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PubMed1985

Differential permeability of pineal capillaries to lanthanum ion in the rat (Rattus norvegicus), gerbil (Meriones unguiculatus) and golden hamster (Mesocricetus auratus).

Capillaries in the pineal gland of the rat (Rattus norvegicus), gerbil (Meriones unguiculatus) and golden hamster (Mesocricetus auratus) were investigated by means of electron-microscopical tracer studies using lanthanum. The tracer was administered together with the fixative solution by perfusion via the left cardiac ventricle. In the rat, endothelial junctions of fenestrated capillaries are permeable to lanthanum. In the gerbil the tracer does not leave the capillaries, which are of the non-fenestrated type throughout the organ. In the golden hamster the two portions of the pineal system have different types of capillaries. While in the superficial pineal fenestrated capillaries permeable to lanthanum predominate, the deep pineal possesses capillaries that are, without exception, devoid of fenestrations and impermeable to the tracer. It is suggested that differences in the structure of the capillaries are related to differences in the extent of a specialized contact of the pineal gland to the third ventricle.

Animals↗
PubMed1996

Vascular permeability in the peripheral autonomic and somatic nervous systems: controversial aspects and comparisons with the blood-brain barrier.

Endothelium, choroidal epithelium, and arachnoid exclude plasma proteins from most parts of the mammalian central nervous system (CNS). Nerve roots, in contrast, have permeable capillaries and permeable pia-arachnoid sheaths. Diffusion of plasma proteins into the cerebrospinal fluid is probably prevented by slow bulk flow along a pressure gradient from the subarachnoid space into the veins of the roots. In nerves, the perineurium prevents diffusion of proteins from the epineurium into the endoneurium. Capillaries within fascicles are permeable to macromolecules, though less so than the microvessels of roots and ganglia. Endoneurial vascular permeability is lowest in rats and mice, but even in these species albumin is normally present in the extracellular spaces around the nerve fibers. The so-called blood-nerve barrier is not equivalent to the blood-brain barrier. Capillaries in sensory and sympathetic ganglia are fully permeable to macromolecules, and extravasated protein is in contact with neuronal cell bodies and neurites. An impenetrable perineurium surrounds each ganglion, but serves no obvious purpose when the vessels inside are as permeable as those outside. The enteric nervous system lacks a perineurium, and the neurons in its avascular ganglia and tracts are exposed to extracellular fluid formed by permeable vessels in adjacent tissues of the gut. The reasons for excluding macromolecules from some parts of the nervous system are obscure. Carrier-mediated transport, which maintains a constant supply of ions, glucose, and other metabolites to cells in the CNS, would be impossible if larger molecules could diffuse freely. Presumably the metabolic needs of ganglia are adequately met by exchange vessels similar to those of nonnervous tissues. Most of the CNS is protected from exogenous toxic substances that bind to plasma proteins. Peripheral neurons and glial cells are damaged by some such substances because of the lack of blood-tissue barriers.

Animals↗
PubMed1997

Neutral proteases and disruption of the blood-brain barrier in rat.

Blood-brain barrier disruption is common in many neurological diseases. Matrix metalloproteinases are induced in brain injury and increase capillary permeability by attacking the extracellular matrix around cerebral capillaries. Other neutral proteases are also increased in sites of secondary injury, and may contribute to the proteolysis of the blood-brain barrier. Therefore, we studied capillary permeability and histological tissue damage after intracerebral injection of neutrophil elastase, cathepsin G, heparatinase and plasmin. Adult rats were injected intracerebrally with an enzyme. After 1, 4 or 24 h, measurements were made of brain uptake of a radiolabeled tracer, [14C]sucrose. Enzymes that significantly increased capillary permeability were injected into other rats for histological assessment of tissue damage. Elastase increased capillary permeability significantly when compared with controls; maximal damage was seen at 4 h. Plasmin produced smaller increases in permeability at 4 h, exerting its maximal effect on sucrose uptake at 24 h. Cathepsin G had a small effect at 4 h. Heparitinase had no effect. Histologic examination of elastase-injected brains at 24 h revealed multifocal perivascular and intraparenchymal acute hemorrhages accompanied by a polymorphonuclear cell infiltrate. Elastase-injected brains were microscopically similar to saline-injected brains at 1 and 4 h. Plasmin produced fibrinoid changes in the blood vessels at 24 h, coinciding with the maximal increase in capillary permeability. We conclude that neutrophil elastase attacks the capillary extracellular matrix, causing extensive hemorrhage, while plasmin leads to increased vascular permeability and fibrinoid necrosis of blood vessel walls. Differential effects of neutral proteases released secondary to injury could be important in both the acute changes in blood vessel permeability and long-term alterations in vessel structure.

Animals↗
PubMed1985

Capillary permeability-increasing enzyme from the venom of Agkistrodon caliginosus (kankoku-mamushi): activity due to the release of peptide material from a protein in bovine plasma.

When a mixture of the purified capillary permeability-increasing enzyme from A. caliginosus venom and bovine plasma or heated bovine plasma was injected into the depilated skin of the back of a rabbit, the capillary permeability-increasing activity was much greater than that induced by injection of the enzyme alone. The substance which increases capillary permeability was extracted from the incubated mixture of bovine plasma and enzyme with 50-70% ethanol. Its activity was lost when treated with carboxypeptidase A. Thus, it is supposed that the increase in capillary permeability induced by the enzyme is due to a low molecular weight peptide released from a protein in bovine plasma by the action of the enzyme. No liberation by the enzyme of histamine or anaphylatoxins of the complement system was found.

Animals↗
PubMed2000

Vascular hyperpermeability in nephrotic edema.

BACKGROUND/AIM: There is increasing evidence that hypoalbuminemia and the inability of the renal distal tubule to excrete salt are not the only factors responsible for nephrotic edema. We tested the possibility that vascular hyperpermeability also plays a role in the pathophysiology of nephrotic edema in human primary glomerulonephritis. METHODS: We investigated the capillary permeability by means of a standardized test using albumin labelled with technetium (99mTc-albumin) in 20 healthy adults and in 101 nephrotic adult patients comprising 60 patients with idiopathic nephrotic syndrome (INS; minimal-change nephropathy and segmental glomerulosclerosis), 32 with idiopathic membranous nephropathy (IMN) and 9 patients with idiopathic type I membranoproliferative glomerulonephritis (MPGN). The patients and healthy controls were also compared with a group of women (n = 25) with idiopathic cyclic edema, a disease in which an increase in capillary permeability plays a pivotal role. The capillary permeability measured by the Landis isotope test is normal in edematous patients with cardiac and renal impairment unrelated to glomerular disease, cirrhosis, hypothyroidism, lymphatic obstruction and diuretic abuse. As values were not normally distributed, nonparametric analysis of variance was used (Kruskal-Wallis test), and patient groups were compared with healthy controls and with women with idiopathic cyclic edema by means of the two-tailed nonparametric Mann-Whitney test. The effects of high-dose steroids and Ginkgo biloba extract (Tanakan); an agent able to improve capillary permeability) were analyzed by means of the two-tailed nonparametric Wilcoxon test. RESULTS: The capillary permeability was significantly increased (Mann-Whitney test) in each glomerular disease group compared with the healthy controls. 99mTc-albumin extravasation values (%; median and range in parentheses were the following: healthy controls 0 (0-8.4); idiopathic cyclic edema patients 11.5 (8-24), p < 0.001; INS 20 (0-50), p < 0.0001; IMN 12.5 (0-40), p < 0.001, and MPGN 10 (0-40), p < 0.05. An increase in capillary permeability exceeding the upper limit of control values (>8% of 99mTc-albumin extravasation) was observed in 88% of INS, in 53% of IMN and in 44% of MPGN patients. The increase in capillary permeability (%) was greater in idiopathic nephrotic patients than in idiopathic cyclic edema patients (p < 0. 005, Mann-Whitney test) and was markedly reduced in nephrotic patients receiving high-dose steroids (n = 8) [before 25 (8-40); after 0 (0-25), p < 0.005 (Wilcoxon's test)] and high doses of G. biloba extract (n = 16) [before 30 (8-50); after 2.5 (0-20, p < 0. 0005 (Wilcoxon's test)]. CONCLUSIONS: We conclude that capillary permeability is severely altered in most of the nephrotic patients with primary glomerulonephritis. These results strongly suggest that the capillary hyperpermeability plays a role in the pathophysiology of nephrotic edema in primary glomerular disease, especially in INS. We postulate that this widespread abnormality in capillary permeability is related to the release of vascular permeability factor and other cytokines by immune cells.

Adolescent↗
PubMed1992

Vasogenic brain edema induced by arachidonic acid: role of extracellular arachidonic acid in blood-brain barrier dysfunction.

The effects of free arachidonic acid on the capillary permeability of normal rat brains were studied by measuring the regional uptake of [14C]aminoisobutyric acid by a quantitative autoradiographic technique. Intracerebral infusion of sodium arachidonate increased capillary permeability in a dose-dependent manner up to a concentration of 2 mmol/L. A high dose of arachidonic acid (more than 5 mmol/L) produced marked tissue destruction around the injection site (needle track) and increased capillary permeability less than 2 mmol/L arachidonic acid did. A time-course study demonstrated that about 80% of the maximum increase in capillary permeability produced by arachidonic acid was observed within 2 hours after the infusion was initiated. In addition, capillary permeability gradually increased with time up to 24 hours, after which it declined to about half of the maximum increase 48 hours after infusion. These effects of arachidonic acid on capillary permeability were localized within about 1.6 mm around the injection site. Pretreatment with dexamethasone did not completely, but did significantly, inhibit the arachidonic acid-induced increase in capillary permeability. The inhibitory effect of dexamethasone was completely suppressed by the administration of actinomycin D, which inhibits de novo protein synthesis, 1 hour before the treatment with dexamethasone. These results suggest that arachidonic acid, which is released and accumulated in the extracellular space, increases the capillary permeability of the brain in at least two different ways. One is the direct action of the arachidonic acid itself, which can stimulate perturbation of the membrane of the capillary endothelial cells, thus promoting an increase in capillary permeability.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Vascular perfusability and capillary macromolecular permeability in the mechanically induced rabbit hydrosalpinx.

The mechanically induced rabbit hydrosalpinx, a frequently studied animal model of human hydrosalpinges, was examined to determine the variations, in vascular perfusion and capillary albumin permeability, which occur in hydrosalpinges. At laparotomy, 4 adult female virgin rabbits underwent isthmic and ampullary occlusion with small tantalum clips. 4 weeks later, fluorescein isothiocyanate-labelled bovine serum albumin (FITC BSA: molecular weight 67,000) was injected intravenously 5 min before oviduct excision. Examination of tubal sections by incident light fluorescent microscopy demonstrated poor interplical vascular perfusability and markedly reduced interplical capillary permeability to FITC BSA in both isthmic and ampullary segments of hydrosalpinx. These observations imply that, in the experimental rabbit hydrosalpinx, interplical deciliation is probably vascular in origin; furthermore the marked decrease in capillary macromolecule permeability may explain the serous fluid collection within the hydrosalpinx. Poor fecundity following microsurgical restoration of tubal patency in hydrosalpinges is possibly due to the failure of this decrease in submucosal capillary perfusability and macromolecular permeability to resolve.

Animals↗
PubMed2000

Effects on capillary fluid permeability and fluid exchange of albumin, dextran, gelatin, and hydroxyethyl starch in cat skeletal muscle.

OBJECTIVE: To evaluate the peripheral hemodynamic effects in a skeletal muscle in vivo model of the four commercially available colloid solutions, 20% human albumin, 6% dextran-70, 6% hydroxyethyl starch 200/0.5 (HES), and 3.5% urea-linked gelatin. DESIGN: Controlled laboratory study. SETTING: University research laboratory. SUBJECTS: Fifteen adult cats. INTERVENTIONS: The isolated, autoperfused, and denervated calf muscles of the cat hindlimb were placed in a plethysmograph. The colloids tested were given intra-arterially to the muscles in increasing rates of clinically relevant doses. MEASUREMENTS AND MAIN RESULTS: Arterial blood flow, arterial and venous blood pressures, total vascular resistance, tissue volume changes, and capillary filtration coefficient were measured before, during, and after the colloid infusions. The altered capillary filtration coefficient reflects a change in capillary fluid permeability. The capillary filtration coefficient was decreased by albumin and dextran, not affected by HES, and increased by urea-linked gelatin. Albumin induced transcapillary fluid absorption, gelatin induced transcapillary filtration, and no transcapillary fluid exchange was observed with dextran and HES. After discontinuation of the infusions, HES and gelatin induced a rebound transcapillary filtration. No such effect was seen after dextran and albumin. All colloids increased muscle blood flow. CONCLUSION: We conclude that capillary fluid permeability is decreased by albumin and dextran, unchanged by HES, and increased by gelatin. This and the differences in the rebound effect may contribute to the differences in the plasma volume expanding properties of the respective colloid. The increased blood flow induced by the colloids was more an effect of reduced vascular tone than of lowered blood viscosity.

Albumins↗
PubMed1980

Role of complement activation in a model of adult respiratory distress syndrome.

The adult respiratory distress syndrome is characterized by arterial hypoxemia as a result of increased alveolar capillary permeability to serum proteins in the setting of normal capillary hydrostatic pressures. Because bacterial sepsis is prominent among the various diverse conditions associated with altered alveolar capillary permeability, we studied the effect of bacteremia with attendant complement activation on the sequestration of microorganisms and the leakage of albumin in the lungs of guinea pigs. Pneumococci were injected intravenously into guinea pigs and their localization was studied. Unlike normal guinea pigs, complement-depleted guinea pigs did not localize injected bacteria to the lungs. Preopsonization of organisms did not correct this defect in pulmonary localization of bacteria in complement-depleted animals, suggesting that a fluid-phase component of complement activation was required. Genetically C5-deficient mice showed no pulmonary localization of bacteria. C5-sufficient mice demonstrated the usual pulmonary localization, thus further suggesting that the activation of C5 might be important in this localization. The infusion of activated C5 increased alveolar capillary permeability to serum proteins as assayed by the amount of radioactive albumin sequestered in the lung. Neutropenic animals did not develop altered capillary permeability after challenge with activated C5. Thus, complement activation through C5, in the presence of neutrophils, induces alterations in pulmonary alveolar capillary permeability and causes localization of bacteria to the pulmonary parenchyma. Complement activation in other disease states could potentially result in similar clinical manifestations.

Capillary Permeability↗
PubMed1980

Role of hyaluronidase in immediate hypersensitivity reaction.

Hyaluronidase (Hydase) activity in 48-hr homologous passive cutaneous anaphylaxis (PCA) increased about one and one-half times the control for 5 min after challenge with antigen, then gradually decreased and disappeared after 30 min. Change in Hydase activity correlated well with the increase in capillary permeability by PCA. DSCG and BPS given intravenously 10 min prior to challenge produced increases in capillary permeability and Hydase activity caused by PCA was inhibited. Chlorpheniramine inhibited the increase of the capillary permeability, but not the acceleration of Hydase. Prednisolone neither affected the capillary permeability nor the Hydase activity. Similar results were also obtained in in vitro studies. An increase in the capillary permeability caused by PCA, histamine, or 5-HT was additionally augmented by Hydase. Thus, Hydase appears to be involved in the increase in the capillary permeability caused by an immediate hypersensitivity reaction.

Animals↗
PubMedDate not supplied

Extended theory of the early diffusion of multiple indicators: bounds on permeability ratios, with applications to intestinal capillaries.

The determination of ratios of capillary permeabilities to multiple indicators is secured by constructing upper bounds on effects of early back-diffusion following a single arterial injection. The analysis does not exclude highly extracted indicators, and it allows for effects of asymmetric blood-tissue exchange and of tissue concentration gradients. The concept of flow limitation of uptake is delimited operationally. It is shown how to identify effects of heterogeneity of uptake for data sets extended over large ranges of rate of blood flow. These new methods are used to show, for several sets of previously published data from muscle, that back-diffusion cannot change appreciably the permeability ratios determined previously without any quantification of back-diffusion. The main application is to data published by Perry and Granger (1981) on the permeability of cat intestinal capillaries to raffinose and inulin. The permeability ratios deduced from these data imply paradoxically restricted diffusion; it is shown that this cannot be attributed to effects of back-diffusion, heterogeneity of extraction, or of solvent drag. It is shown that the paradox is removed if tissue-to-blood permeability to raffinose is at least double the blood-to-tissue permeability, possibly as part of the active transport of sugars from the intestinal lumen. It is shown that corresponding results on permeability ratios in dog gastric capillaries are not paradoxical (against the standard of unrestricted diffusion) under symmetric permeability to raffinose.

Animals↗
PubMed1982

The effect of intravenous steroids on alveolar-capillary membrane permeability in pulmonary acid injury.

The treatment of pulmonary aspiration of gastric contents remains largely empirical. The purpose of the present study was to evaluate the effect of methylprednisolone administration (30 mg/kg) on alveolar-capillary membrane permeability after pulmonary acid aspiration in dogs. Alveolar-capillary membrane permeability was assessed by several methods. Extravascular lung water volume (EVLW), extravasation of 125I-serum albumin (RISA) into lung parenchyma, and albumin leak into the alveolar spaces were measured. EVLW increased progressively from 5.5 +/- 0.6 to 20.0 +/- 2.3 ml/kg in Group I (Acid) and from 5.4 +/- 1.2 to 22.1 +/- 3.1 ml/kg in Group II (Acid + Steroids) over the 5 hours after acid injury. The ratio of Lung Extravascular RISA to Plasma RISA was 0.56 +/- 0.14 and 0.58 +/- 0.14 in Group I and Group II, respectively (normal = 0.19 +/- 0.06). The tracheal albumin to plasma albumin ratio remained near 1.0 from 2 hours to 5 hours post-aspiration in both groups. This study demonstrated that pulmonary acid injury resulted in a marked increase in alveolar-capillary permeability to albumin, smaller solutes, and water which was not ameliorated by the administration of methylprednisolone.

Adrenal Cortex Hormones↗
PubMed2002

Analysis and characterization of relative permeability and capillary pressure for free surface flow of a viscous fluid across an array of aligned cylindrical fibers.

In LCM processes of fiber-reinforced composite manufacturing, resin is injected into a closed mold with a preplaced stationary fiber preform. If these preforms are created from fiber tows, resin progression at the microlevel during infiltration is often non-uniform. Consequently, macroscopic description of the filling phase requires a theory of flow through unsaturated porous media in which the transition (partly saturated) region must be taken into account. Unsaturated flows must consider surface tension effects; therefore, capillary pressure and relative permeability must be included in governing equations. This paper presents a methodology to determine relative permeability and macroscopic capillary pressure for simple flows. The results lead to important conclusions and the methodology can be generalized to other flow fields.

Journal Article↗
PubMed2000

Pharmacologic aspects of a phlebotropic drug in CVI-associated edema.

Several phlebotropic drugs, or edema-protecting drugs, are available, the most important of which are found in the gamma-benzopyrone family (flavonoids). gamma-Benzopyrones can be plant extracts, semisynthetic preparations, or synthetic preparations. This family is divided into two different groups: flavones and flavonols, and flavanes (flavanones). The flavone group contains various types of molecule and includes diosmin. Here we discuss the pharmacologic aspects in edema associated with chronic venous insufficiency (CVI) of one of the reference phlebotropic drugs, micronized purified flavonoid fraction (MPFF), a semisynthetic preparation from the diosmin group, which represents the latest improvement in flavonoid formulation. Before we detail the pharmacologic aspects, a brief summary of the pathophysiology of edema in CVI is necessary. Several factors are implicated: the veins, which create the conditions favorable to edema; the microcirculation, which is the site of fluid transfer into the interstitial tissue; and the lymphatics, which have a limited possibility to reduce edema. Major discoveries are currently being made in CVI and the microcirculation. Results of studies show that MPFF decreases capillary permeability and increases capillary resistance, which could partly be explained by inhibition of leukocyte activation, migration, and adhesion. This inhibition is linked to a significant decrease in plasma levels of endothelial adhesion molecules (VCAM-1 and ICAM-1) after MPFF treatment. Thus, the CVI-induced damage to the microcirculation is counteracted by MPFF. The lymphatic system is also improved by MPFF treatment. The lymphagogue activity of MPFF has been demonstrated in experimental animal models and confirmed by microlymphographic measurement in patients suffering from severe CVI. The pharmacologic activity of MPFF in lymphedema was observed in a study using an animal model of acute lymphedema and in a study in patients with upper limb lymphedema secondary to breast cancer treatment. All these findings point to the importance of acting on each factor involved in the formation and maintenance of edema. This pharmacologic activity is indeed reflected by the clinical efficacy on edema observed during treatment with MPFF.

Animals↗