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PubMed1997

An Electron Paramagnetic Resonance Spin-Probe Study of Membrane-Permeability Changes with Seed Aging.

We developed an electron paramagnetic resonance spin-probe technique to study changes in the barrier properties of plasma membranes in wheat (Triticum aestivum L.) seeds during aging under dry storage. The estimation of these barrier properties was based on the differential permeability of membranes for the stable free radical 4-oxo-2,2,6,6-tetramethyl-1-piperidinyloxy and the broadening agent ferricyanide. The line-height ratio between the water and lipid components in the electron paramagnetic resonance spectra of 4-oxo-2,2,6,6-tetramethyl-1-piperidinyloxy (R value) allowed for the quantitative assessment of the plasma membrane permeability in small samples, enabling separate studies of the axis, scutellum, aleurone layer, and starchy endosperm tissue. High R values corresponded to low permeability and vice versa. Starchy endosperm cells had completely permeable plasma membranes even in mature, viable seeds. The loss of germinability with aging coincided with a considerably increased plasma membrane permeability of the embryo axis cells, but not of the scutellum and aleurone layer cells. The threshold R value for the individual axes associated with viability loss was established at 5 to 6, with the total ranging from 0 to more than 12. We suggest that the R value of an individual axis is the result of contributions from all individual cells, each of them characterized by a different permeability. The loss of viability, therefore, corresponds to the accumulation of cells having permeability above a critical level.

Journal Article↗
PubMed1994

Rectification properties and Ca2+ permeability of glutamate receptor channels in hippocampal cells.

Excitatory amino acids exert a depolarizing action on central nervous system cells through an increase in cationic conductances. Non-NMDA receptors have been considered to be selectively permeable to Na+ and K+, while Ca2+ influx has been thought to occur through the NMDA receptor subtype. Recently, however, the expression of cloned non-NMDA receptor subunits has shown that alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors are permeable to Ca2+ whenever the receptor lacks a particular subunit (edited GluR-B). The behaviour of recombinant glutamate receptor channels predicts that Ca2+ would only permeate through receptors that show strong inward rectification and vice versa, i.e. AMPA receptors with linear current-voltage relationships would be impermeable to Ca2+. Using the whole-cell configuration of the patch-clamp technique, we have studied the Ca2+ permeability and the rectifying properties of AMPA receptors, when activated by kainate, in hippocampal neurons kept in culture or acutely dissociated from differentiated hippocampus. Cells were classified according to whether they showed outward rectifying (type I), inward rectifying (type II) or almost linear (type III) current-voltage relationships for kainate-activated responses. AMPA receptors of type I cells (52.2%) were mostly Ca(2+)-impermeable (PCa/PCs = 0.1), while type II cells (6.5%) expressed Ca(2+)-permeable receptors (PCa/PCs = 0.9). Type III cells (41.3%) showed responses with low but not negligible Ca2+ permeability (PCa/PCs = 0.18). The degree of Ca2+ permeability and inward rectification were well correlated in cultured cells, i.e. more inward rectification corresponded to higher Ca2+ permeability.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed2006

Luminal hypotonicity increases duodenal mucosal permeability by a mechanism involving 5-hydroxytryptamine.

AIM: To investigate whether 5-hydroxytryptamine (5-HT) participates in the mediation of the hypotonicity-induced increase in duodenal mucosal permeability. METHODS: Proximal duodenum in anaesthetized rats was perfused in situ with a hypotonic NaCl solution and effects on duodenal motility, net fluid flux, mucosal permeability [blood-to-lumen clearance of (51)Cr-ethylenediaminetetraacetic acid (EDTA)] and the release of 5-HT into the luminal solution studied in the presence of the cyclooxygenase inhibitor indomethacin. RESULTS: Perfusion of the duodenum with 50 mm NaCl increased mucosal permeability eightfold, increased the luminal output of 5-HT twofold and induced net fluid absorption. This rise in permeability was enhanced 25% by 5-HT (3 x 10(-3) m), reduced by the 5-HT(3)-receptor antagonists granisetron (10(-4)-3 x 10(-4) m) or ondansetron (10(-5)-10(-4) m) or by the 5-HT(4) receptor antagonist SB 203186 (10(-4) m). The 5-HT(3/4) receptor antagonist tropisetron, at 10(-4) m, did not affect while 3 x 10(-4) and 3 x 10(-3) m augmented the hypotonicity-induced increase in mucosal permeability. Lidocaine (1.1 x 10(-3) m) similarly potentiated while tetrodotoxin (TTX) (5 x 10(-5) m) inhibited the hypotonicity-induced increase in mucosal permeability. Compared with animals treated with indomethacin alone ondansetron and granisetron augmented (by 30-40%) while tropisetron and lidocaine reduced (by 60-70%) the hypotonicity-induced net fluid absorption. Tetrodotoxin and all 5-HT receptor antagonists, except tropisetron, depressed duodenal motility. CONCLUSIONS: Luminal hypotonicity increases duodenal mucosal permeability by a neural mechanism involving 5-HT acting on 5-HT(3) and 5-HT(4) receptors. 5-HT also appears to participate in the regulation of the hypotonicity-induced fluid flux.

Anesthetics, Local↗
PubMed1996

Autoradiographic mapping of local cerebral permeability to bilirubin in immature rats: effects of hyperbilirubinemia.

Kernicterus is characterized by the accumulation of bilirubin mainly into subcortical brainstem nuclei. Inasmuch as premature infants are more susceptible to kernicterus, we hypothesized that the cerebral permeability to bilirubin could vary by cerebral region and with age. Therefore, in the present study, we measured the blood-to-brain transfer constant (Ki) of [3H]bilirubin in 6-8 rats at postnatal age 10 (P10) or 21 d (P21) in basal conditions and after a bilirubin perfusion to explore age-related and bilirubin-induced changes in the cerebral permeability to the dye. Blood-to-brain transfer of [3H]bilirubin was measured in 39 brain regions by quantitative autoradiography in 15-min experiments. Rats exposed to unlabeled bilirubin received a loading dose of 160 mg/kg over 15 min followed by a 90-min bilirubin perfusion at a speed of 64 mg/kg/h. At P10, cerebral permeability to bilirubin ranged from 0.07 to 0.12 microL/g/min, except in the auditory nerve, dentate nucleus, hypothalamus, and thalamus where it reached 0.41-0.47 microL/g/min. At P21, Ki of bilirubin was significantly lower than at P10 and ranged from 0.03-0.06 microL/g/min in most brain areas. In P10 bilirubin-exposed rats, permeability to bilirubin significantly increased over control levels in all brain regions but three. The largest increases (> 350%) were recorded in the sensory regions, most limbic areas, hypothalamus, and thalamus. At P21, hyperbilirubinemia induced increases in blood-to-brain transfer of bilirubin of 50-200% in 16 brain areas, except in the hippocampus, sensory-motor cortex, and thalamic nuclei where they reached 200-433%. Thus, it appears that the immature rat brain (P10) is very permeable to bilirubin. The increased permeability with preexposure to the dye, especially in brain regions which are affected in infants with kernicterus, could be related either to the large decrease in the value of the albumin:bilirubin ratio between control (15-16) and hyperbilirubinemic conditions (1.7-1.8) and/or to an increased permeability to bilirubin.

Age Factors↗
PubMed2003

Simultaneous mapping of blood volume and endothelial permeability surface area product in gliomas using iterative analysis of first-pass dynamic contrast enhanced MRI data.

We describe a novel method for the calculation of endothelial permeability surface area product from dynamic contrast enhanced MRI. The technique uses iterative estimation to automatically decompose tissue residue function into intravascular and extravascular components, which are subsequently used to generate tumour blood volume, which is equal to relative cerebral blood volume calculated from T(1) weighted images and corrected for contamination by contrast agent leakage (rCBV(T1)(corrected), and endothelial permeability (k(fp)) maps. The technique was assessed in patients with cerebral glioma (n=5) by examining the reproducibility of endothelial permeability and rCBV(T1)(corrected) between two separate examinations conducted with a 2-day interval. The technique produces maps of endothelial permeability that appear to be free of any contribution from intravascular contrast agent. Maps of rCBV(T1)(corrected) show close correlation with maps of blood volume calculated from independently acquired dynamic susceptibility weighted MRI examinations, with no evidence of residual permeability effects. The results were highly reproducible with strong intra-class correlation between the two examinations for mean values and for 97.5 percentiles of endothelial permeability and rCBV(T1)(corrected). The excellent reproducibility of this technique and the ability to calculate endothelial permeability and rCBV(T1)(corrected) values from rapidly acquired data sets offer considerable advantages over conventional approaches and support the use of this methodology for therapeutic monitoring or trials of novel therapeutic agents.

Aged↗
PubMed1999

[Effects of ventilation and surfactant perturbation on alveolocapillary permeability].

OBJECTIVE: To investigate the effects of large tidal volume ventilation (LTVV) and surfactant dysfunction induced with dioctyl sodium sulphoccinate (DOSS) on alveolocapillary permeability, and on the surface tension of lung tissue extract (LTE). METHODS: The permeability index of tecthnetium-99m labelled human serum albumin (99mTc-HSA) was used to characterize the alveolocapillary permeability after LTVV and surfactant dysfunction permeability index, dynamic respiratory compliance (Cdyn), arterial blood gas (ABG), wet lung weight and surface tension of LTE were measured in four groups of rabbits: (1) controls; (2) LTVV; (3) DOSS; and (4) DOSS + LTVV. RESULTS: Cdyn and ABG were stable throughout the experiment in all groups. The wet lung weight was (1.85 +/- 0.16) g/kg, (2.50 +/- 0.27) g/kg, (1.88 +/- 0.12) g/kg and (2.65 +/- 0.13) g/kg in four groups respectively. It was significantly increased in LTVV and DOSS + LTVV groups compared with controls and DOSS (P < 0.01). The permeability index was 0.10 +/- 0.04, 0.72 +/- 0.14, 0.13 +/- 0.03 and 0.79 +/- 0.17 in four groups respectively. There was a significantly increased permeability index in LTVV and DOSS + LTVV groups compared with controls and DOSS (P < 0.01). There was no difference of surface tension of LTE among all groups. CONCLUSIONS: The results of this study suggest that the increased alveolocapillary permeability, pulmonary edema and lung injury are induced by LTVV rather than DOSS. The mechanisms of HSA transferring alveolocapillary membrane from different directions are different.

Animals↗
PubMed2006

Microvascular and epithelial permeability measurements in laboratory animals.

Disruption of the mucosal permeability barrier is an acute life-threatening consequence of intestinal transplantation. The major aim of organ preservation techniques is to maintain the mucosal barrier and its function. Thus, assessment of microvascular and epithelial permeability is an important tool to determine the efficacy of therapeutic interventions. The use of murine models is particularly advantageous, as numerous immunological approaches (e.g., monoclonal antibodies) and genetically modified animal strains have been developed. Large animal models are also useful because they allow online detection of mucosal permeability changes. In this review, we summarize the available methodologies for measuring microvascular and epithelial permeability in the intestines of laboratory animals. We describe the advantages of various photometric and intravital microscopic methods for the assessment of microvascular permeability. Techniques that determine the inward and outward direction of mucosal permeability changes (including radioenzymatic, fluorimetric, and intravital microscopy methods) are also discussed.

Animals↗
PubMed1984

The effect on dentine permeability of time following cavity preparation in dogs.

Cavities were prepared into the dentine of mandibular first molars of anaesthetized dogs. Conical plastic chambers were cemented into the cavities to permit quantitation of dentine permeability using a fluid-filtration technique. There was a progressive fall in dentine permeability every hour for the 6 h of study, to about 20 per cent of zero time values. The fall in dentine permeability could be delayed but not prevented, by filtering fluid across the dentine into the pulp. Similar experiments on teeth from which the pulps had been removed showed no change or a slight increase in permeability with time. No change in dentine permeability was seen in dogs killed after the zero time measurement and followed for an extra 6 h. This decrease of dentine permeability in response to cavity preparations only occurs in teeth with intact pulps.

Animals↗
PubMed1985

Peritoneal permeability in the rat: modulation by microfilament-active agents.

A model of peritoneal dialysis in the rat was used to determine the effects of cytochalasins on ultrastructure and peritoneal permeability to molecules of varying molecular weight. The permeability to urea, inulin, and plasma albumin were determined after intraperitoneal administration of cytochalasin B (2 to 10 X 10(-6) M) and cytochalasins D and E (2 X 10(-6) M). Cytochalasin B (20 X 10(-6) M) increased the permeability to inulin, urea, and albumin by 30, 60, and 150%, respectively. These effects were, to a large degree, reversible. Cytochalasins D and E produced greater increments in permeability for all molecules; this increase was only partially reversible. Ultrastructure analysis by scanning electron microscopy revealed extensive development of membrane protuberances (zeiotic knobs) on mesothelial cells exposed to cytochalasin B. A return to a normal apical cell surface was apparent although incomplete at 24 hr. Tight junctions were not grossly altered and major changes in intramembranous junctional strands were not observed. The major effect of cytochalasins on the cell surface may be responsible for the increased permeability to urea, predominately a transcellular probe. Inulin, which follows a paracellular route, was less affected. Altered protein permeability may be due to the action of cytochalasin on the exposed capillary endothelium in subdiaphragmatic areas where the mesothelium is discontinuous.

Animals↗
PubMed2001

Effect of eicosapentaenoic acid (EPA) on tight junction permeability in intestinal monolayer cells.

UNLABELLED: The purpose of this study is to evaluate the effect of C18 and C20 long chain fatty acids on tight junction permeability in a model of intestinal epithelium. METHODS: Confluent Caco-2 cells on porous filters with double chamber system were used to measure fluorescein sulfonic acid (FS) permeability and transepithelial electrical resistance (TEER). Lactate dehydrogenase release and ultrastructure were evaluated. Effect of 200 microM eicosapentaenoic acid (EPA, C20:5 n-3), arachidonic acid (AA, C20: 4 n-6), alpha-linoleic acid (ALA, C18: 3 n-3), linoleic acid (LA, C18: 2 n-6), or oleic acid (OA, C18: 1 n-9) enrichment in the culture medium during 24 hours were compared. The effect of the cyclooxygenase inhibitor, indomethacin, lipoxygenase inhibitors, NDGA or AA861, and antioxidant, BHT, was evaluated as a mechanism to change tight junction permeability. RESULTS: Caco-2 cells formed polarized columnar epithelial cells with densely packed microvilli and well developed junctional complexes. Addition of EPA enhanced FS permeability to 3.0+/-1.6-fold and lowered TEER to 0.59+/-1.2-fold vs. control with concentration dependency without cell injury (P<0.01-0.05). OA, AA or LA did not change, but ALA enhanced tight junction permeability. Indomethacin and AA861 normalized the changes mediated by EPA. CONCLUSIONS: EPA affects tight junction permeability in intestinal monolayer cells specifically and concentration dependently via cyclooxygenase and lipoxygenase products.

Caco-2 Cells↗
PubMed2003

Dextran modulates microvascular permeability: effect in isotonic and hypertonic solutions.

Hypertonic saline solutions with Dextran (HSD) have been advocated for rapid restoration of intravascular volume. Dextran is thought to increase the duration of action of hypertonic saline (HS) by selectively partitioning the water in the vascular space that has been drawn out of cells by HS. The goal of this study was to define the microvascular permeability modulating activity of Dextran in both isotonic and hypertonic solutions. We hypothesized that Dextran would decrease hydraulic permeability (Lp). Using the modified Landis micro-occlusion technique, single rat mesenteric venules were perfused with either normal Ringers (NR) with 135 mM NaCl or HS with 185 mM NaCl. In sequential cannulations of the venules, 1%, 2%, and 3% of Dextran was added to the NR perfusion (n = 6) and the HS perfusion (n = 6). The Lp was measured at baseline and after perfusion with each Dextran concentration. Baseline Lp measurements for NR and HS solutions were 1.01 +/- 0.034 and 5.14 +/- 1.02, respectively. In the NR group, the 2% and 3% Dextran decreased permeability below baseline levels to 0.79 +/- 0.028 (P < 0.0001) and 0.66 +/- 0.028 (P < 0.0001), respectively. In the HS group, the 2% and 3% Dextran decreased permeability to 1.65 +/- 0.53 (P < 0.0001) and 0.99 +/- 0.2 (P < 0.0001), respectively. All values for Lp are x10(-7) cm s(-1) x cm H2O(-1). The addition of Dextran to isotonic and hypertonic solutions results in a decrease in microvessel permeability. This effect is more pronounced with the perfusion of hypertonic solutions. The results demonstrate the oncotic potential of Dextran and its ability to hold water in the vascular space. Dextran may have a beneficial effect when used for resuscitation with HS by decreasing microvascular permeability and augmenting intravascular volume.

Animals↗
PubMed1987

Quantitative assessment of the permeability of the rat blood-retinal barrier to small water-soluble non-electrolytes.

1. The passive permeability of the blood-retinal barrier (b.r.b.) to the water-soluble non-electrolytes, sucrose and mannitol, was determined using a multiple time point-graphical approach as has been used in the assessment of blood-brain barrier (b.b.b.) permeability. 2. The calculated permeability surface area product for the b.r.b. for sucrose was 0.44 (+/- 0.081 S.E. of mean) X 10(-5) ml g-1 s-1 (n = 20) and for mannitol was 1.25 (+/- 0.30) X 10(-5) ml g-1 s-1 (n = 18). These values are similar and comparable to those found for the capillaries in the brain (P greater than 0.05) and significantly different from zero (P less than 0.01). 3. Data on the concentrations of sucrose in different parts of the eye show that the permeability of the blood-retinal barrier, rather than the more permeable blood-aqueous barrier permeability, was being measured by our technique.

Animals↗
PubMed1990

Permeability of neutral vs. anionic dextrans in cultured brain microvascular endothelium.

The luminal surface of vascular endothelium contains glycocalyx residues that establish an overall negative charge. Recent evidence has suggested that local endothelial surface charge properties may account for the permeability properties of various macromolecules. It has also been suggested that altered membrane charge on the luminal side may play a role in thrombogenesis and atherogenesis. The relationship of macromolecule charge to endothelial cell permeability was examined in vitro using mouse brain microvessel endothelial cells grown to confluence on a nitrocellulose filter separating a double-chamber system. Endothelial permeability to 4K and 10K fluorescein-labeled neutral dextrans was compared with the permeability to 4K and 10K fluorescein-labeled anionic dextrans (sulfated). After 1 h, there was significantly greater permeability of neutral fluorescein-labeled dextran than of anionic fluorescein-labeled dextran in each particle size. In addition, there was significantly greater permeability of 4K than 10K fluorescein-labeled dextrans of either charge. The findings indicate that charge in addition to size plays an important role in the movement of macromolecules across cultured microvascular endothelial cells.

Animals↗
PubMed1978

Permeability changes in Necturus proximal tubule during volume expansion.

The permeability of Necturus proximal tubule to hydrophilic nonelectrolytes of varying molecular size was studied under control conditions and during isotonic expansion of the animal's extracellular volume. Transepithelial permeability was measured in perfused tubular segments under conditions of zero net water flux. During volume expansion, tubular permeability to urea increased slightly, whereas mannitol decreased slightly and permeability to sucrose was significantly decreased. Volume expansion had a greater effect on osmotic flow parameters; the NaCl reflection coefficient decreased from 0.64 to 0.47 (summer animals) and from 0.41 to 0.27 (winter animals). Osmotic water flux and hydraulic conductivity increased but only in the lumen-to-capillary direction. Reflection coefficients of nonelectrolytes measured at the apical surface were reduced during volume expansion for probing molecules greater than 3 A in radius and were unchanged for smaller molecules, less than 3 A, suggesting two pore populations. We propose that an increase in tight-junction permeability can account for modification of osmotic flow parameters, whereas the whole thickness of the epithelium, particularly the intercellular space, plays the dominant role in regulation of diffusional permeability.

Animals↗
PubMed1992

Cyclooxygenase inhibition prevents PMA-induced increase in pulmonary vascular permeability to albumin.

In a previous study, we demonstrated that phorbol myristate acetate-(PMA) induced injury in isolated blood-perfused rabbit lungs was characterized by increased pulmonary vascular resistance (PVR) and permeability to water as measured by fluid filtration coefficient (Kf). The Kf increase was prevented by pretreatment with three cyclooxygenase inhibitors, indomethacin, ibuprofen, and meclofenamate. Other studies have shown that PMA causes a decrease in pulmonary vascular surface area, probably due to the increase in arterial resistance. Measurement of Kf requires increased microvascular pressure, and therefore Kf estimates the permeability of the entire vascular bed. Thus the permeability of the flowing vessels may be overestimated by Kf. In this study, we chose to investigate the effect of PMA on vascular permeability to protein by measuring albumin leak. Because this measurement does not require a hydraulic stress, it is more likely to reflect the permeability of flowing vessels. PMA administration (5 x 10(-8) M) caused significant increases in both PVR and 125I-labeled bovine serum albumin leak. Cyclooxygenase inhibition with indomethacin, ibuprofen, or meclofenamate prevented the PMA-induced increase in albumin leak without affecting the PVR increase. These results suggest that cyclooxygenase-mediated products of arachidonic acid mediate the PMA-induced increase in vascular permeability to both water and protein.

Albumins↗
PubMed1979

Alveolar-capillary membrane permeability. Correlation with functional, radiographic, and postmortem changes after fluid aspiration.

An index of permeability of the alveolar-capillary membrane was derived from the relative extraction from the lung into arterial blood of 2 tracers, 125I-antipyrine and 51Cr-ethylenediaminetetraacetate. The effect on this index of aspirating 2 ml of isotonic saline, distilled water, or 10(-1) M hydrochloric acid per kg of body weight was studied in 3 groups of rabbits. The severity and time course of changes in the permeability index were correlated with changes in lung mechanics, gas exchange, serial chest roentgenograms, ratio of extravascular lung water to dry weight, and histologic findings. Aspiration of saline produced no change in the permeability index; aspiration of water produced a large mean +/- SEM increase in the index, from a baseline of 0.025 +/- 0.002 to 1,050 +/- 0.054 (P less than 0.001), but this value returned to baseline 15 min later. After hydrochloric acid, the permeability index increased from a baseline of 0.027 +/- 0.003 to 1.068 +/- 0.098 (P less than 0.005), with no evidence of resolution after 60 min. Changes in lung mechanics, gas exchange, and roentgenograms were smallest after aspiration of distilled water and greatest after aspiration of hydrochloric acid. The functional changes after aspiration of water and saline recovered at a rate proportional to the known clearance rates of these liquids from the lung. The changes after hydrochloric acid either showed no tendency toward recovery or, in the case of the roentgenograms, worsened with time. There were no detectable histologic abnormalities or an increase in the ratio of extravascular lung water to dry weight after aspiration of water or saline, but there were extensive histologic abnormalities and a 70 per cent increase in lung water after acid. The increase in the permeability index after aspiration of water was too transient to exert a deleterious effect. In contrast, the persistence of the increase in the permeability index after hydrochloric acid was associated with persistent functional changes attributable to the considerable increase in lung water.

Animals↗
PubMed1992

Glycation of albumin, not glomerular basement membrane, alters permeability in an in vitro model.

The effects of glycation of either albumin, a plasma protein, or GBM were examined in an in vitro model of GBM permeability. Albumin was incubated with glucose in vitro, and nonglycated and glycated albumin were separated by affinity chromatography. Rat GBM was glycated either in vivo after the induction of diabetes or in vitro after incubation with 25 mM glucose. 150 micrograms of GBM was consolidated in an ultrafiltration cell, and albumin permeability across the GBM filter was assessed at an applied pressure (50 mmHg) selected to approximate glomerular capillary pressure in vivo. The sieving coefficient of glycated albumin was greater than the sieving coefficient of nonglycated albumin (0.25 +/- 0.03 vs. 0.10 +/- 0.02; P < 0.05). GBM glycated in vivo in diabetic rats exhibited native albumin and water permeability that was indistinguishable from that for GBM from control rats. Similarly, GBM glycated in vitro by incubation with 25 mM glucose exhibited water and albumin permeability identical to that for GBM incubated in buffer. Thus, the glycation of albumin, but not of GBM, leads to enhanced permeability in an in vitro GBM filtration system. Increased permeability of glycated albumin may contribute to albuminuria and/or renal injury in states of increased circulating glycated albumin such as diabetes and experimental galactosemia.

Animals↗
PubMed1990

[The effect of procyanidolic oligomers on vascular permeability. A study using quantitative morphology].

In normal conditions vascular permeability is precisely regulated by mechanisms which involve among others the macromolecules of extracellular matrix of the vascular wall. Permeability for a given substance will vary according to the anatomical localisation of the vessel determining also its structure and composition. In some pathological conditions, such as inflammation or diabetes, permeability can be abnormally increased. Increased permeability can be reproduced by i.v. collagenase injection. This permeability increase can be quantified by image analysis using appropriate tracers such as FITC-dextrans or horse-radish peroxidase, on histological sections from control and collagenase treated rats, pretreated or not with procyanidolic oligomers (PCO). We studied cerebral capillaries, aorta and cardiac muscle capillaries. It could be shown that previous treatment of animals with procyanidolic oligomers prevented the permeability increase produced by collagenase injection.

Animals↗