Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Capillary Permeability”

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

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

At least 1,459 records · Page 81Linked to original sources
PubMed1991

Greater permeability of the neonatal lung. Postnatal changes in surface charge and biochemistry of porcine pulmonary capillary endothelium.

Capillary permeability is partly determined by the distribution of anionic charge on the endothelial cell membrane and organelles and on the biochemical composition of these structures. Therefore the pulmonary capillaries of 18 Large White pigs aged less than 10 minutes, 1 week, and 6 months (six animals at each age) were perfused with cationized ferritin and the peroxidase conjugated lectins Dolichos bifloris, concanavalin A, Triticum vulgaris, and Ricinus communis type 2. Lectins bind to the carbohydrate cell surface antigen for which each shows monosaccharide specificity. The ultrastructural localization of each substance on the capillary endothelial cell was studied, and the length of labeled cell membrane was measured. The proportion of intracellular vesicles containing cationized ferritin was also determined. Binding of cationized ferritin to cell membrane and the number of cationized ferritin-labeled vesicles decreased between birth and 1 week (p less than 0.01 for both). Binding of lectins Triticum vulgaris and Dolichos bifloris decreased between birth and 1 week (p less than 0.01 for both) and between 1 week and adulthood (p less than 0.01 for Dolichos bifloris). Binding of concanavalin A and Ricinus communis type 2 showed a nonsignificant increase with age. Thus the area of pulmonary endothelial cell membrane and the proportion of vesicles with a negative charge decreased after birth, and the distribution of cell surface glycoconjugates also changed. Because these microdomains form differentiated pathways that help control transcellular movement of water and solutes, the findings help explain the greater permeability of the newborn lung.

Animals↗
PubMed1995

Healthy lungs tolerate repetitive collapse and reopening during short periods of mechanical ventilation.

The possible occurrence of lung damage if alveolar units are allowed to collapse and reopen breath by breath during mechanical ventilation with normal tidal volumes was investigated. Anaesthetised, paralysed, open chest rabbits were subjected to either intrathoracic negative (NEEP; n = 6) or positive (PEEP; n = 6) end-expiratory pressure during volume controlled mechanical ventilation. Both experimental settings were preceded by a 30 min control period and followed by a 30 min recovery period during which a PEEP of 0.2 kPa was maintained. Pao2 and pulmonary compliance deteriorated significantly in the NEEP group during the experimental period and compared to ventilation with PEEP. Partial restoration of lung mechanics and blood gases was achieved during the recovery period. After an alveolar recruitment manoeuvre, this recovery was complete. Lung clearance studied by depositing an aerosol of technetium-99m-labelled diethylenetriamine pentaacetate (99mTc-DTPA) in the alveoli, was significantly faster during ventilation with NEEP compared to the PEEP group (P = 0.0002) as well as the control period (P = 0.0029). It did not recover completely during the recovery period but remained significantly faster. Light microscopic histology was normal in both groups with no evidence of inflammation or epithelial disruption. We conclude that previously healthy rabbit lungs show only a transient disturbance of lung mechanics and blood gases with repetitive collapse and re-expansion. The integrity of the alveolar microstructure is preserved. The disturbance in the alveolo-capillary permeability persists and may indicate surfactant related alveolo-capillary barrier dysfunction.

Animals↗
PubMed1979

Experimental retinal branch vein occlusion in rhesus monkeys. III. Histopathological and electron microscopical studies.

Experimental retinal vein occlusion in monkeys was followed by an immediate increase in capillary permeability which was accompanied by retinal oedema. This functional capillary change was followed at about 6 hours after occlusion by structural damage to the capillary wall. Thrombus formation occurred in the damaged vessels, and areas of stasis were thus produced with associated retinal haemorrhages. Finally, there was complete loss of the capillary endothelium and pericytes, and the acellular capillaries were invaded by proliferating glial cell processes, so producing permanent capillary closure.

Animals↗
PubMed2003

Arteriovenous pairing: a determinant of capillary exchange.

Venuloarteriolar signaling helps mediate microvascular function and dysfunction. Mediators produced at venular sites of inflammation appear to constrict arterioles and increase capillary permeability. In contrast, venules beneficially dilate arterioles to enhance capillary flow according to metabolic demand. These mechanisms are altered with cardiovascular risk factors, contributing to microvascular complications.

Animals↗
PubMed1977

Nephron function and perinatal homeostasis.

A) The proximal nephron and perinatal regulation of extracellular volume. 1. The glomerular capillary permeability coefficient (Kf) changes mainly because of an increasing capillary hydraulic conductance (Lp) within the autoregulatory range of renal perfusion pressure. 2. Proximal tubule hydrostatic hydraulic conductance and response to transmural protein concentration gradients is high during perinatal adaptation. 3. Proximal tubule paracellular shunt pathways are more important for absorption during differentiation than at maturity. 4. Basolateral membrane area of the single epithelial segment (10(-6) micron2 mm-1) increases and the typical basal labyrinth architecture develops. 5. The activity of the transport enzyme Na-K-ATPase increases in parallel to the basolateral membrane area to result in a constant number of enzyme sites during normal ontogeny. B) The distal nephron and perinatal regulation of extracellular osmotic activity. 6. Inner medullary urea content increases at osmotic equilibrium between interstitium and collecting duct. 7. The loop of Henle gradually dilutes the isotonic luminal fluid in the course of perinatal differentiation. 8. The thick ascending segment of the loop of Henle differentiates its anisotonic transport by increasing the Na-Chloride transport at constant hydraulic conductivity. 9. Ultrastructure and N-A-K-ATPase activity of the diluting segment (TAL) change greatly during ontogeny. 10. The centrifugal pattern of renal maturation from the juxtamedullary towards the superficial cortical layers leads to an intracortical profile of structure and function.

Adenosine Triphosphatases↗
PubMed1992

Circumventricular organ capillaries.

Most circumventricular organs (CVOs) have unusually dense and permeable capillary networks that facilitate secretion of or tissue penetration by circulating substances, unlike other nervous system structures wherein blood-brain barrier (BBB) properties of the capillary endothelium limit solute permeability. In this brief review, I shall discuss new facts from recent experiments, and draw on interpretations from previous studies, to illustrate how capillary systems vary both between and within some CVOs, how closely microvascular properties coincide topographically with the distribution and density of neuropil, transmitter substances and hormonal binding sites, and how physiological data can be combined with morphological descriptions of capillary beds to accent specialized processes of blood-brain solute exchange in individual CVOs. The emphasis of this paper is on exchange microvessels of the rat area postrema (AP), subfornical organ (SFO) and median eminence (ME) which are regions of dense binding for several hormones and contain appreciable numbers of neurons (AP and SFO) or neural terminations that may be part of the sensing apparatus for humoral messengers of homeostatic systems. The work is intended to highlight established concepts about the process of blood monitoring by CVOs, summarize new morphological and physiological characteristics of their capillaries, and provide clues to novel research that could foster further understanding of these curious sentinel and secretory organs of the brain.

Animals↗
PubMed1996

[Threshold values of colloid-osmotic pressure, serum albumin or protein during perioperative period].

The water flux across the capillary membrane is directly related to a gradient of hydrostatic and colloid osmotic forces. The membrane is not an absolute barrier to proteins. Any change in the capillary permeability tends to decrease the plasmatic colloid osmotic pressure. The interstitial space includes a perimicrovascular space and a compliant connective tissue space, where oedema accumulates. The lymphatics may easily drain excess filtration, but cannot clear constituted oedema. Primarily, the risk of pulmonary oedema determines the lower limit of the colloid osmotic pressure. During the perioperative period, any extrapolation of the colloid, osmotic pressure from protidaemia or albuminaemia would be approximate. Two major conclusions can be drawn from the results of Guyton and Lindsey. First, in the absence of left ventricular failure, a 50% decrease in colloid osmotic pressure does not increase extravascular lung water. Second, in the case of left ventricular failure, when the left atrial pressure exceeds 10 mmHg, a 50% decrease in colloid osmotic pressure significantly increases the risk of pulmonary oedema. In these experiments, an impairment in capillary membrane permeability is likely. As a result, the threshold at which extravascular water starts to accumulate cannot be precisely defined. However, in the perioperative period, capillary membrane permeability is frequently altered by the acute phase reaction. Finally, in most perioperative clinical situations, a 50% decrease in colloid osmotic pressure may not require any treatment.

Blood Proteins↗
PubMed2004

[Role of p38 mitogen-activated protein kinase signal transduction pathway in the acute lung injury of severely burned rats].

OBJECTIVE: To investigate the role of p38 mitogen-activated protein kinase (MAPK) signal transduction pathway in the acute lung injury of severely burned rats. METHODS: Forty-eight adult healthy rats were randomly divided into three groups: sham group, burn control group, and burn + SB203580 group. A third-degree burns over 30% total body surface area rat model was used and pulmonary capillary permeability, lung water content, pulmonary histology and p38 MAPK activity were measured at 24 hours postburn. RESULTS: Burn trauma resulted in increased pulmonary capillary leakage permeability (42.5 +/- 4.7 vs. 12.1 +/- 1.4, P < 0.01), elevated lung water content (P < 0.05), and worsen histologic condition. There was a significant activation of p38 MAPK at 24 hours postburn compared with control. SB203580 inhibited the activation of p38 MAPK, reduced the pulmonary capillary leakage permeability (24.7 +/- 2.9 vs. 42.5 +/- 4.7, P < 0.01), decreased lung water content, and prevented burn-mediated lung injury. CONCLUSION: The activation of p38 MAPK is one important aspect of the signaling event that contributes to burn-induced lung injury.

Animals↗
PubMed2001

Vascular localization of heparan sulfate proteoglycans in retinas of patients with diabetes mellitus and in VEGF-induced retinopathy using domain-specific antibodies.

PURPOSE: The Steno hypothesis (Deckert et al. ) states that in diabetes mellitus (DM), changes in vascular heparan sulfate proteoglycan (HSPG) expression are involved in systemic endothelial dysfunction and increased capillary permeability. In diabetes-induced glomerular capillary leakage, loss of HSPG and its side chains has been documented. This study aimed to investigate whether microvascular leakage in diabetic retinopathy (DR) is also associated with altered expression of HSPG in retinal microvessels. METHODS: Serial cryosections of post-mortem eyes of 22 subjects with DM and 7 controls were stained with antibodies against the core proteins of the basement membrane HSPGs agrin (Abs Bl31 and JM72) and perlecan (Ab 1948), and four antibodies against heparan sulfate side chains (HS) (Abs JM403, HepSS1, JM13, 3G10). Moreover, we investigated Cynomolgus monkey eyes injected with vascular endothelial growth factor (VEGF)-A, as a model of retinal microvas-cular leakage. The endothelial antigen PAL-E was used to detect microvascular leakage. RESULTS: In the retina of all controls and DM cases, agrin and perlecan core proteins and HS as recognized by JM403 and 3G10 were expressed in the walls of microvessels. Staining for JM13 was variable between cases, but unrelated to microvascular leakage as determined by PAL-E. Staining for HepSS1 was absent in all human retinal microvessels. In monkey retinas, HSPG staining was identical to that in human retinal tissues, except for the staining for HepSS1, which was found absent in control monkey eyes but which was positive in VEGF-injected eyes. CONCLUSIONS: Increased microvascular permeability in human DR is not associated with changes in expression of the HSPGs studied, whereas high amounts of VEGF may induce increased expression of the HS side chain epitope recognized by HepSS1. These results suggest that the mechanism underlying retinal leakage is different from diabetic glomerular capillary leakage.

Aged↗
PubMed1989

Protective effect of a 21-aminosteroid on the blood-brain barrier following subarachnoid hemorrhage in rats.

The effects of subarachnoid injection of blood on blood-brain barrier permeability to albumin was assessed in a rat model. Subarachnoid injection of blood caused a significant sixfold increase in Evans blue extravasation, whereas sham operation or NaCl injection had no effect. In addition, subarachnoid injections of arachidonic acid or FeCl2 increased blood-brain barrier permeability to Evans blue 16- and 10-fold, respectively. The capillary permeability after subarachnoid injection of blood was normalized by pretreatment with a novel 21-aminosteroid, U-74006F, that has antioxidant and antilipolytic activity. Pretreatment with U-74006F also reduced the vascular leakage induced by subarachnoid injection of arachidonic acid or FeCl2 by 50% and 45%, respectively. We conclude that damage to membrane lipids by peroxidative and/or lipolytic processes is involved in the subarachnoid hemorrhage-induced blood-brain barrier opening and that U-74006F protects the blood-brain barrier against the effects of subarachnoid hemorrhage by preventing or limiting these pathologic membrane lipid changes.

Animals↗
PubMed1988

Pancreatitis-induced acute lung injury. An ARDS model.

Cerulein-induced acute pancreatitis in rats is associated with acute lung injury characterized by increased pulmonary microvascular permeability, increased wet lung weights, and histologic features of alveolar capillary endothelial cell and pulmonary parenchymal injury. The alveolar capillary permeability index is increased 1.8-fold after a 3-hour injury (0.30 to 0.54, p less than 0.05). Gravimetric analysis shows a similar 1.5-fold increase in wet lung weights at 3 hours (0.35% vs. 0.51% of total body weight, p less than 0.05). Histologic features assessed by quantitative morphometric analysis include significant intra-alveolar hemorrhage (0.57 +/- 0.08 vs. 0.12 +/- 0.02 RBC/alveolus at 6 hours, p less than 0.001); endothelial cell disruption (28.11% vs. 4.3%, p less than 0.001); and marked, early neutrophil infiltration (7.45 +/- 0.53 vs. 0.83 +/- 0.18 PMN/hpf at 3 hours, p less than 0.001). The cerulein peptide itself, a cholecystokinin (CCK) analog, is naturally occurring and is not toxic and in several in vitro settings including exposure to pulmonary artery endothelial cells, Type II epithelial cells, and an ex vivo perfused lung preparation. The occurrence of this ARDS-like acute lung injury with acute pancreatitis provides an excellent experimental model to investigate mechanisms and mediators involved in the pathogenesis of ARDS.

Animals↗
PubMed1987

Diabetogenic action of streptozotocin: essential role of membrane permeability.

A single high dose of streptozotocin was found to cause a transient increase in islet capillary permeability 2-4 h after administration. Staining of areas of increased vascular permeability by Evans blue showed that islets, but not exocrine tissue, were affected. The permeability increase seems to involve vasoactive substances released by mast cells. A mast cell inhibitor (disodium cromoglycate) and a serotonin antagonist (methysergide) were found protective. Furthermore, administration of methysergide partially prevented the development of hyperglycaemia in streptozotocin-treated rats. In mice, almost full protection from diabetes development was reached by both methysergide and disodium cromoglycate. Our observations indicate an important role of mast cell controlled membrane permeability in this model of beta-cell destruction and diabetes development.

Animals↗
PubMed2002

Breakdown of the blood-brain barrier and neuropathological changes induced by Phoneutria nigriventer spider venom.

The blood-brain barrier (BBB) is responsible for selective flux of substances between blood and brain. The selective permeability of the BBB is crucial for the maintenance of the brain microenvironment homeostasis, and alterations in the barrier may be involved in many pathophysiological processes. Phoneutria nigriventer armed spider venom produces excitatory signals and symptoms in humans, and its recognized neurotoxic action suggests a potential ability to alter BBB permeability. The aim of the present study was to investigate the capacity of P. nigriventer venom (PNV) in promoting BBB breakdown in adult rats. After intravenous injection of 850 micro g/kg of the whole venom, BBB lesions were evaluated after 18 h to 9 days by ultrastructural methods using the extracellular tracer lanthanum nitrate. Clinical signs and symptoms of rats showed acute neurotoxicity, with some of the animals presenting convulsions, but which were clinically resolved by 12 h post-envenoming. The results showed that PNV is able to increase BBB permeability, particularly in the hippocampus. Changes were first detected in arterioles and post-capillary venules 18 h to 5 days after venom inoculation. The increased permeation of the extracellular tracer peaked on day 1, representing about 42% of the examined vessels (P<0.01). This appeared to occur by both transendothelial and intercellular routes, i.e., by pinocytic transport and through interendothelial junctions. Concomitantly, the surrounding tissue showed vasogenic edema and swollen astrocytic processes, without inflammatory infiltrates. The peak of the edema occurrence was observed on day 3, in about 60% of the vessels (P<0.001). Enhanced capillary permeability was observed on day 9, and affected 36% of all capillaries (P<0.05). The affected capillaries were characterized by increased number of pinocytotic vesicles, which, in addition, were filled with the extracellular tracer, but without visible transport through the interendothelial pathway. This study demonstrates that systemic PNV inoculation induces BBB breakdown through trans- and paracellular routes. It is concluded that BBB breakdown is an event not associated with the acute neurotoxicity exhibited by the rats.

Animals↗
PubMed1984

A distributed model of peritoneal-plasma transport: theoretical considerations.

Transport of water-soluble substances between the peritoneal cavity and the plasma was modeled with a distributed approach. The model includes diffusion and convection through tissue as well as membrane transport across blood capillaries, which are assumed to be distributed uniformly in the tissue. Lymphatic uptake via the diaphragm is also included. Transport in the remainder of the body is modeled by a system of compartments. The resulting system of mass balances and rate equations is solved numerically to provide predictions of peritoneal volume and concentrations in plasma, peritoneal fluid, and tissue surrounding the cavity. The model sensitivity is explored by varying key parameters to determine whether the changes would have a significant effect on model output. Key parameters include peritoneal surface area, tissue diffusivity, capillary permeability, tissue void fraction, and hydrostatic and osmotic pressures in the capillaries and interstitium.

Absorption↗
PubMed1988

Myocardial serotonin exchange: negligible uptake by capillary endothelium.

The extraction of serotonin from the blood during transorgan passage through the heart was studied using Langendorff-perfused rabbit hearts. Outflow dilution curves of 131I- or 125I-labeled albumin, [14C]sucrose, and [3H]serotonin injected simultaneously into the inflow were fitted with an axially distributed blood-tissue exchange model to examine the extraction process. The model fits of the albumin and sucrose outflow dilution curves were used to define flow heterogeneity, intravascular dispersion, capillary permeability, and the volume of the interstitial space, which reduced the degrees of freedom in fitting the model to the serotonin curves. Serotonin extractions, measured against albumin, during single transcapillary passage, ranged from 24 to 64%. The ratio of the capillary permeability-surface area products for serotonin and sucrose, based on the maximum instantaneous extraction, was 1.37 +/- 0.2 (n = 18), very close to the predicted value of 1.39, the ratio of free diffusion coefficients calculated from the molecular weights. This result shows that the observed uptake of serotonin can be accounted for solely on the basis of diffusion between endothelial cells into the interstitial space. Thus it appears that the permeability of the luminal surface of the endothelial cell is negligible in comparison to diffusion through the clefts between endothelial cells. In 18 sets of dilution curves, with and without receptor and transport blockers or competitors (ketanserin, desipramine, imipramine, serotonin), the extractions and estimates of the capillary permeability-surface area product were not reduced, nor were the volumes of distribution. The apparent absence of transporters and receptors in rabbit myocardial capillary endothelium contrasts with their known abundance in the pulmonary vasculature.

Animals↗
PubMed1975

Influence of histamine- and 5-hydroxytryptamine-containing thyroid mast cells on thyroid blood flow and permeability in the rat.

The possible significance of thyroid mast cells in the regulation of thyroid blood flow and capillary permeability was investigated in rats whose TSH secretion had been eliminated by exogenous T4. Mast cells were identified by their abundance of metachromatic granules, and their content of histamine and 5-hydroxytryptamine (5-HT) was examined by fluorescence histochemistry. Thyroid histamine levels were determined by fluorometry. The tissue uptake of 86Rb was used as an indicator of blood flow and permeability. Numerous histamine- and 5-HT-containing mast cells were found within the thyroid and in connective tissue adjacent to the thyroid, whereas juxtathyroidal muscle tissue was virtually devoid of mast cells. Administration of compound 48/80 evoked a prompt depletion of 5-HT, histamine and metachromatic granules from thyroid mast cells, and a concomitant increase in the thyroidal uptake of 86Rb. The 86Rb uptake by juxtathyroidal muscle tissue was unaffected. Exogenous 5-HT and histamine both induced prompt increments in thyroidal 86Rb uptake, and 5-HT also stimulated 86Rb uptake in juxtathyroidal muscle tissue. TSH, previously shown to induce a gradual amine release from mast cells within, but not outside, the thyroid, evoked a gradual increase in thyroidal, but not in muscular, uptake of 86Rb. The findings support the concept that, in the rat, histamine and/or 5-HT, released from intrathyroidal mast cells by TSH, stimulate thyroid blood flow and/or permeability.

Animals↗
PubMed1988

Altered lung vascular permeability during intermittent haemodialysis.

Hypoxia is known to develop during intermittent haemodialysis. To investigate if increased pulmonary capillary permeability to protein contributes to this phenomenon, a dual-isotope technique using Indium-labelled transferrin and Technetium-labelled red blood cells was used. Lung vascular permeability was measured in eight patients with dialysis-dependent chronic renal failure immediately before and during intermittent haemodialysis with cuprophane membranes. As a group there was a significant increase in lung vascular permeability during the early stages of haemodialysis, compared to predialysis values (P less than 0.05) and this increase occurred during the period when the patients were leucopenic and maximally hypoxic. During the haemodialysis period, but not the predialysis period, the permeability index was also significantly increased compared to a group of eight controls (P less than 0.05). These results suggest that increased vascular permeability may contribute to dialysis-induced hypoxia and that this may relate to neutrophil activation within the pulmonary vascular bed.

Adolescent↗
PubMed1984

Increased peritoneal permeability in rats with alloxan-induced diabetes mellitus.

Increased capillary permeability to small and large molecules has been demonstrated in several organs of human diabetics and in animal models of the disease. To assess the effects of diabetic microangiopathy on peritoneal clearances, peritoneal dialysis was performed in normal rats, rats with gentamicin-induced acute renal failure, and rats with mild and severe alloxan-induced diabetes mellitus. Peritoneal clearances of urea, inulin, and albumin were significantly increased in the severely diabetic rats compared with other groups. Microscopic examination revealed abnormally small adipose cells in the peritoneums of the severely diabetic rats, associated with a generally malnourished appearance. Vascular abnormalities attributable to diabetes mellitus, such as capillary basement membrane layering and neovascularization, were demonstrated in the peritoneums+ of both mildly and severely diabetic rats, though not to a greater extent in either group. We conclude that, as in many other parts of the body, peritoneal permeability to small, middle and large molecules is increased in early, severe, untreated diabetes mellitus.

Acute Kidney Injury↗