Increase of microvascular permeability is one of the most important pathological events in the pathogenesis of trauma and burn injury. Massive leakage of fluid from vascular space leads to lose of blood plasma and decrease of effective circulatory blood volume, resulting in formation of severe tissue edema, hypotension or even shock, especially in severe burn injury. Fluid resuscitation has been the only valid approach to sustain patient's blood volume for a long time, due to the lack of overall and profound understanding of the mechanisms of vascular hyperpermeability response. There is an emerging concept in recent years that some so-called barrier stabilizing mediators play a positive role in preventing the increase of vascular permeability. These mediators may be released in response to proinflammatory mediators and serve to restore endothelial barrier function. Some of these stabilizing mediators are important even in quiescent state because they preserve basal vascular permeability at low levels. This review introduces some of these mediators and reveals their underlying signaling mechanisms during endothelial barrier enhancing process.
Burns ; Capillary Permeability ; Fluid Therapy ; Humans ; Permeability

No abstract available.
Angiotensin II* ; Angiotensins* ; Capillary Permeability ; Female ; Ovarian Hyperstimulation Syndrome

Immune cells (leukocytes or white blood cells) move actively and sensitively based on body conditions. Despite their important role as protectors inside the body, it is difficult to directly observe the spatiotemporal momentum of leukocytes. With advances in imaging technology, the introduction of two-photon microscopy has enabled researchers to look deeper inside tissues in a three-dimensional manner. In observations of immune cell movement along the blood vessel, vascular permeability and innate immune cell movements remain unclear. Here, we describe the neutrophil extravasation cascade, which were observed using a two-photon intravital imaging technique. We also provide evidence for novel mechanisms such as neutrophil body extension and microparticle formation as well as their biological roles during migration.
Blood Vessels ; Capillary Permeability ; Cell Movement ; Leukocytes ; Microscopy ; Neutrophils*

BACKGROUND: Exposure to hyperoxia causes extensive injury to lung tissue, which resembles the pathologic changes of the adult respiratory distress syndrome. To observe the relationship between the pulmonary oxygen toxicity and duration of exposure to oxygen, 100% oxygen was exposed to Wistar rats. METHODS: 35 rats were partitioned into 5 groups (n=7 in each group). Gr. I breathed room air. Gr. II, III, IV and V were exposed to 99~100% oxygen for 24 hrs, 48 hrs, 60 hrs and 72 hrs. Wet lung/body weight (WW/BW), dry lung/body weight (DW/BW), wet/dry lung weight (WW/DW) and I-albumin flux ratio were measured in each group. RESULTS: After exposure for 72 hrs in Gr. V, 3 rats were dead. WW/BW in Gr. I was 0.69+/-0.04 and increased to 1.10+/-0.28 in Gr.II (P<0.05), which was maintaind until 60 hrs. It showed marked increase in Gr. V; 2.16+/-0.60. DW/BW, WW/DW and I-albumin flux ratio increased after 48 hrs of hyperoxia. WW/BW and DW/BW in Gr. V and I-flux ratio in Gr. IV showed significant increase compared with Gr. I, II and III. CONCLUSIONS: The results suggest that pulmonary capillary permeability begins to change after 24 hrs of hyperoxia and that definite permeability change to albumin and fluid accumulation in the lung are demonstrable from 48 hrs-exposure to 99~100% oxygen and aggravated by duration of oxygen exposure.
Animals ; Capillaries* ; Capillary Permeability* ; Hyperoxia ; Lung ; Oxygen* ; Permeability ; Rats* ; Rats, Wistar ; Respiratory Distress Syndrome, Adult

The epithelium, including the respiratory system, acts as a selective gate between the outside environment and underlying tissue. Epithelial cells are polarized due to the formation of the apical junctional complex, which includes adherent junctions and tight junctions. Endothelial cells are one of the most important cellular constituents of blood vessels. Endothelial junctional proteins play important roles in tissue integrity as well as in vascular permeability, leukocyte extravasation, and angiogenesis. This review focuses on the apical junctional complex in respiratory diseases.
Blood Vessels ; Capillary Permeability ; Endothelial Cells ; Epithelial Cells ; Epithelium ; Leukocytes ; Permeability ; Respiratory System ; Tight Junctions

Systemic capillary leak syndrome (SCLS) is a condition that's caused by the shift of fluid and protein from the intravascular space to the interstitial space as a result of repetitive episodes of capillary hyperpermeability. The pathogenesis of SCLS is still unclear, but there's recently been a report showing this syndrome in association with monoclonal gammopathy. This syndrome can be a fatal disease because cardiovascular collapse can occur in the initial capillary leak phase. Although theophylline, diuretics, terbutaline, steroids, calcium antagonist, Ginkgo biloba extracts and plasmapheresis have been suggested as medication, none of them have been proven to be effective. Considering that this disease is self-limiting, conservative treatment in the acute phase is believed to be very important. Because hypoalbuminemia is very a common manifestation of SCLS, Pentastarch, which has a higher molecular weight than albumin, could be efficient to prevent cardiovascular collapse. We used 10% Pentastarch during the acute SCLS attacks of 2 patients and the patients both showed a dramatic response. Pentastarch may be helpful to treat SCLS in its initial capillary leak phase by the elevating blood pressure, and this might contribute to somewhat decreasing the acute mortality of SCLS.
Adult ; Capillary Leak Syndrome/diagnosis/*drug therapy/etiology ; Capillary Permeability ; Female ; Hetastarch/*therapeutic use ; Humans ; Plasma Substitutes/*therapeutic use

BACKGROUND: Rhinovirus infection of the airways results in increased permeability of the airway vascular endothelium with the influx of plasma proteins, including lipids such as LDL. In vitro studies on the effect of oxLDL on leukocytes has shown many proinflammatory effects on multiple leukocytes. We hypothesized that oxLDL is one mechanism for recruiting granulocytes to the airways during a RV infection. Therefore, chemotaxis and transendothelial migration, in response to nLDL, was determined for these granulocytes. METHODS: nLDL was oxidized with 5mM Cu2SO4 for 20-24 hours. 3-5×10(5) cells were loaded into the Transwell filter while the chemotatic agonists were placed in the lower well for chemotaxis. Confluent monolayers on HPMEC were grown on Transwell filters for transendothelial migration. The filters were washed and eosinophils and neutrophils loaded on to the filter with the chemotatic agonist was were placed in the lower well. The wells were incubated for 3 hours. The number of migrating cells was counted on a hemocytometer. RESULTS: OxLDL, but not nLDL, is chemotatic for eosinophils and neutrophils. The level of granulocytes chemotaxis was dependent on both the concentration of LDL and its degree of oxidation. OxLDL stimulates eosinophil and neutrophils migration across HPMEC monolayers (±IL-1β preactivation) in a dose dependent manner. CONCLUSION: Increased vascular permeability during a RV infection may lead to the influx and oxidation of LDL. The resulting oxLDL. is one possible mechanism for the recruitment of neutrophils and eosinophils to the airway interstitial matrix. Once in the airways, granulocytes can further interact with oxLDL to promote airway inflammation.
Blood Proteins ; Capillary Permeability ; Chemotaxis ; Endothelium, Vascular ; Eosinophils* ; Granulocytes ; Inflammation ; Leukocytes ; Neutrophils* ; Permeability ; Rhinovirus ; Transendothelial and Transepithelial Migration

The endothelial glycocalyx (EG) is a gel-like layer lining the luminal surface of healthy vascular endothelium. Recently, the EG has gained extensive interest as a crucial regulator of endothelial funtction, including vascular permeability, mechanotransduction, and the interaction between endothelial and circulating blood cells. The EG is degraded by various enzymes and reactive oxygen species upon pro-inflammatory stimulus. Ischemia-reperfusion injury, oxidative stress, hypervolemia, and systemic inflammatory response are responsible for perioperative EG degradation. Perioperative damage of the EG has also been demonstrated, especially in cardiac surgery. However, the protection of the EG and its association with perioperative morbidity needs to be elucidated in future studies. In this review, the present knowledge about EG and its perioperative implication is discussed from an anesthesiologist's perspective.
Blood Cells ; Capillary Permeability ; Endothelium, Vascular ; Glycocalyx* ; Oxidative Stress ; Permeability ; Phenobarbital ; Reactive Oxygen Species ; Reperfusion Injury ; Thoracic Surgery

Porphyromonas gingivalis, one of the major periodontal pathogens, is implicated in the initiation and progression of periodontal disease. The initial stages of periodontal inflammation are accompanied by vascular hyperpermeability. In our present study, we report that the P. gingivalis lipopolysaccharide (LPS) increases the mRNA expression of interleukin-8 (IL-8), a major inducer of vascular permeability, in vascular endothelial cells. P. gingivalis LPS also stimulated the induction of IL-8 secretion in endothelial cells. The P. gingivalis LPS-induced expression of IL-8 was primarily modulated by nuclear factor-kappaB (NF-kappaB). P. gingivalis LPS significantly enhanced the vascular permeability both in vitro and in vivo, and a blockade of the IL-8 receptor decreased the P. gingivalis LPS-induced vascular permeability. Taken together, these results suggest that P. gingivalis LPS increases vascular permeability through the NF-kappaB-dependent production of IL-8 in vascular endothelial cells.
Capillary Permeability ; Endothelial Cells ; Inflammation ; Interleukin-8 ; Periodontal Diseases ; Porphyromonas ; Porphyromonas gingivalis ; RNA, Messenger

We have experienced a reexpansion pulmonary edema(RPE) during general anesthesia. This patient has undertaken the decortication operation due to right sided massive pleural effusion and fibrothorax. Generally reexpansion pulmonary edema is believed to oceur only when a chronically collapsed lung is rapidly reexpanded by evacuation of large amount of air or fluid in pneumothorax and pleural effusion. The pathogenesis of RPE is unknown and is probably multifactorial. The implicated etiologies are chronicity of collapse, technique of reexpansion, increased pulmonary vascular permeability, airway obstruction, loss of surfactant and pulmonaty artery pressure changes. The outcome of RPE may be fatal, so physician treating lung collapse must be aware of the possible causes and endeavor to prevent the occurrence of this complieation.
Airway Obstruction ; Anesthesia, General* ; Arteries ; Capillary Permeability ; Humans ; Lung ; Pleural Effusion ; Pneumothorax ; Pulmonary Atelectasis ; Pulmonary Edema*