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PubMed1985

Cardiac and vascular effects of elliptinium in guinea pigs. Involvement of a histaminergic mechanism.

This work reports a study of the effects of elliptinium on heart rate, arterial blood pressure and capillary permeability in guinea-pigs. The variations in capillary permeability are determined by spectrophotometric assay of skin Evans blue. Elliptinium induces dose-independent tachycardia and dose-related hypotension. For the highest dose (6 mg/kg), elliptinium induces lethal collapse . Elliptinium increases capillary permeability and this effect, particularly marked at 1 mg, i.d., is partially antagonized by mepyramine-cimetidine association. These results are discussed in comparison with those obtained with elliptinium on other parameters, with histamine and with different antitumoral agents. The increase in capillary permeability raises the question of its relevance to the anticancer activity of elliptinium.

Alkaloids↗
PubMed1993

Some properties of a capillary permeability-increasing enzyme-2 from the venom of Agkistrodon caliginosus (Kankoku-Mamushi).

Capillary permeability-increasing enzyme-2 (CPI-enzyme-2) consists of a single polypeptide chain with an isoelectric point of pH 3.5. The enzyme is composed of 369 amino acid residues, based on a mol. wt of 44,000, and contains 20.3% carbohydrate. Both arginine ester hydrolytic and capillary permeability-increasing activities of the enzyme were inhibited by treatment with diisopropylfluorophosphate, indicating that the enzyme is a serine proteinase. The N-terminal amino acid sequence shows homology with that of CPI-enzyme-1 and similarity to those of batroxobin or kallikrein-like enzyme from other snake venoms.

Agkistrodon↗
PubMed1997

Capillary permeability-increasing enzyme-2 from the venom of Agkistrodon caliginosus (kankoku-mamushi): activity resulting from the release of peptides from fibrinogen.

When a mixture of the purified capillary permeability-increasing enzyme-2 from agkistrodon caliginosus venom and rabbit plasma was injected into the depilated skin of the back of rabbits, the capillary permeability-increasing activity was much greater than that induced by injection of the enzyme alone. To isolate the active substance, the mixture was subjected to reversed-phase high-performance liquid chromatography. Among the active peptides, five peptides were purified and their amino acid sequences were analyzed. These peptides were derived from the amino-terminal portion of the B beta-chain of fibrinogen. After the enzyme was incubated with rabbit fibrinogen, the three peptides were purified from the incubation mixture by high-performance liquid chromatography, and their amino acid compositions and amino acid sequences were determined. From these results, it was determined the peptides were derived from the amino-terminal portion of the B beta-chain of fibrinogen. This result indicates that the increase in capillary permeability induced by the enzyme is due to the peptides released from rabbit fibrinogen.

Agkistrodon↗
PubMed1997

Effect of TYB-2285 on passive cutaneous anaphylaxis in rats.

1. TYB-2285 (1-30 mg/kg p.o.) inhibited ovalbumin (OA)- and dinitrophenyl-Ascaris (DNPAs)-induced passive cutaneous anaphylaxis (PCA) in a dose-dependent manner. 2. The ED50 of TYB-2285 and ketotifen fumarate on OA-induced PCA were 0.5 and 3.9 mg/kg, respectively. The ED50 of TYP-2285 and amlexanox on DNP-As-induced PCA were 3.5 and 0.9 mg/ kg, respectively. 3. TYB-2285 (3-30 mg/kg p.o.) inhibited histamine consumption at the PCA site. 4. Unlike cyproheptadine or amlexanox, TYB-2285 (30 mg/kg p.o.) did not inhibit histamine-, serotonin-, ascites-, 48/80-, or A23187-induced capillary permeability. It inhibited dextran-induced capillary permeability slightly. 5. These results demonstrate that TYB-2285 inhibits PCA by inhibiting histamine release, although it does not inhibit capillary permeability.

Animals↗
PubMed1993

The single-pass cerebral extraction and capillary permeability-surface area product of several putative cerebral blood flow imaging agents.

We have determined cerebral blood flow (CBF) and the single-pass cerebral extraction (E) of several putative agents for external imaging of CBF. Simultaneous measurements of blood flow and extraction were performed in 106 rats. For all agents, comparison of linear and exponential regressions of E on CBF indicates that this relationship can be described as linear over the range of flows studied. Analysis of covariance indicates that the extraction of 123I-IMP, 67Cu-PTSM and 99mTc-HMPAO is higher than that of 99mTc-Cl(DMG)3(2MP) and 99mTc-ECD, particularly at flows above the normal range. Accordingly, for 123I-IMP, 67Cu-PTSM and 99mTc-HMPAO, the slope of the linear regression equation for the relationship between brain capillary permeability surface area product (PS) and CBF is higher than that for 99mTc-Cl(DMG)(3)2MP and 99mTc-ECD. PS varies as a linear function of CBF over the range of flows studied. At a CBF level that corresponds to normal regional CBF for human cortex, 0.5 ml/g/min, all the agents have a single-pass extraction of approximately 70% or greater. While all the agents detected changes in CBF in the normal to ischemic range, at higher flows 123I-IMP, 67Cu-PTSM and 99mTc-HMPAO showed substantially greater fidelity to true CBF than 99mTc-Cl(DMG)(3)2MP and 99mTc-ECD.

Animals↗
PubMed1990

Possible mechanism of vasogenic brain oedema induced by arachidonic acid.

Free arachidonic acid was infused into normal rat brains and the effect of arachidonic acid on capillary permeability was investigated by measuring the regional uptake of 14C-aminoisobutyric acid with a quantitative autoradiographic method. Arachidonic acid increased capillary permeability in a dose-dependent manner up to 2 mM. A high dose of arachidonic acid (greater than 5 mM) produced a profound tissue destruction around the needle track and less increased capillary permeability than 2 mM arachidonic acid. Time-course study disclosed that arachidonic acid markedly increased capillary permeability within 2 hours after infusion, and continued to increase with time to 24 hours. The effect of 48 hours infusion was about a half of that at 24 hours, indicating that the effect of arachidonic acid was partially reversible. Pretreatment with dexamethasone significantly inhibited the arachidonic acid-induced increase in capillary permeability and the administration of actinomycin D 1 hour before the pretreatment with dexamethasone suppressed the inhibitory effect of dexamethasone. These results suggest that arachidonic acid, which is deposited in the extracellular space, increases brain capillary permeability by two different ways. One is the direct detergent effect of arachidonic acid, and the other is the effect of arachidonic acid that is released from the membrane by the activation of phospholipase A2.

Animals↗
PubMed1985

[Effect of a course of pentoxifylline (trental) treatment on microcirculatory and central hemodynamic functions in chronic ischemic heart disease patients].

The author studied the effect of trental therapy lasting one month on the functions of the microcirculation and central hemodynamics in 45 patients with chronic coronary heart disease (CHD). It was established that as regards the clinical response to the treatment all the patients could be distributed into 2 groups: responsive and refractory to therapy. In patients who responded to the treatment (36 persons), the rate of the microlymph flow and capillary permeability substantially increased. The increase in capillary permeability led to a lowering in the CPV and BCV, which in turn gave rise to a reduction in the parameters of the cardiac output. There were no changes on the whole in the microhemodynamics. In patients refractory to therapy, trental treatment did not bring about any changes in the central hemodynamics, microhemodynamics or lymphodynamics. Capillary permeability dropped with a high degree of significance. The data obtained point to the necessity of a differential approach to the treatment of CHD patients with trental.

Adult↗
PubMed1982

Fine structural studies on ependymal paracellular and capillary transcellular permeability in the subcommissural organ of the guinea pig.

Morphological investigations on the permeability of intercellular junctions between ependymal cells and between capillary endothelial cells in the subcommissural organ (SCO) of the guinea pig have been carried out using freeze-fracturing and tracer experiments with horseradish peroxidase (HRP). The ependymal junction reveals a moderately developed network of tight junctional strands surrounding the tall ependymal cell. The apical portion of this junctional network tends to form nearly complete strands, whereas the basal portion usually shows irregular, fragmented strands often arranged in hairpin-like structures. The passage of intraventricularly infused HRP is blocked, leaving unstained areas, at the level of membrane fusions. At the same time the lateral intercellular space below the junction is densely stained, probably due to invasion from the basal side through adjacent ordinary ependymal junctions. The SCO capillary endothelium shows a high distribution density of pinocytotic vesicles. Vesicular transport of intravascularly injected HRP is observed, but no HRP penetration occurs through the endothelial junction. The active participation of vesicles in tracer movement is shown in preparations fixed before administration of HRP. Extravasation of this tracer is indicated to some degree in the SCO capillary, but permeability here appears to be comparable to that of ordinary brain capillaries. Accordingly, the SCO ependymal tight junction seems to form an effective barrier not to blood plasma or similar materials but to apically secreted substances, preventing them from spreading back into SCO intercellular spaces.

Animals↗
PubMed1992

[Usefulness of vitamin A binding protein as a marker for capillary endothelial permeability].

We performed a preliminary study to assess the usefulness of Vitamin A binding protein (VABP) as a gamma-camera marker for capillary endothelial permeability. We used a guinea pig model of endotoxin (LPS) induced acute lung injury. We calculated the concentration ratio of either 125I-albumin or 125I-VABP in lung tissue to that in plasma (tissue plasma ratio; T/P) as a parameter of capillary endothelial permeability. 99mTc-diethylene triamine pentaacetic acid (DTPA) was used as a marker for pulmonary interstitial volume. We estimated wet to dry lung weight ratio as a parameter of lung water accumulation (W/D). LPS increased the T/P of 125I-albumin and W/D, suggesting the development of permeability edema. The T/P for 125I-VABP was also increased, indicating that 125I-VABP can be used to detect elevated capillary endothelial permeability. In both groups, LPS and saline, the T/P was higher for 125I-VABP than for 125I-albumin. These data suggest that the pulmonary capillary endothelium is more permeable to VABP than albumin.

Animals↗
PubMed1997

Peripheral circulatory effects of pump perfusion on cat skeletal muscle with and without prostacyclin.

The present study analyses the peripheral circulatory effects of pump perfusion on a sympathectomized cat skeletal muscle in terms of effects on segmental vascular resistances (large-bore arterial vessels, arterioles and veins), hydrostatic capillary pressure, capillary filtration coefficient, transcapillary filtration and autoregulation of blood flow. The effect of prostacyclin during pump perfusion was analysed to evaluate whether it interferes with the pump-induced vascular alterations, especially if it reduces transcapillary filtration through its capillary permeability decreasing effect. Pump perfusion initiates a marked vasodilation (from 17.3 to 10.1 PRU), an increase in hydrostatic capillary pressure, and a marked inhibition of myogenic reactivity and of autoregulation of blood flow. There was a slow restoration of vascular tone reaching a steady-state level somewhat below the autoperfusion value within 2 h. Pump perfusion did not change the capillary filtration coefficient, indicating that the capillary permeability was not increased. This implies that short-term pump-induced capillary leakage is more an effect of increase in hydrostatic capillary pressure, perhaps in combination with increased number of open capillaries, than of an increase in capillary permeability. Prostacyclin decreased capillary permeability by at least 22% but simultaneously increased hydrostatic capillary pressure, resulting in an unchanged filtration compared with the situation just after the starting of the pump. The results obtained show that experiments using pump perfusion should be interpreted with care due to the interference with normal peripheral vascular control. The results give reasonable explanations of the lowered blood pressure and transcapillary fluid loss during the clinical use of a heart-lung machine.

Animals↗
PubMed1983

Changes of the blood-brain barrier in experimental metastatic brain tumors.

An experimental model for blood-borne cerebral metastases was developed by introducing Walker 256 carcinoma cells selectively into the intracranial internal carotid artery of rats. This model was used to study the regional capillary permeability of rat brain and metastatic brain tumors of various sizes with the aid of 14C alpha-aminoisobutyric acid (AIB) quantitative autoradiography. The regional capillary permeability varied with the anatomical location and size of the tumor. Intraparenchymal tumors less than 1 mm in diameter showed no increased permeability to AIB. As the tumors enlarged over 1 mm in diameter, the permeability in the intraparenchymal tumors increased proportionally, but remained less than one-third of capillary permeability of subcutaneously transplanted tumors. Capillary permeability in the peripheral invasive part and necrotic center was less than in the viable part of large tumors. Capillary permeability in metastatic tumors of the choroid plexus and meninges was significantly higher than in tumors of the brain parenchyma. The results suggest that the uptake of chemotherapeutic agents that do not cross the blood-brain barrier easily varies with the anatomical location and size of the metastatic tumors.

Animals↗
PubMed2001

Host factors influencing the preferential localization of sterically stabilized liposomes in Klebsiella pneumoniae-infected rat lung tissue.

PURPOSE: To gain insight into the host factors influencing liposome localization at sites of bacterial infection. METHODS: In a unilateral Klebsiella pneumoniae pneumonia rat model, capillary permeability and number of circulating leukocytes was quantified and related to the degree of liposome target localization. RESULTS: Liposome localization was highest in the hemorrhagic zone of infection, a zone characterized by markedly increased capillary permeability and high bacterial numbers. Both liposome localization and capillary permeability correlated positively with severity of infection. Lung instillation of other inflammatory stimuli, such as lipopolysaccharide or 0.1 M HCl inducing increased capillary permeability, also promoted liposome localization. As liposomal target localization in leukopenic rats was similar to that in immunocompetent rats, contribution of circulating leukocytes seems limited. Intrapulmonary distribution of liposomes shows that leukocytes at the target site are involved in liposome uptake after extravasation. CONCLUSIONS: Increased capillary permeability plays a crucial role in liposome localization at the infected site, whereas contribution of leukocytes is limited. These results suggest inflammatory conditions that could benefit from liposomal drug delivery. The involvement of leukocytes in liposome uptake at the target site could be important information in the selection of appropriate drugs.

Animals↗
PubMed2001

Microvascular permeability is increased in both types of diabetes and correlates differentially with serum levels of insulin-like growth factor I (IGF-I) and vascular endothelial growth factor (VEGF).

Vascular endothelial growth factor (VEGF) and insulin-like growth factor-I (IGF-I) both play a pivotal role in diabetic microangiopathy. This study assessed the relationship between capillary permeability as a marker of endothelial dysfunction and serum VEGF and IGF-I levels in normotensive diabetics. Subjects were 10 Type 1 (6/4, male/female, age: 30 [mean] +/- 5 [SD] years, HbA1c: 7.5 +/- 1.1 %), 13 Type 2 diabetics (9/4, m/f; 63 +/- 7 years, 8.3 +/- 1.8 %), and 24 age- and sex-matched control subjects. We determined nailfold capillary permeability by intravital fluorescence videomicroscopy after intravenous injection of sodium-fluorescein. Serum VEGF, free and total IGF-I, IGF binding protein (IGFBP)-1, IGFBP-3, and insulin levels were measured by specific immunoassays. Capillary permeability was increased in both types of diabetes patients compared to age- and sex-matched controls. In Type 1 diabetics, fluorescence light intensities increased over time, reaching significance 30 minutes after dye injection. Type 2 diabetics already revealed an early onset of elevated fluorescence light intensities after one minute. Capillary permeability showed a significant positive correlation with VEGF levels in Type 1 diabetics, (r = 0.76, p < 0.05; 20 min after dye injection) but with free IGF-I levels in type 2 diabetics (r = 0.65, p < 0.05; 5 min after dye injection). IGFBP-3 correlated negatively with capillary permeability in both diabetes types, whereas IGFBP-1 levels correlated positively in Type 2 patients. In conclusion, capillary permeability is increased in both types of diabetes mellitus. However, VEGF and IGF-I may differentially affect microvascular permeability depending on the diabetes type.

Adult↗
PubMed2002

Intraventricular infusion of vascular endothelial growth factor promotes cerebral angiogenesis with minimal brain edema.

OBJECTIVE: Therapeutic cerebral angiogenesis, i.e., using angiogenic factors to enhance collateral vessel formation within the central nervous system, is a potential method for cerebral revascularization. Vascular endothelial growth factor (VEGF) is a potent endothelial cell mitogen that also increases capillary permeability, particularly in ischemic tissue. The purpose of this study was to assess the angiogenic and capillary permeability effects of chronic intraventricular infusion of exogenous VEGF in nonischemic brain tissue, because many patients with impaired cerebrovascular reserve do not exhibit chronic cerebral ischemia. METHODS: Recombinant human VEGF(165) was infused into the right lateral ventricle of rats at a rate of 1 microl/h for 7 days, at concentrations of 1 to 25 microg/ml, with osmotic minipumps. Control animals received vehicle only. Vessels were identified in laminin immunohistochemical analyses. Capillary permeability and brain edema were assessed with Evans blue extravasation, [(3)H]inulin permeability, and brain water content measurements. RESULTS: Vessel density was dose-dependently increased by VEGF(165) infusions, with significant increases occurring in animals treated with 5 or 25 microg/ml, compared with control animals (P h 0.01). Significant enlargement of the lateral ventricles was observed for the highest-dose group but not for animals treated with other doses. Capillary permeability was assessed in animals treated with a dose of 5 microg/ml. An increase in capillary permeability in the diencephalon was identified with Evans blue extravasation and [(3)H]inulin permeability assessments; however, the brain water content was not significantly increased. CONCLUSION: Chronic intraventricular infusions of VEGF(165) increased vascular density in a dose-dependent manner. There seems to be a therapeutic window, because infusion of VEGF(165) at a concentration of 5 microg/ml resulted in a significant increase in vessel density with minimal associated brain edema and no ventriculomegaly.

Animals↗
PubMed1991

The permeability of capillaries in the eustachian tube mucosa.

The transendothelial passage of horseradish peroxidase (HRP) and diffusion of HRP into the pericapillary space, injected intravenously into cats, was studied at the light and electron microscopic level in the mucosa of the eustachian tube. The permeability of capillaries in the pharyngeal two-thirds of the tube was higher than in the tympanic one-third though all the subepithelial capillaries were of the continuous type. In the lamina propria of the subepithelium in the pharyngeal two-thirds much HRP was found 10 min after its intravenous injection, but in the tympanic one-third, it was absent in the perivascular spaces. The capillaries of the pharyngeal two-thirds had many projections and marginal folds inside the capillary lumen and large pinocytotic vacuoles containing HRP as well as many micropinocytotic vesicles. On the other hand, the capillaries in the tympanic one-third had many micropinocytotic vesicles too, but only a few large pinocytotic vacuoles.

Animals↗
PubMed1981

Increased alveolar-capillary membrane permeability by monocrotaline.

To study the effect of monocrotaline on the pulmonary alveolar-capillary membrane permeability, cardiac catheterization, extravascular lung water content and absorption of 14C-compounds from the rat lungs in combination with morphological observations were studied in the early stage of monocrotaline intoxications. Purified monocrotaline or its pyrrole was administered to rats with various doses. Single dose of 50 mg/kg of monocrotaline was enough to induce pulmonary hypertension 4 weeks later, but neither immediate nor direct pressor effect was observed by monocrotaline or active pyrrole. Only 3 to 5 mg/kg of pyrrole was enough to produce alveolar flooding with increased extravascular lung water content and accelerated absorption of 14C-mannitol and 14C-inulin from lungs 24 hours after administration. In contrast with fast and potent effect of pyrrole, effect of monocrotaline was mild and delayed in development. These findings suggested that monocrotaline increased the porosity of not only endothelial but also alveolar membrane by active metabolite.

Animals↗
PubMed1991

The permeability of capillaries among the small granule-containing cells in rat superior cervical ganglia: an ultrastructural lanthanum tracer study.

The permeability of blood capillaries associated with small granule-containing (SGC) cells in rat superior cervical ganglia was investigated at ultrastructural level by employing ionic lanthanum as an electron dense tracer. In rat superior cervical ganglia, the majority of blood capillaries were nonfenestrated. Both fenestrated and nonfenestrated capillaries were observed in the area associated with SGC cells. Lanthanum tracer was observed in the luminal surface, the interendothelial cleft and the subendothelial perivascular spaces of both fenestrated and nonfenestrated capillaries associated with SGC cells. The external lamina of the Schwann cell which surrounded the neurons, nerve fibres and SGC cells were clearly delineated by the lanthanum tracer. Furthermore, the perineuronal space, the periaxonal space, and the pericellular space of the SGC cells were readily accessible to the lanthanum ion. The results demonstrated an absence of blood-nerve barrier, blood-ganglionic and blood-SGC cell barrier to the lanthanum ion in the parenchymal area of the SGC cells in rat superior cervical ganglia. It is proposed that lanthanum may pass through the endothelial cells via 1) the fenestrae of fenestrated capillaries, 2) the intercellular junctions of both fenestrated and nonfenestrated capillaries, i.e., a paracellular pathway; and 3) the process of endocytosis/exocytosis, i.e., a transcellular pathway, to reach the subendothelial space and be distributed in the parenchyma of SGC cells in rat superior cervical ganglia.

Animals↗
PubMed1990

Role of xanthine oxidase and neutrophils in ischemia-reperfusion injury in rabbit lung.

This study evaluated the effect of ischemia-reperfusion (I-R) on pulmonary capillary permeability in isolated rabbit lungs and the roles of xanthine oxidase (XO), aldehyde oxidase (AO), and neutrophils (PMN) in producing this lung injury. Effects of XO and AO were studied by inactivation with a tungsten-enriched diet (0.7 g/kg) and inhibition of XO by allopurinol (100 microM) or AO by menadione (3.5 microM). PMN effects were studied by preventing endothelial adhesion with the monoclonal antibody IB4 (10 microM). Vascular permeability was evaluated by determining the capillary filtration coefficient (Kf,c) measured before and after I-R in all experimental conditions. Reperfusion after 2 h of ischemia significantly increased pulmonary capillary permeability (Kf,c changed from 0.096 +/- 0.014 to 0.213 +/- 0.025 ml.min-1. cmH2O-1.100 g-1), and this increase was blocked by the addition of catalase (50,000 U) at reperfusion (baseline Kf,c was 0.125 +/- 0.023 and 0.116 +/- 0.014 ml.min-1.cmH2O-1.100 g-1). XO inactivation with the tungsten-supplemented diet and XO inhibition with allopurinol prevented the Kf,c increase observed after I-R (0.183 +/- 0.030 to 0.185 +/- 0.033 and 0.126 +/- 0.018 to 0.103 +/- 0.005 ml.min-1.cmH2O-1.100 g-1). Inhibition of AO had no effect on I-R injury (Kf,c 0.108 +/- 0.011 to 0.167 +/- 0.014 ml.min-1.cmH2O-1.100 g-1). Preventing PMN adhesion resulted in significant attenuation of the change in Kf,c associated with I-R (0.112 +/- 0.032 to 0.090 +/- 0.065 ml.min-1.cmH2O-1.100 g-1). We conclude that XO and PMN adherence, but not AO, are involved in the increased capillary permeability associated with I-R.

Aldehyde Oxidase↗