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PubMed1995

The blood-ocular barrier in type I diabetes without diabetic retinopathy: permeability measurements using fluorophotometry.

For the evaluation of a possible malfunction of the blood-retinal (BRB) and the blood-aqueous barrier (BAB) in type I diabetes without manifest angiopathy, after i.v. injection of sodium fluorescein, the permeability of BRB (P) and the diffusion coefficient of BAB [P(a)] were studied simultaneously by fluorophotometry in 34 eyes of 34 type I diabetics (HbA1c = 6.6 +/- 0.9%) without retinopathy whose ages ranged from 19 to 38 years (30.5 +/- 5); diabetes' duration was between 5 and 18 years. Fluorescein angiography was performed to exclude nonperfused areas. In all, 34 eyes of 34 healthy volunteers whose ages ranged between 23 and 34 years (28.5 +/- 3.3) served as controls; in this group, fluorophotometry was performed twice to evaluate reproducibility. The mean BAB diffusion coefficient in diabetics [P(a) = 5.3 +/- 1.8/min] was significantly increased (p = 0.00003) as compared to controls [P(a) = 3.7 +/- 0.7/min]; BRB permeability in diabetes (P = 3.2 +/- 1.4 x 10(-7) cm/s) was raised with this elevation being of lower significance (p = 0.019; controls: P = 2.6 +/- 0.7 x 10(-7) cm/s). We found a decrease in BRB permeability depending on diabetes' duration (r = -0.15; p = 0.007) that was not significant in BAB (r = -0.1; p = 0.24). No correlation was found to exist between permeability and HbA1c values either in BAB or in BRB. The reproducibility in controls was 9% in BRB determinations and 12% in BAB measurements. These results may suggest that early structural alterations without the manifestation of retinopathy possibly cause elevation in BRB permeability and are even more obvious in BAB permeability. Whereas the reliability of vitreous fluorophotometry in detecting early BRB malfunction has to be judged critically, anterior segment fluorophotometry is a reliable procedure for the monitoring of BAB affection in type I diabetes without retinopathy.

Adult↗
PubMed1997

Gender differences in intima-media permeability to low-density lipoprotein at atherosclerosis-prone aortic sites in rabbits. Lack of effect of 17 beta-estradiol.

Premenopausal women are protected from coronary heart disease, and premenopausal nonhuman primates are protected from atherosclerosis, the underlying cause of coronary heart disease. Estrogen is thought to account for this protection in females, and part of this protection is independent of the effects on risk factors, including lipoprotein levels. This study considered the hypothesis that reduced intima-media permeability to low-density lipoproteins (LDL) may account for the protection from atherosclerosis and coronary heart disease in premenopausal females and that this effect might be mediated by estrogen. Intima-media permeability to LDL was determined in male and female rabbits made hypercholesterolemic by feeding them 0.5% cholesterol for 8 days. The diet of half of the female rabbits was supplemented with 17 beta-estradiol (4 mg/d) during cholesterol feeding and the preceding 4 weeks. Estrogen treatment in the female rabbits did not influence the intima-media permeability to LDL. However, intima-media permeability to LDL for branch sites of the abdominal aorta and aortic arch (regions highly susceptible to atherosclerosis) was 43% and 38% lower, respectively, in male rabbits than in female rabbits: (2.93 +/- 0.39 microL/h/g, (n = 8), vs 6.28 +/- 0.86 microL/h/g, (n = 16), P < .001, and 4.69 +/- 0.28 microL/h/g, (n = 8) vs 7.57 +/- 0.75 microL/h/g, (n = 16), P < .02). In contrast, intima-media permeability to LDL in 7 of 8 aortic sites relatively resistant to atherosclerosis did not differ between male and female rabbits. These data suggest that the protection from atherosclerosis associated with female sex and estrogen is mediated by mechanism(s) other than reduction in intima-media permeability to LDL.

Animals↗
PubMed1991

Thrombolytic therapy causes an increase in vascular permeability that is reversed by 1-deamino-8-D-vasopressin.

BACKGROUND: To examine the effect of plasminogen activator therapy on vascular permeability, we used a modified rabbit mesenteric model of extravascular tissue accumulation of radiolabeled albumin. METHODS AND RESULTS: Albumin deposition was measured after saline, tissue-type plasminogen activator (t-PA; 0.86 mg/kg for 1 hour followed by 0.29 mg/kg for 2 hours), or t-PA plus 1-deamino-8-D-arginine vasopressin (DDAVP; 0.6 mg/kg/hr for 30 minutes) infusion in animals with or without aspirin (ASA; 15-mg/kg bolus) pretreatment. In animals not given ASA, t-PA caused a 240% increase in tissue [125I]albumin accumulation over time (p less than 0.001). DDAVP prevented the rise in albumin accumulation normally seen with t-PA alone (p less than 0.05) in animals not given ASA. In animals pretreated with ASA, t-PA similarly caused an increase in tissue albumin accumulation, but this was significantly attenuated from that of animals not given ASA (p less than 0.03). Interestingly, DDAVP failed to block the response to t-PA in the animals given ASA. Because increases in vascular permeability correlated with increases in bleeding time (r = 0.37, p less than 0.03), these data suggest that the effect of plasmin generation on vascular permeability may contribute to the bleeding tendency seen with thrombolytic therapy. The ability of DDAVP to reverse the bleeding tendency and bleeding time may be due in part to its reversal of the increased vascular permeability induced by the administration of plasminogen activators. CONCLUSIONS: These data show that plasminogen activation causes an increase in vascular permeability that is inhibited by DDAVP; ASA blunts this action of t-PA and prevents the DDAVP blockade of the increase in permeability induced by t-PA in this rabbit model.

Albumins↗
PubMed2005

Cdc42 regulates adherens junction stability and endothelial permeability by inducing alpha-catenin interaction with the vascular endothelial cadherin complex.

The endothelial adherens junctions (AJs) consist of trans-oligomers of membrane spanning vascular endothelial (VE)-cadherin proteins, which bind beta-catenin through their cytoplasmic domain. beta-Catenin in turn binds alpha-catenin and connects the AJ complex with the actin cytoskeleton. We addressed the in vivo effects of loss of VE-cadherin interactions on lung vascular endothelial permeability and the role of specific Rho GTPase effectors in regulating the increase in permeability induced by AJ destabilization. We used cationic liposomes encapsulating the mutant of VE-cadherin lacking the extracellular domain (DeltaEXD) to interfere with AJ assembly in mouse lung endothelial cells. We observed that lung vascular permeability (quantified as microvessel filtration coefficient [K(f,c)]) was increased 5-fold in lungs expressing DeltaEXD. This did not occur to the same degree on expression of the VE-cadherin mutant, DeltaEXDDeltabeta, lacking the beta-catenin-binding site. The increased vascular permeability was the result of destabilization of VE-cadherin homotypic interaction induced by a shift in the binding of beta-catenin from wild-type VE-cadherin to the expressed DeltaEXD mutant. Because DeltaEXD expression in endothelial cells activated the Rho GTPase Cdc42, we addressed its role in the mechanism of increased endothelial permeability induced by AJ destabilization. Coexpression of dominant-negative Cdc42 (N17Cdc42) prevented the increase in K(f,c) induced by DeltaEXD. This was attributed to inhibition of the association of alpha-catenin with the DeltaEXD-beta-catenin complex. The results demonstrate that Cdc42 regulates AJ permeability by controlling the binding of alpha-catenin with beta-catenin and the consequent interaction of the VE-cadherin/catenin complex with the actin cytoskeleton.

Antigens, CD↗
PubMed1987

Change in (dP/dt)max as an index of myocardial microvascular permeability.

We frequently study processes that alter microvascular permeability in the heart. Myocardial microvascular permeability has been estimated by determining the filtration independent reflection coefficient for beta-lipoprotein (sigma beta-LIPO). This technique requires the measurement of myocardial lymph flow rate and the lymph-to-plasma protein concentration ratio. Unfortunately, it is a nonsurvival procedure. An index of myocardial microvascular permeability was needed that could be determined in experimental preparations without sacrificing valuable chronically instrumented animals. We attempted to relate changes in myocardial microvascular permeability and myocardial edema formation to some index of myocardial performance. In 33 acute, anesthetized dogs (with normal or disrupted myocardial microvasculatures), we measured systemic arterial pressure, systemic venous pressure, coronary sinus pressure, left ventricular pressure, the maximum rate of change in left ventricular pressure (dP/dt)max, myocardial lymph flow rate, and myocardial extravascular fluid volume. Following an increase in coronary sinus pressure, the amount of edema fluid entering the myocardium varied as a function of myocardial microvascular permeability. Further, as the heart became edematous, (dP/dt)max changed with respect to time [delta(dP/dt)max/delta t]. Finally, a significant relation was found between sigma beta-LIPO and delta(dP/dt)max/delta t. Since coronary sinus pressure can be elevated and delta(dP/dt)max/delta t can be measured in chronic animals, this technique may be useful for evaluating myocardial microvascular permeability on a long-term survival basis.

Animals↗
PubMed1989

Lipoxygenase products induce neutrophil activation and increase endothelial permeability after thrombin-induced pulmonary microembolism.

We examined the mechanism of the neutrophil (PMN)-dependent increase in pulmonary vascular permeability to protein after thrombin-induced pulmonary microembolism. Humoral factors that activate PMNs after thrombin-induced pulmonary microembolism were characterized in pulmonary lymph obtained from unanesthetized sheep challenged with intravenous infusion of alpha-thrombin. Time-dependent increases in PMN migration, aggregation, and superoxide anion (O2-) generation were induced by the pulmonary lymph obtained within 20 minutes after thrombin infusion. The pulmonary lymph neutrophil activating factors present in ether extracts of lymph had retention times of leukotriene B4 (LTB4) and monohydroxyeicosatetraenoic acids (HETEs) by high-performance liquid chromatography. The postthrombin lymph samples containing the LTB4 and HETEs increased PMN O2- generation and endothelial monolayer permeability to 125I-albumin in the presence of PMNs layered on the endothelial monolayers. Control lymph samples replete with LTB4, 5-HETE, and 15-HETE induced increases in PMN O2- generation and endothelial monolayer permeability to 125I-albumin in the presence of PMNs layered on the endothelial monolayers. Maximal increases in PMN O2- production and endothelial permeability occurred when LTB4, 5-HETE, and 15-HETE were coincubated with PMNs, indicating a synergistic action of these mediators in inducing PMN activation. Endothelial monolayer permeability to 125I-albumin did not increase with postthrombin lymph samples obtained after pretreatment with the 5-lipoxygenase inhibitor, L-651,392. The results indicate that lipoxygenase products generated in the lungs after thrombin-induced microembolism contribute to increased endothelial permeability secondary to PMN activation.

Animals↗
PubMed2001

Role of nitric oxide in vascular permeability after combined burns and smoke inhalation injury.

Patients with severe burn and/or smoke inhalation injury suffer both systemic and pulmonary vascular hyperpermeability. We hypothesized that nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) plays a role in the changes in microvascular permeability seen with this injury. To test the hypothesis, we administered mercaptoethylguanidine (MEG), a selective iNOS inhibitor, to conscious sheep subjected to a combined smoke inhalation and third-degree burn injury to 40% of total body surface area. The sheep were surgically prepared for chronic study with lung and prefemoral lymph fistulas in order to estimate microvascular permeability. Both the groups and a control group of animals showed an increase in iNOS protein and message in their lungs. The control animals showed significant increases in either plasma or lymph NO2-/NO3- (NOx) concentration at 24 h after injury, with associated cardiac depression and hemoconcentration. The airway epithelium stained for nitrotyrosine. In the treatment group, NOx did not increase significantly in plasma or lymph throughout the experiment, there was no nitrotyrosine staining, hemodynamic depression was not observed, and the fluid requirement was significantly less than in the control group. Changes in pulmonary microvascular permeability were significantly suppressed by inhibition of iNOS. However, there was no significant difference between the two study groups in the microvascular permeability of burned tissue. These data suggest that NO produced by iNOS plays an important role in the changes in systemic and pulmonary microvascular permeability in combined smoke inhalation/third-degree burn injury, but does not affect the vascular permeability of third-degree-burned tissue in this type of injury.

Animals↗
PubMed1982

Oxygen-radical-mediated permeability edema and vasoconstriction in isolated perfused rabbit lungs.

Oxygen radicals have been implicated in the pathogenesis of permeability pulmonary edema. To determine directly if O2 radicals can cause increased alveolar-capillary membrane (ACM) permeability and low-pressure permeability edema, we chemically produced O2 radicals in the sale perfusates of isolated rabbit lungs. The O2 radicals generated by xanthine oxidase caused protein-rich edema and increases in lung perfusion pressures that were inhibitable by catalase (hydrogen peroxide scavenger) or dimethylthiourea (hydroxyl radical scavenger) but not by superoxide dismutase. To determine the effect of O2 radicals on ACM permeability without interference from increased perfusion pressures, we used papaverine to maintain baseline perfusion pressures during O2 radical exposure and then assessed ACM integrity by evaluating the response of isolated lungs to elevated outflow pressures (10 mmHg for 10 min). Under these conditions, increased ACM permeability manifested by weight gains and lavage albumin accumulations occurred in lungs treated with xanthine oxidase but not in control lungs. We conclude that O2 radicals can cause increased ACM permeability and vasoconstriction in isolated lungs.

Animals↗
PubMed1983

Granulocytes and phorbol myristate acetate increase permeability to albumin of cultured endothelial monolayers and isolated perfused lungs. Role of oxygen radicals and granulocyte adherence.

Human granulocytes and phorbol myristate acetate (PMA) increased permeability to albumin of monolayers of cultured endothelial cells grown on micropore filters. Granulocytes from a patient with chronic granulomatous disease and PMA did not increase endothelial permeability to albumin, demonstrating that the increase in permeability is dependent on granulocyte-derived oxygen radicals. When granulocytes were separated from the endothelial cells by a micropore filter, granulocytes and PMA no longer increased endothelial permeability to albumin, demonstrating that PMA-stimulated granulocytes must be closely approximated to endothelial cells to increase endothelial permeability. The relevance of these in vitro findings to an intact microvasculature was confirmed by demonstrating that agents that reduce granulocyte adherence to endothelium reduce edema formed in isolated lungs by granulocytes and PMA, an oxygen radical dependent process. Pretreatment of granulocytes with cytochalasin B or addition of 2% dextran to isolated lung perfusates reduced granulocyte adherence and markedly reduced edema formation in isolated lungs. These studies demonstrate that PMA-stimulated granulocytes must be closely apposed to endothelial cells to increase endothelial permeability through an oxygen-radical-dependent mechanism, and they suggest that reduction of granulocyte adherence may protect against granulocyte-dependent edema.

Animals↗
PubMed1985

Deterioration of oxygenation and abnormal lung microvascular permeability during resolution of leukopenia in patients with diffuse lung injury.

To determine whether circulating leukocytes contribute to gas exchange abnormalities in diffuse lung injury, we retrospectively examined oxygenation in 6 patients who met 3 criteria: leukopenia caused by marrow aplasia from remission-inducing chemotherapy for myelogenous leukemia, the eventual resolution of leukopenia, and concurrent acute respiratory failure diagnosed clinically as increased permeability pulmonary edema. Four of the 6 patients abruptly developed overt clinical evidence of pulmonary dysfunction within the 96 h preceding the resolution of the peripheral leukopenia. In all 6 patients, the alveolar to arterial oxygen tension difference increased between leukocyte counts. The mean value for the alveolar to arterial oxygen tension difference for the group doubled during this period (148 +/- 37 mmHg 3 days prior to resolution; 290 +/- 37 mmHg 1 day after resolution; p less than 0.05). As an index of lung capillary permeability, we measured the lung permeability-surface area product for urea (PSu) for an additional patient with oxygen toxicity and drug-induced leukopenia whose hypoxemia increased immediately before the resolution of leukopenia. The PSu in this patient was high, in the range previously reported as being highly specific for increased permeability pulmonary edema with a fatal outcome. We conclude that such diffuse lung injury resembling the adult respiratory distress syndrome can occur in leukopenic patients, but the resolution of leukopenia in such patients may be associated with worsening oxygenation and with abnormally high pulmonary microvascular permeability. These observations do not prove a causal relationship but provide a clinical parallel to several leukocyte-depletion studies reported in animal models of increased permeability pulmonary edema that implicate white blood cells in the pathogenesis of hypoxemia and lung edema.

Adult↗
PubMed1999

Early events in naphthalene-induced acute Clara cell toxicity: comparison of membrane permeability and ultrastructure.

Naphthalene causes severe dose- and site-selective injury to mouse nonciliated bronchiolar (Clara) epithelial cells. Toxicity is characterized by exfoliation of injured Clara cells into the airway lumen 24 h after exposure. The purpose of this study was to define the temporal pattern of intracellular changes immediately following naphthalene treatment, with the goal of identifying critical early events involved in cytotoxicity. Mice were injected with naphthalene or carrier and were killed 1, 2, 3, and 6 h after treatment (PT). Loss of membrane integrity was assessed by ethidium homodimer-1 permeability and confocal microscopy. Cell morphology and ultrastructure were evaluated using high-resolution light and electron microscopy. Permeable cells were found only in terminal bronchioles and increased in abundance with time PT. At 2 and 3 h PT, when most Clara cells had early signs of injury, few permeable cells were detected. Many Clara cells had apical membrane blebs that contained abundant, swollen, smooth endoplasmic reticulum (SER) and few other organelles. By 6 h PT many Clara cells were membrane-permeable. However, many permeable Clara cells lacked apical blebs and SER was less abundant in these cells. Cytoplasmic blebbing may be a mechanism to protect the cell by isolating and removing damaged SER. We conclude that the early stages of injury include SER swelling and bleb formation which precede increases in cell membrane permeability after acute naphthalene injury to bronchiolar Clara cells in vivo.

Animals↗
PubMed1992

Attenuation of ozone-induced airway permeability in rats by pretreatment with cyclophosphamide, FPL 55712, and indomethacin.

Exposure of rats to ozone (O3) produces an increase in airway permeability and a concomitant influx of polymorphonuclear leukocytes in the lung. These observations raise the possibility that the inflammatory cells play a role in the cellular injury and increased airway permeability after O3 exposure. This study was therefore designed to determine if the inflammatory cells or their products are essential for the O3 effect. In a series of experiments, rats were rendered leukopenic with cyclophosphamide, treated with leukotriene B4 (LTB4), or with the inhibitors of lipoxygenase or cyclooxygenase products of arachidonic acid, followed by exposure to O3. A 2-h exposure to 0.8 ppm O3 caused a significant increase in the flux of proteins and albumin in bronchoalveolar lavage (BAL) and elevated the transport of 99mTc-diethylenetriaminepentaacetate (99mTc-DTPA) from trachea to blood. The treatment with cyclophosphamide caused a significant reduction in the circulating and pulmonary leukocytes and prevented an increase in tracheal mucosal permeability to 99mTc-DTPA and the protein and albumin flux in BAL. While the intratracheal instillation of LTB4 did not affect the permeability, tracheal permeability and albumin levels in BAL in rats treated with LTD4 antagonist FPL 55712 and exposed to O3 were lower than in the untreated O3-exposed rats. Pretreatment with indomethacin also prevented the O3 effects, as reflected by the decreased protein and albumin flux in BAL and 99mTc-DTPA transport from trachea to blood. These data show a reduction in the effect of O3 by agents that affect leukocytes or their products. The results support a mechanism of increased permeability that is dependent upon inflammatory cells and their products.

Albumins↗
PubMed2006

Integrin alphavbeta5 regulates lung vascular permeability and pulmonary endothelial barrier function.

Increased lung vascular permeability is an important contributor to respiratory failure in acute lung injury (ALI). We found that a function-blocking antibody against the integrin alphavbeta5 prevented development of lung vascular permeability in two different models of ALI: ischemia-reperfusion in rats (mediated by vascular endothelial growth factor [VEGF]) and ventilation-induced lung injury (VILI) in mice (mediated, at least in part, by transforming growth factor-beta [TGF-beta]). Knockout mice homozygous for a null mutation of the integrin beta5 subunit were also protected from lung vascular permeability in VILI. In pulmonary endothelial cells, both the genetic absence and blocking of alphavbeta5 prevented increases in monolayer permeability induced by VEGF, TGF-beta, and thrombin. Furthermore, actin stress fiber formation induced by each of these agonists was attenuated by blocking alphavbeta5, suggesting that alphavbeta5 regulates induced pulmonary endothelial permeability by facilitating interactions with the actin cytoskeleton. These results identify integrin alphavbeta5 as a central regulator of increased pulmonary vascular permeability and a potentially attractive therapeutic target in ALI.

Amides↗
PubMed2005

Regulation of aquaporin water permeability in the lens.

PURPOSE: To examine Ca(2+)- and pH-mediated regulation of water permeability of endogenously expressed aquaporin (AQP)0 in lens fiber cells and AQP1 in lens epithelial cells. METHODS: Large, right-side-out membrane vesicles were formed from freshly isolated groups of lens fiber cells. Osmotic shrinking or swelling of these vesicles was used to determine the water permeability of endogenously expressed AQP0. The results were compared with those in similar studies of freshly isolated lens epithelial cells, which endogenously expressed AQP1, and of oocytes, which exogenously expressed AQP0. RESULTS: In the lens or in oocytes, decreasing external pH from 7.5 to 6.5 caused a two- to fourfold increase in the water permeability of mammalian AQP0. Several lines of evidence suggest that this effect is mediated by the binding of H(+) to a histidine in the first extracellular loop (His40). Lens AQP1 lacks His40 and also lacks pH sensitivity. Increasing Ca(2+) caused a two- to fourfold increase in the water permeability of endogenous AQP0. The Ca(2+) effect on mouse AQP0 was a 2.5-fold increase in the lens, whereas in oocytes, it was a 4-fold decrease. In either environment, the effect was mediated through calmodulin, most likely through its binding to the proximal domain of the C terminus. Lens AQP1 does not have a similar domain and does not have calcium sensitivity. CONCLUSIONS: In either the lens or oocytes, Ca(2+) and H(+) appear to affect the same mechanism, probably either the open probability of the water channel, or open-channel permeability. The difference between calcium's effects in lens versus oocytes was remarkable and is not understood. However, in the lens, Ca(2+) and H(+) are both increased in inner fiber cells, and so in the physiologically relevant environment, both may act to increase the water permeability of AQP0.

Amino Acid Sequence↗
PubMed1974

Normal glomerular permeability and its modification by minimal change nephrotic syndrmone.

It has been suggested that the glomerular basement membrane restricts the passage of large molecules only, the barrier to filtration of smaller molecules being at the level of the epithelial slit pore. This hypothesis was investigated by measuring glomerular permeability to (125)I-labeled polydisperse polyvinyl pyrrolidone (PVP) in 16 children with idiopathic nephrotic syndrome (INS) and in 6 children of comparable age who had no evidence of renal disease. Studies were performed in the patients with INS before, during, and after treatment with steroids. PVP in blood and urine samples was separated according to molecular size by solumn chromatography, to permit the calculation of permeability to inert macromolecules of sizes ranging from 8,000 mol wt. In untreated INS, glomerular permeability to molecules > 40 A was normal; permeability to smaller molecules was markedly reduced, frequently to 20% or less of normal. There was an average decrease in inulin clearance (C(in)) of 24%. Glomerular permeability and C(in) returned to normal in INS treated with steroids only when proteinuria disappeared. The results support the concept, derived from studies with ultrastructural tracers, that the final barrier to filtration may be at the level of the epithelial slit pore. Thus fusion of the epithelial foot processed with obliteration of the slit pores was associated with impaired passage of smaller molecules of PVP into the urine. Reversal of the pathologic abnormality resulted in return of permeability to normal. The decreased C(in) seen in INS may not reflect true glomerular filtration rate, but may result from restricted passage of inulin molecules (mol wt 5,000) through the epithelial slit pore.

Adolescent↗
PubMed1990

Improvement of capillary permeability in patients with venous hypertension after treatment with TTFCA.

The VSC (vacuum suction chamber) device, a new system to evaluate local capillary permeability, was used with laser Doppler flowmetry to study variations of permeability and of the microcirculation in 10 normal subjects; in 22 patients with moderate, superficial venous hypertension; and in 12 patients with postphlebitic limbs and severe venous hypertension. All these patients had distal (ankle and foot edema) in the evening. After a first assessment these subjects were studied again after two weeks without treatment and after two weeks' treatment with total triterpenic fraction of centella asiatica (TTFCA), tablets, 60 mg, tid. The VSC produces a wheal on the skin of the perimalleolar region that disappears (in average) in less than sixty minutes in normal subjects. The disappearance time (DT) is greater in conditions of increased capillary filtration and permeability. The three groups of subjects (normal and those with superficial and severe venous hypertension) had significantly different, increasing disappearance time of the wheals at the first observation. There were no significant changes after two weeks' observation, but after 2 weeks' treatment with TTFCA, there was a significant decrease of DT both in limbs with superficial and with deep venous incompetence. The improvement (decrease) of the abnormally increased capillary permeability was associated with a significant improvement of the microcirculation and symptoms (studied by an analogue scale line). In conclusion this study showed a combined improvement of the microcirculation and capillary permeability after treatment with TTFCA and the possibility of using the VSC to evaluate the effects of drugs (or other treatment) on local capillary permeability in patients with venous hypertension.

Adult↗
PubMedDate not supplied

Luminal glutamine perfusion alters endotoxin-related changes in ileal permeability of the piglet.

BACKGROUND: The objective of this study was to investigate whether luminal perfusion with glutamine or with oxygenated glutamine solutions prevents endotoxin-induced changes in mucosal permeability. METHODS: Three 15-cm segments of distal ileum were isolated in anesthetized 21-day-old piglets (n = 4) and perfused (50 mL/h) with Ringer's lactate solution, Ringer's lactate solution with 2% glutamine (wt/vol), glutamine, or glutamine purged with oxygen at 37 degrees C for 280 minutes. Plasma-to-lumen clearances of 51Cr-EDTA and urea were measured to assess mucosal permeability. At time 0 minutes, loading and maintenance IV infusions of markers were begun. Baseline permeabilities were obtained from time 60 to 80 minutes, and IV endotoxin (50 micrograms/kg) was introduced from time 80 to 140 minutes. RESULTS: Results are expressed as the ratio of the clearances of the two probes (CEDTA/CUREA). Permeability increased from baseline in loops perfused with Ringer's lactate solution vs loops perfused with glutamine purged with oxygen and with glutamine alone (p < .01). Saturation with oxygen was without effect inasmuch as glutamine alone negated permeability increases. Intestinal myeloperoxidase activity did not differ with perfusate (p > .05). CONCLUSIONS: These data suggest that endotoxin-induced permeability changes can be prevented or delayed by the supply of luminal glutamine at the time of insult.

Animals↗
PubMed1991

The permeability of oral mucosa.

In discussing permeability, we are describing one of the fundamental barrier functions of oral mucosa. Despite assumptions to the contrary, the oral mucosa is not a uniformly, highly permeable tissue like gut, but shows regional variation. The keratinized areas, such as gingiva and hard palate, are least permeable and nonkeratinized lining areas are most permeable. This variation appears to reflect differences in the types of lipid making up the intercellular permeability barrier in the superficial layers of the epithelium. Differences in permeability may be related to regional differences in the prevalence of certain mucosal diseases and can be utilized to advantage for local and systemic drug delivery.

Animals↗