5-fold. With the apposition of bare corneal stroma to the conjunctiva and Tenon's capsule, the permeability decreased further (4-fold).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

[Disordered permeability of the glomerular filter for middle- and high-molecular serum proteins in various morphologic types and stages of chronic glomerulonephritis].

Investigation of glomerular filter permeability for serum immunoglobulins and albumins in 83 patients with chronic glomerulonephritis (CGN) with nephrotic proteinuria has shown that in mesangioproliferative glomerulonephritis permeability for IgM is rare, for IgA and IgG moderately raised; in a marked but not maximum degree of permeability for albumins, it is characterized by considerable variability. In maximum permeability for albumins there is a tendency to the reduction of the ratio of IgA and IgM clearances to albumin clearance, and variability of these indices. In membranous CGN the structure of nephron permeability for serum proteins is identical but it remains unchanged with a sharp rise of albumin fractional clearance. In mesangiocapillary CGN permeability for IgM is more frequent and enhanced for IgG. in focal-segmental glomerular hyalinosis/sclerosis and diffuse-fibroplastic GN permeability for IgG is considerably raised unrelated to a degree of permeability for albumins. Sclerotic changes are accompanied by elevated permeability for IgG.

Adolescent↗