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PubMed1992

[Anti-inflammatory and analgesic actions of artificial and fermentative Ganoderma sinense (AFGS)].

Both AFGS and natural Ganoderma sinense (NGS) have obvious anti-inflammatory and analgesic effects for arthritis in rats induced by carrageenan and the pain reaction in mice induced by hot scalding as well as HAC-induced writhing. AFGS also can reduce the edematous swelling of mice's ears, reduce the capillary permeability of mice skin and obviously inhibit cotton pellets granuloma implanted in rats. It can promote cytophagy capacity of the reticular endothelial cells in mice. No irritation on the gastric mucosa in rats has been observed.

Animals↗
PubMed1991

The role of platelet-activating factor in the pulmonary response to inhaled bacterial endotoxin.

Quantitative morphometric analyses were carried out on animals subjected to aerosols of bacterial endotoxin (LPS) to further define the role of platelet-activating factor (PAF) in the development of pulmonary injury. Hamsters were exposed to either saline aerosol or dilute aerosols of LPS (4 micrograms/m3) for standard lengths of time. Within each aerosol exposure group, animals were further subdivided into groups receiving either the PAF receptor binding antagonist, RP 48740, or saline injections. LPS inhalation resulted in decreased fixed lung volume, increased sequestration of polymorphonuclear leukocytes and platelets in pulmonary capillaries, increased type I epithelial and endothelial cellular volumes, increased cellular interstitium, and increased endothelial pinocytotic vesicles. Treatment with RP 48740 either attenuated or abolished the ability of inhaled LPS to induce these structural alterations. The PAF antagonist also inhibited LPS-induced increases in pulmonary capillary permeability. It is concluded that PAF is one of the major injury-promoting mediators released upon inhalation exposure to environmentally realistic concentrations of bacterial endotoxin. A major but not exclusive target of this mediator is the pulmonary vascular endothelium.

Animals↗
PubMed1978

Influence of counter-irritation by carrageenin on inflammatory reactions induced by prostaglandins, serotonin, histamine, compound 48/80, carrageenin and Freund's complete adjuvant.

The carrageenin edema of rat paw and the primary phase of rat adjuvant arthritis were significantly inhibited by carrageenin whereas the increase of skin capillary permeability induced by prostaglandins (PGs) and further irritants as well as the secondary phase of adjuvant arthritis were mostly not significantly affected. Inhibitory effects after single carrageenin injection do not seem to be mediated by the complement system because total complement activity remained unaffected.

Animals↗
PubMed1981

Concurrent increases in resistance and transport after coronary obstruction in dogs.

We have extended earlier studies on coronary vascular permeability-surface area (PS) for [14C]sucrose to include observations of the transcoronary flow resistance before and after partial occlusion of the left anterior descending coronary artery. Multiple-tracer (MT) studies were conducted on 13 anesthetized dogs by inserting an isotope mixture (125I-albumin, 51Cr-red blood cells, [14C]sucrose, 3HOH) into a cannula connecting the carotid and the left anterior descending coronary artery. Analysis of blood sampled from the coronary sinus allowed calculation of PS, extravascular 3HOH volume (VT), and extravascular [14C]sucrose volume (VS). Flow reduction significantly reduced VT and VS and increased PS/VT relative to base line. Coronary resistance distal to the obstruction (R) decreased significantly immediately after flow reduction but then, over the low-flow period, increased significantly above this initial low-flow value. The mean R during reduced flow normalized to R immediately after flow reduction (Ri) correlated significantly with PS/VT during ischemia. Because R/Ri is not correlated with VT alone, we speculate that capillary permeability alterations may play a role in the deterioration of myocardial perfusion during ischemia.

Animals↗
PubMed1987

The origin of proteinuria at high altitude.

Urinary protein excretion was measured before and after the intravenous infusion of lysine in 14 normal subjects after 4-6 days' acclimatization at 4846 m. Urinary albumin excretion before lysine was elevated in 11 subjects but alpha 1-microglobulin was detected in only four. After lysine a large increase in albumin excretion occurred in all subjects. Together with the absence of alpha 1-microglobulin before lysine this implies that increased glomerular capillary permeability is the major cause of proteinuria after acclimatization to high altitude. The estimated minimum glomerular fluid albumin concentration was increased two to three fold above the published values in normal controls.

Acclimatization↗
PubMed1987

Modulation of normobaric pulmonary oxygen toxicity by hydroxyl radical inhibition.

The effects of hydroxyl radical inhibition on an experimental model of normobaric pulmonary oxygen toxicity have been studied. The metal ion chelator, desferrioxamine (which inhibits hydroxyl-radical generation) or the hydroxyl-radical scavenger, dimethylthiourea (DMTU), were administered in an attempt to block hydroxyl-radical-mediated tissue injury. Lung injury was monitored in Sprague-Dawley rats by examining lung histology and bronchoalveolar lavage and by assessing pulmonary capillary permeability using the 125I-albumin lung permeability index and the lung weight:body weight ratio. Control animals had lung permeability indices 0.183 +/- 0.005 and lung weight to body weight ratio of 4.50 +/- 0.10 (all as mean +/- SEM). With increased duration of exposure to hyperoxia, there was a progressive increase in pulmonary inflammation, with thickening of alveolar membranes and atelectasis and a progressive increase in lung permeability indices (0.434 +/- 0.088 at 24 hrs; 0.954 +/- 0.165 at 48 hrs; and 1.55 +/- 0.214 at 60 hrs); and lung weight to body weight ratio (5.28 +/- 0.11 at 24 hrs; 6.54 +/- 0.23 at 48 hrs; and 8.91 +/- 0.51 at 60 hrs). Treatment with desferrioxamine provided significant protection from lung injury after 24 hrs of hyperoxia (eg., lung permeability indices 0.250 +/- 0.018; lung weight to body weight ratio 4.68 +/- 0.14, both p less than 0.025; cf. 24-hr hyperoxia controls) but no reduction in pulmonary injury was observed after 48 and 60 hrs of hyperoxia exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Administration of tourniquet. I. Are edema and oxidative stress related to each other and to the duration of ischemia in reperfused skeletal muscle?

One hindlimb of mice was subjected to 60, 90 and 120 min ischemia by application of a tourniquet followed by a 60-min reperfusion period. An additional experimental group received a tourniquet for 90 min without subsequent reperfusion. The soleus muscle (from the contralateral side also as control) was removed and evaluated for muscle weight, protein weight, protein content, and glutathione concentrations. Ischemia alone without subsequent reperfusion did not produce significant changes. With postischemic reperfusion, the protein content and muscle weight increased, probably because of an increased capillary permeability, leading to muscle edema. Oxidative stress was also present during reperfusion, correlating well with the changes in protein content. The intensity of these alterations appeared to depend on the period of ischemia.

Animals↗
PubMed2003

Preventive effect of phosphoenolpyruvate on hypoxemia induced by oleic acid in Guinea pigs.

Oleic acid-induced hypoxemia is an animal model of acute respiratory distress syndrome (ARDS). Increased capillary permeability is a cause of hypoxemia in lung injury. Endothelial cells form a major capillary barrier, and disruption of the barrier appears to involve a decreased level of ATP in the cells. Phosphoenolpyruvate (PEP) is an endogenous substance that is one of the ATP precursors and can cross some cell membranes via anion exchanger. We examined the effect of PEP on oleic acid-induced lung injury in guinea pigs. An intravenous injection of oleic acid (15 microl/kg) caused severe hypoxemia. Pretreatment with PEP at a dose of 2, 20, or 200 micromol/kg attenuated the oleic acid-induced decrease in the arterial partial pressure of oxygen in a dose-dependent manner. Furthermore, PEP attenuated the oleic acid-induced increase in vascular permeability in the proximal and distal bronchi, as indicated by the extravascular leakage of Evans Blue dye. The combination of PEP with ATP (4 micromol/kg) showed no additional inhibitory effect on oleic acid-induced lung injury, compared with PEP alone. We suggest that PEP is a promising candidate to prevent hypoxemia in acute lung injuries associated with increased vascular permeability, such as ARDS.

Animals↗
PubMed1986

Distributed model of blood-bone exchange.

An understanding of bone physiology obtained from a knowledge of fluid spaces and their associated barriers may lead to better management of bone pathologies. Such information can be obtained by mathematically modelling the results of multiple tracer outflow dilution techniques, which in our case were performed on the canine tibia. Hence, a computer model was developed to describe the exchange processes of tracers between blood and bone. Capillary permeability, bone binding and the vascular, interstitial fluid and bone volumes of distribution were used as parameters in the equations describing the system, which also used published morphometric bone data. Parameter estimates were then derived by the use of optimization procedures.

Animals↗
PubMed1998

Plasma volume in acute hypoxia: comparison of a carbon monoxide rebreathing method and dye dilution with Evans' blue.

Exposure to acute hypoxia is associated with changes in body fluid homeostasis and plasma volume (PV). This study compared a dye dilution technique using Evans' blue (PV[Evans']) with a carbon monoxide (CO) rebreathing method (PV[CO]) for measurements of PV in ten normal subjects at sea level and again 24 h after rapid passive ascent to high altitude (4,350 m). Hypobaric hypoxia decreased arterial oxygen saturation to 79 (74-83)% (mean with 95% confidence intervals). The PV(Evans') remained unchanged from 3.49 (3.30-3.68) l at sea level to 3.46 (3.24-3.68) l at high altitude. In contrast PV(CO) decreased from 3.39 (3.17-3.61) l at sea level to 3.04 (2.75-3.33) l at high altitude (P < 0.05). Compared with sea level, this resulted in an increase of the mean bias between the two methods [from 0.11 (-0.05-0.27) l at sea level to 0.43 (0.26-0.60) l at high altitude] so that the ratio between PV(Evans') and PV(CO) increased from 1.04 (0.99-1.09) at sea level to 1.15 (1.06-1.24) at high altitude (P < 0.05). In conclusion, the two methods were not interchangeable as measures of hypoxia-induced changes in PV. The mechanism responsible for the bias remains unknown, but it is suggested that the results may reflect a redistribution of albumin caused by the combined effects in hypoxia of both an increased capillary permeability to albumin and a decrease in PV. As a result, the small perivascular compartment of albumin beyond the endothelium may increase without changes in the overall albumin distribution volume.

Acute Disease↗
PubMed1984

Reexpansion pulmonary edema after pneumothorax.

Spontaneous pneumothorax is a common disorder that is easily recognized and treated. Occasionally reexpansion of the collapsed lung is complicated by unilateral pulmonary edema, heralded by tachypnea, unilateral rales, and profuse expectoration of frothy secretions within several hours of reexpansion. Severe morbidity and death may result. Increased duration of pneumothorax and the use of suction are important factors in the generation of reexpansion pulmonary edema. Increased pulmonary capillary permeability rather than hydrostatic transudation is believed to underlie its development. For patients with pneumothorax of prolonged duration close observation in an intensive care unit for 24 hours after evacuation of air and the routine use of supplemental oxygen during and after lung reexpansion seem indicated.

Capillary Permeability↗
PubMed1998

Analysis of the paired-tracer method of determining cell uptake.

The paired-tracer method has been used extensively for determining cell uptake of numerous substances, although the method of calculating uptake has no published theoretical support. We have investigated the effect of capillary permeability of the tracers on v, the uptake rate calculated directly from the ratio of tracer venous concentrations. For a simple mathematical model of plasma-tissue movement of lactate and an analytic expression for v, it has been shown that values of v calculated in the first moments after tracer injection depend almost entirely on the differences in tracer permeability-surface area product (PS). The model indicates v would never give the correct value of cell uptake. It is also shown that PS differences alone can explain the published values for lactate uptake obtained from v in skeletal muscle of the rat and dog.

Animals↗
PubMed1998

Test of a two-pathway model for small-solute exchange across the capillary wall.

We previously proposed a two-pathway model for solute and water transport across vascular endothelium (Fu, B. M., R. Tsay, F. E. Curry, and S. Weinbaum. J. Biomech. Eng. 116: 502-513, 1994) that hypothesized the existence of a continuous slit 2 nm wide along tight junction strands within the interendothelial cleft in parallel with 20 x 150-nm breaks in tight junctions. We tested this model by measuring capillary permeability coefficients (P) to a small solute (sodium fluorescein, radius 0.45 nm), assumed to permeate primarily the 2-nm small pore, and an intermediate-sized solute (FITC-alpha-lactalbumin, radius 2.01 nm) excluded from the small pore. Mean values of the paired diffusive permeability coefficients, Psodium fluorescein and PFITC-alpha-lactalbumin, were 34.4 and 2.9 x 10(-6) cm/s, respectively, after corrections for solvent drag and free dye (n = 26). These permeabilities were accounted for by transport through the large-break pathway without the additional capacity of the hypothetical 2-nm pathway. As a further test we examined the relative reductions of Psodium fluorescein and PFITC-alpha-lactalbumin produced by elevated intracellular cAMP. Within 20 min after the introduction of rolipram and forskolin, Psodium fluorescein and PFITC-alpha-lactalbumin decreased to 0.67 and 0.64 times their respective baseline values. These similar responses to permeability decrease were evidence that the two solutes were carried by a common pathway. Combined results in both control and reduced permeability states did not support the hypothesis that a separate pathway across tight junctions is available for solutes with a radius as large as 0.75 nm. If such a pathway is present, then its size must be smaller than that of sodium fluorescein.

Animals↗
PubMed2001

[Hydrothorax during diagnostic laparoscopy].

An 83-yr-old, 44-kg woman with a 2-month history of abdominal distension received diagnostic laparoscopy. Except for chronic treated hypertension, she was healthy. The preoperative chest X-ray demonstrated small pleural effusion occupying the lower left hemithorax, but she did not present with dyspnea or chest pain. After premedication with intravenous ranitidine 50 mg, anesthesia was induced with thiopental 150 mg, vecuronium 7 mg and maintained by 1-2% sevoflurane in 50% N2O/O2. SpO2 decreased after insufflation of CO2, but breath sound was audible on both lungs. At completion of operation, chest X-ray revealed the left hemilateral hydrothorax and 650 ml of pleural fluid was suctioned. Blood gas improved and the tracheal tube was removed. The diagnosis of tuberculous peritonitis was established by the demonstration of granulomas of the peritoneum. We speculated on four reasons for the increased pleural effusion on the left thorax: 1) Increase of systemic and capillary pressure caused by CO2 insufflation. 2) Increase of capillary permeability by tuberculous pleuritis. 3) Decrease of colloid osmotic pressure by hypoalbuminemia. 4) Decreased pleural fluid removal because of venous compression caused by increased intrathoracic pressure. Peritoneal insufflation of CO2 to create the pneumoperitoneum may induce hydrothorax in patients with tuberculous pleuritis.

Aged↗
PubMed1996

Lung injury in the microembolic model of acute pancreatitis and amelioration by lexipafant (BB-882), a platelet-activating factor antagonist.

Acute pancreatitis is associated with the development of pulmonary dysfunction in a number of patients. The aim of this study was to determine whether acute lung injury was a feature of the microembolic model of pancreatitis in rats and to assess the therapeutic effect of lexipafant (BB-882), a potent platelet-activating factor antagonist, on the lung injury. Acute pancreatitis was induced by microembolisation of the pancreas with 20-microns polystyrene microspheres. After 12 h tissue capillary permeability was assessed by an Evans blue dye (EBD) extravasation technique and compared with that in control animals. A further group of animals received an intraperitoneal injection of BB-882 (5 mg/kg) 30 min after the induction of pancreatitis. There was a significantly increased tissue content of EBD in the pancreas and lungs of the group of animals with acute pancreatitis (p < 0.05). BB-882 ameliorated the pulmonary changes when administered after the induction of pancreatitis, as demonstrated by a significant reduction in the EBD content of the lungs (p < 0.01). Increased pulmonary vascular permeability is an early feature of the microembolic model of acute pancreatitis and these changes appear to be modified by the administration of BB-882, providing further evidence for the potential role of platelet-activating factor antagonists in the treatment of acute pancreatitis and its complications.

Acute Disease↗
PubMed1970

Consumption of kininogen in the submandibular salivary gland when activated by chorda stimulation.

1. A method is described for determination of kininogen 1 (substrate mainly for plasma kallikrein) and kininogen 2 (substrate for glandular kallikrein) independently in cat plasma.2. In anaesthetized cats the arterial inflow to, and venous outflow from, the submandibular salivary gland were isolated: a roller pump giving constant volume inflow was interposed in the arterial circuit.3. Venous blood was collected at rest, during and after stimulation of the chorda tympani, and its content of kininogens 1 and 2 were estimated. Kininogen 2 was reduced up to 60% by chorda stimulation, whereas the level of kininogen 1 was unchanged.4. On close arterial infusion of bradykinin or histamine in amounts which produce large vascular effects, including increased capillary permeability, the venous blood levels of both kininogens 1 and 2 were unchanged.5. It is concluded that the selective loss of kininogen 2 on chorda stimulation results from the release of kallikrein into the tissue spaces and reflects the extent of kinin formation within the gland.

Animals↗
PubMed1998

[Synthesis and antiinflammatory activity of 2-(E)-benzylidene-5-(N-substituted aminomethyl) cyclopentanones].

Nineteen kinds of 2-(E)-benzylidene-5-(N-substituted aminomethyl) cyclopentanones were synthesized via Mannich reaction or amine exchange reaction and identified spectrometrically. One compound exhibited significant antiinflammatory activity, showing obvious inhibitory effect on xylene-induced mice ear swelling, carrageenin-induced rats paw edema and increased capillary permeability induced with acetic acid in mice. Its ED50 values in these inflammatory models were calculated to be 67.8 mg.kg-1, 25.3 mg.kg-1 and 41.8 mg.kg-1 respectively, nearly equal to those of ibuprofen and aspirin.

Animals↗