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PubMed1983

[Lymph flow from the lungs in conditions of normal capillary permeability].

The source of the lung lymph formation was studied in 8 experiments on dogs and in 30 experiments on isolated lungs. The former revealed the effect of bronchial vessels ligature upon the lung lymph outflow, the latter series aided to trace the lymph flow in perfusion of the lung artery's vessels and bronchial vessels. The section of bronchial vessels decreased by 4-6 times the lymph outflow. No lymph outflow was observed in perfusion of isolated lungs whereas in perfusion of bronchial vessels the lymph flow was directly related to the pressure level in the bronchial vessels. These vessels are concluded to be of the primary importance for the lung lymph formation.

Animals↗
PubMed1982

Permeability of intestinal capillaries: effects of fat absorption and gastrointestinal hormones.

The purpose of this study was to determine whether the postprandial increase of intestinal lymphatic protein flux is due to an increased capillary permeability. Intestinal lymph flow and lymph (L) and plasma (P) protein concentrations were measured at various venous pressures under control conditions, after cream feeding, and during intraluminal perfusion with a bile-oleic acid solution. The osmotic reflection coefficient (sigma d), a measure of capillary permeability that is independent of surface area, was estimated under all conditions, assuming sigma d = 1 - L/P at high capillary filtration rates. The results acquired indicate that cream feeding and intraluminal perfusion with bile-oleic acid significantly increases intestinal capillary permeability. Pretreatment with indomethacin and antihistamines did not alter the permeability increase induced by intraluminal bile-oleic acid. Intra-arterial infusion of cholecystokinin and secretin did not increase intestinal capillary permeability. These studies indicate that the postprandial increase in intestinal lymphatic protein flux is due at least in part, to an increase in capillary permeability. Cholecystokinin, secretin, histamine, and prostaglandins do not appear to mediate the increased intestinal capillary permeability during fat absorption.

Animals↗
PubMed1989

The pathophysiology of intestinal damage: effects of luminal distention and ischemia.

Intestinal edema, luminal distention, and ischemia are common pathologic processes involved in producing the intestinal damage found during surgical exploration for acute abdominal disorders in the horse. The severity of intestinal edema depends on the degree of altered intravascular forces and changes in capillary permeability. Capillary hydrostatic pressure rises as the less pliable venules and veins become occluded during intestinal obstruction. Concurrently, the production of various endogenous products that damage the vascular wall leads to increases in capillary permeability and protein exudation, causing fluid movement into the interstitium and consequent tissue edema. The information presently available indicates that luminal distention does not produce the morphologic damage observed during natural conditions. However, slight intestinal edema was observed with experimental distention of the equine small intestine. Although the effects of increased luminal pressure appear minor, in the overall scheme of intestine damage, many processes are occurring together, and the luminal distention may be additive in the production of intestinal damage. The intestinal damage occurring during natural obstructions is most likely related to both the severity of the ischemia and the subsequent reperfusion injury. Experimentally, an ischemic insult produces a consistent sequence of mucosal alterations to both the equine small and large intestine. Severity of ischemia may be the limiting factor in determining the clinical outcome in cases in which the ischemic insult is irreversible; however, if the intestinal tissue survives the ischemia, the reperfusion injury may substantially increase the damage, producing an irreversible injury. The proposed mechanisms responsible for the reperfusion injury include the presence of highly reactive cytotoxic oxygen radicals. The intestinal epithelium and vascular endothelium are both capable of producing these unstable compounds. Secondly, the influx and activation of neutrophils may also release oxygen radicals. During experimental ischemia, neutrophils gradually move to the affected area; however, during reperfusion their numbers dramatically increase and may play a significant role in producing intestinal damage. Therapy for intestinal damage involves first determining the viability of the affected intestine. All nonviable bowel should be resected and viable intestine anastomosed. The care and maintenance of intestine of questionable viability are presently based on therapy in humans and experimental information concerning the pathophysiologic mechanisms of intestinal ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Effects of protamine, heparinase, and hyaluronidase on endothelial permeability and surface charge.

We undertook studies in the isolated perfused rat lung to determine 1) the effects of endothelial charge neutralization with the polycation protamine sulfate on microvascular permeability, lung water, and anionic ferritin binding to the endothelium and 2) the role of heparan sulfate and hyaluronate, negatively charged cell surface glycosaminoglycans, on permeability. Capillary permeability was determined by tissue 125I-albumin accumulation in isolated perfused rat lungs. In control lungs the 5-min albumin uptake was 0.50 +/- 0.05 cm3.s-1.g dry tissue-1 X 10(-3). It was increased by 132 +/- 7.8% (P less than 0.001) by protamine (0.08 mg/ml) and 65 +/- 12% (P less than 0.01) by heparinase (5 U/ml), whereas hyaluronidase (25 NFU/ml) was without effect. In control lungs total water was 4.83 +/- 0.15 ml g/dry tissue. Protamine increased lung water 12 +/- 2% (P less than 0.05). Heparinase caused a 9 +/- 3% increase (P less than 0.05), and hyaluronidase had no effect. Electron microscopy demonstrated that protamine increased anionic ferritin binding to the surface of endothelial cells. We conclude that protamine sulfate neutralization of negative charge in the pulmonary microcirculation leads to increased microvascular permeability. Heparin sulfate may be responsible for this charge effect.

Animals↗
PubMed1990

Mechanisms of pulmonary edema induced by tumor necrosis factor-alpha.

We tested the hypothesis that human recombinant tumor necrosis factor-alpha (TNF) promotes pulmonary edema by neutrophil-dependent effects on the pulmonary vasculature. The isolated guinea pig lung was perfused with phosphate-buffered Ringer's solution with or without human neutrophils. The infusion of neutrophils (9 x 10(6) total) into lungs isolated after the in vivo administration of TNF (3.2 x 10(5) units/kg) resulted in weight gain (+1.951 +/- 0.311 g versus -0.053 +/- 0.053 g in control) and an increase in the lung (wet-dry)-to-dry weight ratio (8.3 +/- 0.5 versus 6.0 +/- 0.2 in control), indicating the formation of pulmonary edema. The neutrophil-dependent pulmonary edema induced by TNF was associated with a combination of increased capillary permeability (capillary filtration coefficient [Kf,c], 0.170 +/- 0.048 g/min/cm H2O/g at 30 minutes versus 0.118 +/- 0.008 g/min/cm H2O/g at baseline) and increased pulmonary capillary pressure (Ppc, 12.8 +/- 0.8 cm H2O at 60 minutes versus 6.0 +/- 0.3 cm H2O at baseline). The Ppc increase was mediated by thromboxane A2 (TXA2) because the TXA2 synthetase inhibitor Dazoxiben (0.5 mM) prevented the effect (Ppc, 6.7 +/- 0.6 cm H2O at 60 minutes with Dazoxiben), and thromboxane B2 (TXB2) levels were increased in the pulmonary venous effluent (5,244 +/- 599 pg/ml at 60 minutes versus 60 +/- 13 pg/ml at baseline). Studies using WEB-2086 (37 microM), a platelet activating factor (PAF) receptor antagonist, indicated that PAF mediated the increased vascular permeability (Kf,c, 0.107 +/- 0.014 g/min/cm H2O/g at 30 minutes using WEB-2086) and, in part, the increased Ppc (Ppc, 8.4 +/- 0.7 cm H2O at 60 minutes using WEB-2086). In addition, alterations of endothelial peripheral actin bands were noted after TNF administration. The data indicate that TNF induces neutrophil-dependent pulmonary edema associated with increased Ppc (mediated by TXA2 and PAF), increased Kf,c (mediated by PAF), and changes in endothelial peripheral actin bands.

Actins↗
PubMed1996

Dynamic contrast-enhanced magnetic resonance imaging reveals stress-induced angiogenesis in MCF7 human breast tumors.

The mechanism of contrast enhancement of tumors using magnetic resonance imaging was investigated in MCF7 human breast cancer implanted in nude mice. Dynamic contrast-enhanced images recorded at high spatial resolution were analyzed by an image analysis method based on a physiological model, which included the blood circulation, the tumor, the remaining tissues, and clearance via the kidneys. This analysis enabled us to map in rapidly enhancing regions within the tumor, the capillary permeability factor (capillary permeability times surface area per voxel volume) and the fraction of leakage space. Correlation of these maps with T2-weighted spin echo images, with histopathology, and with immunohistochemical staining of endothelial cells demonstrated the presence of dense permeable microcapillaries in the tumor periphery and in intratumoral regions that surrounded necrotic loci. The high leakage from the intratumoral permeable capillaries indicated an induction of a specific angiogenic process associated with stress conditions that cause necrosis. This induction was augmented in tumors responding to tamoxifen treatment. Determination of the distribution and extent of this stress-induced angiogenic activity by contrast-enhanced MRI might be of diagnostic and of prognostic value.

Animals↗
PubMed1997

When does the lung die? Kfc, cell viability, and adenine nucleotide changes in the circulation-arrested rat lung.

Lungs harvested from cadaveric circulation-arrested donors may increase the donor pool for lung transplantation. To determine the degree and time course of ischemia-reperfusion injury, we evaluated the effect of O2 ventilation on capillary permeability [capillary filtration coefficient (Kfc)], cell viability, and total adenine nucleotide (TAN) levels in in situ circulation-arrested rat lungs. Kfc increased with increasing postmortem ischemic time (r = 0.88). Lungs ventilated with O2 1 h postmortem had similar Kfc and wet-to-dry ratios as controls. Nonventilated lungs had threefold (P < 0.05) and sevenfold (P < 0.0001) increases in Kfc at 30 and 60 min postmortem compared with controls. Cell viability decreased in all groups except for 30-min postmortem O2-ventilated lungs. TAN levels decreased with increasing ischemic time, particularly in nonventilated lungs. Loss of adenine nucleotides correlated with increasing Kfc values (r = 0.76). This study indicates that lungs retrieved 1 h postmortem may have normal Kfc with preharvest O2 ventilation. The relationship between Kfc and TAN suggests that vascular permeability may be related to lung TAN levels.

Adenine Nucleotides↗
PubMed2001

Engraftment syndrome following hematopoietic stem cell transplantation.

During neutrophil recovery following hematopoietic stem cell transplantation, a constellation of symptoms and signs including fever, erythrodermatous skin rash, and noncardiogenic pulmonary edema often occur. These clinical findings have usually been referred to as engraftment syndrome, or, reflecting the manifestations of increased capillary permeability, capillary leak syndrome. While described most often following autologous stem cell transplantation, a similar clinical syndrome has been observed followed allogeneic stem cell transplantation. Distinction from graft-versus-host disease in the allogeneic setting however, has been difficult. Recent experience with non-myeloablative conditioning for stem cell transplantation, however, reveals that an engraftment syndrome independent of GVHD may occur. In some cases, this engraftment syndrome may be a manifestation of a host-versus-graft reaction (graft rejection). While cellular and cytokine interactions are believed to be responsible for these clinical findings, a distinct effector cell population and cytokine profile have not been defined. Engraftment syndromes are likely associated with an increased transplant-related mortality, mostly from pulmonary and associated multi-organ failure. Corticosteroid therapy is often dramatically effective for engraftment syndrome, particularly for the treatment of the pulmonary manifestations. A proposal for a more uniform definition of engraftment syndrome has been developed in order to allow for a reproducible method of reporting of this complication and for evaluating prophylactic and therapeutic strategies.

Capillary Leak Syndrome↗
PubMed1980

Pleural effusions.

Pleural effusions develop following changes in capillary permeability, capillary hydrostatic pressure, plasma colloid osmotic pressure, or lymphatic drainage. Generalized fluid retention or a transudate suggests a systemic cause while an exudate suggests a local cause. The diagnosis can usually be established by clinical assessment, chest radiography, analysis of pleural fluid, pleural biopsy, and appropriate special investigations. When no cause can be found, particular care should be taken to exclude secondary carcinoma, tuberculosis, pulmonary infarction, and mesothelioma; the patient should be followed-up. Symptomatic malignant effusions may be managed initially by basal intercostal tube drainage alone. For recurrences, local instillation first of tetracycline and then of mustine may be tried. Pleurectomy should be considered if the prognosis is otherwise good.

Alkylating Agents↗
PubMed1979

Permeability of single capillaries compared with results from whole-organ studies.

There are now two experimental approaches to capillary permeability: whole-organ studies and single-capillary experiments. It is not possible to obtain permeability coefficients in the true sense of the word from whole-organ experiments since the capillary surface area is unknown. Other limitations of whole-organ approaches are discussed. Results from 'osmotic transient' experiments are compared with those from 'indicator diffusion' experiments. 'Osmotic transient' experiments give higher values for capillary diffusion capacity than 'indicator diffusion' experiments. Reasonable agreement is obtained when the reflection coefficient is taken into account. Thus far, single-capillary experiments have only provided results from capillaries in the frog mesentery, where the potassium permeability was about 70 X 10(-5) cm . sec-1, or 10 times the value from whole-organ experiments on muscle. The discrepancy may reflect true differences between capillaries in the two tissues or may be caused by methodological limitations. There is a need for comparative studies of permeability with the whole-organ and the single-capillary technique applied to the same tissue.

Animals↗