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Results for “Capillary Permeability”

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At least 1,441 records · Page 80Linked to original sources
PubMed1991

Hemoglobin potentiates oxidant injury in isolated rat lungs.

Isolated perfused rat lungs were subjected to oxidant injury induced by tert-butyl hydroperoxide (t-buOOH), which caused a significant increase in capillary permeability as assessed by the change in the capillary filtration coefficient. t-buOOH caused an increase in the change in the capillary filtration coefficient (delta Kfc) of 0.27 +/- 0.05 ml.min.cmH2O-1.100 g lung tissue-1 (mean +/- SE) that was accompanied by an increase in thiobarbituric acid reactive products of lipid peroxidation in the lung perfusate. The addition of hemoglobin to the perfusate potentiated t-buOOH-induced lung injury as evidenced by a significantly greater (P = 0.007) delta Kfc of 0.43 +/- 0.05. t-buOOH also caused hemoglobin to release large quantities of free iron in vitro. The potentiation of t-buOOH-induced lung injury by hemoglobin was prevented by apotransferrin as evidenced by a significant reduction (P = 0.001) in delta Kfc to 0.13 +/- 0.02. No statistically significant (P greater than 0.05) changes in segmental resistances or pulmonary vascular pressures occurred in any of the lungs injured with t-buOOH when compared with time controls. These results demonstrate that t-buOOH causes an oxidant injury in isolated rat lungs that can be potentiated by free iron released from hemoglobin.

Animals↗
PubMed2004

Beta1-integrins and glomerular injury.

The renal glomerulus is composed of three types of glomerular cells (mesangial cell (MC), endothelial cell and podocyte) and extracellular matrix (ECM) consisting of the glomerular basement membrane (GBM) and mesangial matrix. It constitutes a highly specialized microcirculation in which the permeability characteristics of the capillary wall allow its unique filtration function. The proliferation of MCs, an increase of mesangial ECM and detachment podocyte from GBM are key biological features of progressive glomerulonephritis (GN), leading to glomerular scarring and dysfunction. Thus, the study of the molecular and cellular mechanisms responsible for pathological glomerular alterations may help to elucidate the pathogenesis of progressive glomerular diseases. A growing body of evidence indicates that beta1 integrin family (beta1 integrins), that mainly mediates cell adhesion to ECM, controls cell behaviors such as cell migration, proliferation, apoptosis and ECM assembly. In addition, a correlation between glomerular expression of beta1 integrins and their ligand ECM components is observed in various human and experimental GN, suggesting that altered beta1 integrins-mediated cell behaviors may contribute to the progression of GN. It is now becoming apparent that the expression of glomerular beta1 integrins is not only critical for maintaining the glomerular capillary permeability but it modulates cell signaling pathways regulating the cell phenotypes involved in the progression of glomerular diseases.

Animals↗
PubMed1989

[A clinical study of pulmonary edema on paraquat poisoning by double indicator dilution method using heat and sodium].

We studied the formation of pulmonary edema on 9 patients with paraquat poisoning using thermal-sodium double indicator dilution method for the measurement of lung water. In survivors group (n = 4) extravascular thermal volume (EVTV) was not almost changes. In non-survivors group (n = 5) EVTV increased about three times as much as that in survivors group on 32 hours after admission. EVTV was correlated with PCP-PCOP in both survivors group and non-survivors group (n = 64, r = 0.665, p less than 0.01). But EVTV in non-survivors group was higher than that in survivors group within same PCP-PCOP. In non-survivors group delta EVTV/delta (PCP-PCOP) in 24 hours after admission was correlated with initial PCP-PCOP (r = 0.984, p less than 0.01). We propose that the formation of pulmonary edema on paraquat poisoning is mainly due to the increased capillary permeability, influenced by the increased pressure gradient of capillary barrier.

Adult↗
PubMed1987

Brain microvascular function during cardiopulmonary bypass.

Emboli in the brain microvasculature may inhibit brain activity during cardiopulmonary bypass. Such hypothetical blockade, if confirmed, may be responsible for the reduction of cerebral metabolic rate for glucose observed in animals subjected to cardiopulmonary bypass. In previous studies of cerebral blood flow during bypass, brain microcirculation was not evaluated. In the present study in animals (pigs), reduction of the number of perfused capillaries was estimated by measurements of the capillary diffusion capacity for hydrophilic tracers of low permeability. Capillary diffusion capacity, cerebral blood flow, and cerebral metabolic rate for glucose were measured simultaneously by the integral method, different tracers being used with different circulation times. In eight animals subjected to normothermic cardiopulmonary bypass, and seven subjected to hypothermic bypass, cerebral blood flow, cerebral metabolic rate for glucose, and capillary diffusion capacity decreased significantly: cerebral blood flow from 63 to 43 ml/100 gm/min in normothermia and to 34 ml/100 gm/min in hypothermia and cerebral metabolic rate for glucose from 43.0 to 23.0 mumol/100 gm/min in normothermia and to 14.1 mumol/100 gm/min in hypothermia. The capillary diffusion capacity declined markedly from 0.15 to 0.03 ml/100 gm/min in normothermia but only to 0.08 ml/100 gm/min in hypothermia. We conclude that the decrease of cerebral metabolic rate for glucose during normothermic cardiopulmonary bypass is caused by interruption of blood flow through a part of the capillary bed, possibly by microemboli, and that cerebral blood flow is an inadequate indicator of capillary blood flow. Further studies must clarify why normal microvascular function appears to be preserved during hypothermic cardiopulmonary bypass.

Animals↗
PubMed1998

[Early treatment for body fluid shifts and circulatory derangement in patients with extensive burns].

The initial postburn period is characterized by body fluid shifts and circulatory derangement, or so-called burn shock. The fluid shifts are mainly due to a marked increase in capillary permeability. This loss of capillary integrity is so great that colloid including albumin, readily disperse into the extravascular space. This is limited to the burned area when of 30% or less of the body surface area (BSA) is involved, but is found throughout the entire body when more than 30% of the BSA is involved. The tremendous fluid shifts from the intravascular to the extravascular space result in edema formation and hemoconcentration. Along with the reduction in intravascular volume, there is a rapid reduction in cardiac output which gradually returns to the normal level 24 to 48 hours after burn injury. Therefore fluid resuscitation should be initiated immediately after injury. Currently a number of methods for achieving adequate volume replacement are available. In this paper we review fluid resuscitation methods for patients with extensive burns and also introduce recent topics on new regimens for resuscitation.

Burns↗
PubMed1990

[Roentgenological diagnosis of acute lesions of the lungs with disorders of blood circulation and vascular permeability].

To specify differential and diagnostic criteria of hemodynamic and non-hemodynamic pulmonary edema, canine experimental simulation (15 trials) of different types of abnormal hemodynamic and lung capillary permeability parameters was carried out. The X-ray pictures of 71 patients with and acute diffuse lesion of the pulmonary vascular channel (including 51 with adult respiratory distress and 20 with hemodynamic pulmonary edema) was analysed. The findings substantiated the possibility of making a differential diagnosis of pulmonary edema of various genesis. Symptom complexes, typical of predominantly higher permeability of the lung capillaries and hemodynamic disturbance, were formulated.

Acute Disease↗
PubMed2002

Effects of albumin supplementation on microvascular permeability in septic patients.

Albumin has a stabilizing effect on endothelium and helps maintain capillary permeability to macromolecules. Critically ill patients with sepsis may have profound hypoalbuminemia, but the effect of this hypoalbuminemia on microvascular permeability is unknown. To determine the degree and potential importance of this effect, we measured the transcapillary escape rate (TER) of (125)I-labeled albumin in 12 adult patients fulfilling American College of Chest Physicians/Society of Critical Care Medicine criteria for septic shock. We measured TER over a 90-min baseline period and then repeated these measurements immediately after the rapid infusion of 200 ml of 20% albumin. At baseline, patients had a mean serum albumin concentration of 10.3 +/- 3.8 g/l, which, at 30 min after the albumin infusion, was 18.5 +/- 3.7 g/l. The baseline TER was 6.7 +/- 1.5%/h, with a postinfusion TER of 6.4 +/- 2.1%/h (P = 0.550). Albumin supplementation sufficient to nearly double serum concentrations in profoundly hypoalbuminemic septic patients had no clinically significant effect in reducing microvascular permeability.

Adult↗