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At least 109 records · Page 6Linked to original sources
PubMed1994

Spontaneous leukocyte rolling in venules in untraumatized skin of conscious and anesthetized animals.

Intravital bright-field videomicroscopy was used to investigate whether leukocyte rolling can be observed under normal physiological conditions. We studied skin venules in trained conscious rats and anesthetized rats and mice without touching the skin itself. Leukocyte rolling was spontaneously present in all hindpaw venules of Lewis rats (diam 8-27 microns) and also in all mouse ear venules (Swiss, 13-38 microns; BALB/c, 12-56 microns). Rolling levels (in leukocytes/min, median and range) were 8 (3-15) in conscious rats, 9 (3-19) in anesthetized rats, 30 (5-160) in anesthetized Swiss mice, and 10 (3-22) in anesthetized BALB/c mice. These levels appeared to be independent of time. Noninvasive mechanical stimulation induced an average increase of 32%. Fluorescent labeling of leukocytes in vivo with acridine orange had no influence. In Swiss mice, the rolling velocity was < 50 microns/s for > 75% of the leukocytes (median 31 microns/s); this parameter did not correlate with reduced velocity (17-68 s-1) and hence wall shear rate. Our finding that leukocyte rolling is spontaneously present in skin venules of anesthetized and conscious animals suggests a constant vigilance of the host defense mechanisms in the skin.

Acridine Orange↗
PubMed2005

Pressure-induced leukocyte margination in lung postcapillary venules.

Although pressure elevation in lung postcapillary venules increases endothelial P-selectin expression, the extent to which P-selectin causes lung leukocyte margination remains controversial. To address this issue, we optically viewed postcapillary venules of the isolated blood-perfused rat lung by real-time fluorescence imaging. To determine leukocyte margination in single postcapillary venules, we quantified the fluorescence of leukocytes labeled in situ with rhodamine 6G (R6G). Although baseline fluorescence was sparse, a 10-min pressure elevation by 10 cmH(2)O markedly increased R6G fluorescence. Both stopping blood flow during pressure elevation and eliminating leukocytes from the perfusion blocked the fluorescence increase, affirming that these fluorescence responses were attributable to pressure-induced leukocyte margination. A P-selectin-blocking MAb and the L- and P-selectin blocker fucoidin each inhibited the fluorescence increase, indicating that P-selectin was critical for inducing margination. Time-dependent imaging of blood-borne fluorescent beads revealed reduction of plasma velocity during pressure elevation. After pressure returned to baseline, a similar reduction of plasma velocity, established by manually decreasing the perfusion rate, prolonged margination. Our findings show that in lung postcapillary venules, the decrease in plasma velocity critically determines pressure-induced leukocyte margination.

Animals↗
PubMed2002

Nonendothelial source of nitric oxide in arterioles but not in venules: alternative source revealed in vivo by diaminofluorescein microfluorography.

This study aimed to examine topographic distribution of microvascular NO generation in vivo. To this end, nitrosonium ion (NO+)-sensitive diaminofluorescein diacetate was superfused continuously on the rat mesentery and the fluorescence was visualized in the microvessels through laser confocal microfluorography. Two major sites exhibited a time-dependent elevation of the fluorescence: microvascular endothelia and mast cells. As judged by the fluorescence sensitivity to local application of different inhibitors of NO synthase (NOS), NO availability in arteriolar endothelium and mast cells appeared to be maintained mainly by NOS1, whereas that in venular endothelium greatly depends on NOS3. In venules, the magnitude of inhibitory responses elicited by the inhibitors was positively correlated with the density of leukocyte adhesion. NOS inhibitors significantly reduced, but did not eliminate, the NO+-associated fluorescence in arterioles, capillaries, and venules, suggesting alternative sources of NO in circulation for these microvessels. Immunohistochemistry for NOS isozymes revealed that NOS1 occurred not only in nerve fibers innervated to arterioles but also abundantly in mast cells. Laser flow cytometry of peritoneal cells in vitro revealed abundant expression of NOS1 in mast cells. Interestingly, NOS3 occurred in endothelia of capillaries and venules but not in those of distal arterioles with comparable diameters. These results suggest that the arterioles receive NO from nonendothelial origins involving NOS1 present in nerve terminals and mast cells, whereas venules depend on the endothelial NOS as a major source. Furthermore, nonenzymatic sources of NO from circulating reservoirs constitute a notable fraction throughout different classes of microvessels. The full text of this article is available at http://www.circresaha.org.

Animals↗
PubMed2005

Efficient recruitment of lymphocytes in inflamed brain venules requires expression of cutaneous lymphocyte antigen and fucosyltransferase-VII.

Lymphocyte migration into the brain represents a critical event in the pathogenesis of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). However, the mechanisms controlling the recruitment of lymphocytes to the CNS via inflamed brain venules are poorly understood, and therapeutic approaches to inhibit this process are consequently few. In this study, we demonstrate for the first time that human and murine Th1 lymphocytes preferentially adhere to murine inflamed brain venules in an experimental model that mimics early inflammation during EAE. A virtually complete inhibition of rolling and arrest of Th1 cells in inflamed brain venules was observed with a blocking anti-P-selectin glycoprotein ligand 1 Ab and anti-E- and P-selectin Abs. Th1 lymphocytes produced from fucosyltransferase (FucT)-IV(-/-) mice efficiently tethered and rolled, whereas in contrast, primary adhesion of Th1 lymphocytes obtained from FucT-VII(-/-) or Fuc-VII(-/-)FucT-IV(-/-) mice was drastically reduced, indicating that FucT-VII is critical for the recruitment of Th1 cells in inflamed brain microcirculation. Importantly, we show that Abs directed against cutaneous lymphocyte Ag (CLA), a FucT-VII-dependent carbohydrate modification of P-selectin glycoprotein ligand 1, blocked rolling of Th1 cells. By exploiting a system that allowed us to obtain Th1 and Th2 cells with skin- vs gut-homing (CLA(+) vs integrin beta(7)(+)) phenotypes, we observed that induced expression of CLA on Th cells determined a striking increase of rolling efficiency in inflamed brain venules. These observations allow us to conclude that efficient recruitment of activated lymphocytes to the brain in the contexts mimicking EAE is controlled by FucT-VII and its cognate cell surface Ag CLA.

Adjuvants, Immunologic↗
PubMed1999

C1-esterase inhibitor and its effects on endotoxin-induced leukocyte adherence and plasma extravasation in postcapillary venules.

BACKGROUND: C1-esterase inhibitor (C1-INH) has been shown to have beneficial effects in patients with sepsis. However, the microcirculatory effects of C1-INH during sepsis are unknown. This study investigated the influence of C1-INH on leukocyte-endothelial cell adhesion, vascular leakage, and venular microhemodynamics in postcapillary venules of rat mesentery during endotoxemia. METHODS: Thirty-two anesthetized Wistar rats randomly received 1 of 4 treatments: pretreatment with infusion of C1-INH in a concentration of 7.5 U.kg-1 body weight (C1-INH-7.5 group, n = 8) or in a concentration of 15 U.kg-1 body weight (C1-INH-15 group, n = 8) followed by continuous infusion of Escherichia coli lipopolysaccharide (LPS). The LPS group (n = 8) was pretreated with saline solution 30 minutes before LPS infusion. The control group (n = 8) received equivalent amounts of saline infusion. Leukocyte adherence, red blood cell velocity, and vessel diameters in postcapillary venules of rat mesentery were determined every 60 minutes during a period of 120 minutes using in vivo videomicroscopy. Vascular permeability was determined by measuring the extravasation of fluorescence-labeled albumin. Venular wall shear rate was calculated from mean red blood cell velocity and vessel diameter. RESULTS: LPS infusion induced a decrease in venular wall shear rate and an increase in leukocyte adherence and vascular permeability in postcapillary venules of rat mesentery. All microcirculatory disturbances were attenuated by pretreatment with C1-INH, showing no significant difference between the 2 concentrations. CONCLUSIONS: Pretreatment with C1-INH attenuates endotoxin-induced leukocyte adherence and macromolecular leakage in postcapillary venules of rat mesentery, indicating that complement inhibition might be a therapeutic tool in the treatment of sepsis.

Animals↗
PubMed2004

[Leukocyte adhesion to walls of the rat pial venules in normoxia and during brain ischemia].

With the help of contact optic system direct observations were carried out on leukocyte movements and on the acts of their adhesion to the inner surface of the walls of pial venules of the rats in normoxia and ischemia resulting from ligating two carotid arteries. After ligating the carotid artery and subsequent gradual development of ischemia, an abrupt increase in the number of the acts of adhesion to the walls of pial venules was shown to occur, the leukocytes adhere to each other inside the venules. A complete occlusion of venules and small veins results, which can be one of the reasons for the animal death in brain ischemia.

Animals↗
PubMed1992

Ultrastructural pathology of experimental autoimmune uveitis. Quantitative evidence of activation and possible high endothelial venule-like changes in retinal vascular endothelium.

BACKGROUND: Experimental autoimmune uveitis (EAU) is a highly organ-specific autoimmune disease in which the target is the retinal photoreceptors. It is well recognized as a model of uveoretinitis in humans. The mechanisms that control the homing of sensitized lymphocytes and other leukocytes to the retina is unknown. The aim of this study was to investigate changes in the retinal vasculature that may be involved with aiding leukocyte-endothelial cell interactions and subsequent extravasation of leukocytes into the retina. EXPERIMENTAL DESIGN: Lewis rats immunized with S-antigen were used to produce EAU. The retinal vasculature was assessed by morphologic (light and electron microscopy) and morphometric techniques at various stages in the generation and course of the disease (days 3, 7, 11, 14, 21, 28 and 49 postimmunization) for evidence of endothelial cell (EC) activation and leukocyte-EC interaction. Image analysis of the retinal vessels at the electron microscopic level was performed to detect alterations in the thickness and irregularity of the EC surface, both considered to be important in lymphocyte homing in the high endothelial venules (HEVs) of lymphoid tissues. Control values were obtained from normal eyes, pertussis-only treated animals, and normal lymph node HEVs. RESULTS: The clinical and histopathologic changes in the eyes were consistent with previous descriptions of EAU and included perivasculitis, focal mononuclear infiltrate in the outer retina, and choroid with destruction of the photoreceptor outer segments and eventually loss of large portions of the outer retina. During the course of EAU, a significant proportion of retinal venules underwent both qualitative and quantitative morphologic changes including EC activation evident as increased cytoplasmic organelles, a 230% average increase in mean EC thickness, and a concomitant 4-fold increase in irregularity of the EC, that produced plump irregular EC with deep intercellular clefts. These alterations were maximal at day 21, however from day 11 onward, large numbers of lymphocytes and monocytes were observed adhering to or lodged in the clefts of plump EC, migrating through the EC cytoplasm, or lying beneath the EC. CONCLUSIONS: The characteristics acquired by the retinal venules during EAU are reminiscent of HEVs. This study suggests that tissue-specific changes in the endothelial cells of retinal venules may be responsible for the homing of S-antigen specific autoreactive lymphocytes to the target organ in this model of retinal autoimmunity.

Animals↗
PubMed1991

Presence of nerve fiber collaterals from the sympathetic arteriolar plexus the concomitant venules in dog skeletal muscle.

Previous studies with the local 133Xenon washout method of the local regulation of blood flow in peripheral tissues in man gave evidence for a local veno-arteriolar sympathetic axon reflex which constricts arterioles when the venous transmural pressure is increased 25 mm Hg or more. The present study with the formaldehyde induced histofluorescence technique applied to skeletal muscle biopsies from dogs showed a dense plexus of noradrenergic sympathetic fibers around arterioles. Venules were generally devoid of these fibers. In certain instances sympathetic fibers left the arteriolar network to innervate the concomitant venule directly. Some of these fibers could be seen returning from the venule back to the arteriolar network. We suggest that the adrenergic fibers derived from the sympathetic plexus around the arterioles who innervate the venules can be the anatomical substrate for the local veno-arteriolar sympathetic axon reflex.

Adrenergic Fibers↗
PubMed1978

Penetration of colloidal carbon through post-capillary venules in lymph nodes and Peyer's patches of the guinea-pig: a potential immunogeneic route.

Colloidal carbon injected intravascularly provided a selective marker for post-capillary venules in lymph nodes and Peyer's patches. In the first few minutes a denticulate outline to the lumen was formed by carbon capping the high columnar epithelium and carbon particles were deeply embedded between endothelial cells. Ten minutes after injection carbon had reached the basement membrane and was lying outside this membrane 30 min later, at first free but later engulfed inside macrophages. Carbon was retained in post-capillary venules for the duration of the experiment (8 h). Discontinuities were present in the basement membrane in about one-fifth of venules, and lymphocyte and macrophage penetrating the basement membrane are demonstrated. It is postulated that carbon penetrates the post-capillary venular wall by increased intraluminal hydrostatic pressure arising from contraction of muscles that surrounded the lymphoid tissue in the case of the gut, or skeletal muscle compressing lymph nodes against a bony surface in the axilla, groin or neck. Secondly, if carbon is a model for particulate antigens, then post-capillary venules provide a potential immunogenic route whereby antigens can reach lymphoid tissues from the circulation, as proposed by Burwell (1962) for transplantation antigens.

Animals↗
PubMed1993

Fucoidin, but not yeast polyphosphomannan PPME, inhibits leukocyte rolling in venules of the rat mesentery.

Leukocyte rolling in venules is inhibited by several sulfated polysaccharides, by antibodies to the leukocyte adhesion receptor L-selectin (LECAM-1), and by recombinant soluble L-selectin. The sulfated fucose polymer fucoidin and the polyphosphomannan PPME bind to L-selectin and inhibit L-selectin-mediated lymphocyte adhesion to lymph node high endothelial venules (LN-HEV). We investigated whether fucoidin and PPME also inhibit leukocyte rolling. Rolling leukocyte flux was determined by intravital microscopy in 47 venules (diameter 21 to 50 microns) of the rat mesentery with and without micro-infusion of each reagent through 8-microns glass micropipettes. Micro-infusion (1 mg/mL) or intravenous (IV) injection (25 mg/kg) of fucoidin, but not vehicle, reduced leukocyte rolling by greater than 90%. The half-effective concentration was approximately 2.5 micrograms/mL. Stroboscopic fluorescence video microscopy showed that fucoidin decreased the fraction of rolling leukocytes from 44% of all leukocytes passing the venules in control to less than 1%. PPME micro-infusion (1 mg/mL) or IV injection (14 mg/kg) did not reduce leukocyte rolling. Hence, leukocyte rolling differs from lymphocyte homing with respect to the effect of PPME. This may be related to fucoidin binding to L-selectin with greater affinity than PPME. Alternatively, inflamed venular endothelium may express a ligand for L-selectin different from that constitutively expressed on LN-HEV.

Animals↗
PubMed1975

The postanatal development of high-endothelial venules in lymph nodes of mice.

The postnatal development of high-endothelial venules (HE-venules) in popliteal lymph nodes of normal and athymic mice was studied by light and electron microscopy. In the normal mice, undifferentiated postcapillary HEvenules are already present at birth. During the first four days after birth, ribosomes and mitochondria in the endothelial cells of the venules become more numerous, and the endoplasmic reticulum and in particular the Golgi complexes enlarge. At day four lymphocyte diapedesis through the venules becomes apparent. From the tenth day the HEvenules are structurally mature. However, diapedesis activity still increases till about a month postnatally. In mice with congenital aplasia of the thymus (nude mice) and in neonatally thymectomized mice the development of the HEvenules is similar to that in normal mice. In the athymic mice both lymphocytes and granulocytes migrate through the walls of the HEvenules. However, the blood level of lymphocytes in these mice is far below the value in normal mice. It is concluded that the development of the HEvenules during the first month of life is independent of the blood level of lymphocytes.

Animals↗
PubMed1985

A three-dimensional reconstruction of high endothelial venules in the mouse lymph node: an enzyme-histochemical study.

A three-dimensional reconstruction of high endothelial venules (HE-venules) of an entire mouse lymph node is presented. The reconstruction has been made by means of the histochemical technique for alpha-naphthylacetate esterase. The course of the HE-venules is shown in coherence with lymphocytic aggregates (follicles and unit), which were concomitantly reconstructed. Carbonic anhydrase, glutamate-, and alpha-glycerophosphate dehydrogenase were found in the high endothelia, while calcium-stimulated NA+, K+ ATP-ase and the acetylcholinesterase were localized to the endothelia and/or to the perivascular sheath of the HE-venules and submarginal capillaries.

Acetylcholinesterase↗
PubMed1986

Reactivity of rat pial arterioles and venules to adenosine and carbon dioxide: with detailed description of the closed cranial window technique in rats.

This study describes a closed cranial window technique that allows the observation and measurement of rat pial arterioles and venules in situ. The resolving power of this system is 1-2 microns. Using this sensitive technique, we characterized the responses to 7% carbon dioxide inhalation and adenosine in arterioles (10-70 microns) and venules (15-100 microns). During carbon dioxide inhalation, larger arterioles (greater than 40 microns) dilated more than smaller arterioles (less than 20 microns). There was limited vasoreactivity of pial venules during CO2 inhalation. Dilation of arterioles was initially observed with an adenosine concentration of 10(-8) M. Almost a twofold increase in diameter was noted at 10(-3) M. In contrast to the effect of CO2 inhalation, the degree of dilation with topical application of adenosine was not size dependent. Pial venules did not respond to adenosine. The technique for observation of pial vessels using the closed cranial window and for measurement of vessel diameter by video camera system microscopy is a powerful tool for studying in vivo the cerebral circulation in the rat.

Adenosine↗
PubMed2005

Histology and ultrastructure of the equine lingual tonsil. II. Lymphoid tissue and associated high endothelial venules.

The stratified squamous epithelium of the lingual tonsil of five young horses was infiltrated with CD4 and CD8 positive cells, which were very numerous in the crypt reticular epithelium along with macrophages and IgGb and IgA positive cells. Lymphoid follicles of the lamina propria mucosae consisted of a parafollicular area, corona and germinal centre. The parafollicular area was populated by large numbers of CD4 and CD8 positive lymphocytes as well as macrophages, inter-digitating cells, and a few B-lymphocytes. The germinal centre contained mainly IgGb and IgG(T) positive cells, plasma cells and small numbers of follicular dendritic cells, macrophages, CD4, CD8 and IgA positive cells. Some venules in the parafollicular and inter-follicular areas had features characteristic of high endothelial venules with irregular nuclei and cytoplasmic processes on the luminal surface. In addition to the normal cytoplasmic organelles, a novel vesiculo-vacuolar organelle was observed in small clusters toward the lateral, luminal and abluminal surfaces of these high endothelial venules. These vesiculo organelles along with their stomata and diaphragms, communicated with each other and with inter-endothelial clefts forming a structural basis for enhanced permeability and extravasation of macromolecules. The presence of lymphocytes in the high endothelial venules is consistent with transmural and inter-endothelial passage of these cells.

Animals↗
PubMed2001

Integrin binding to fibronectin and vitronectin maintains the barrier function of isolated porcine coronary venules.

Integrin-mediated endothelial cell-extracellular matrix adhesion plays a critical role in maintaining the structural integrity of microvascular walls. The aim of this study was to evaluate the impact of specific integrin extracellular domain binding to matrix fibronectin and vitronectin on the barrier function of intact microvascular endothelium. The apparent permeability coefficient of albumin was measured in isolated and perfused porcine coronary venules using a fluorescence ratioing technique with the aid of fluorescence microscopy. Inhibition of integrin binding to either fibronectin with GRGDdSP peptide or vitronectin with GPenGRGDSPCA peptide dose-dependently increased venular permeability by 2- to 3-fold. The effects were sustained for more than 60 min and were reversible upon clearance of the peptides. In contrast, the inactive control peptide GRADSP did not significantly affect venular permeability. Pretreatment of the venules with purified human fibronectin and vitronectin, respectively, prevented the hyperpermeability response to GRGDdSP and GPenGRGDSPCA. GRGDSP, a peptide that inhibits integrin binding to both fibronectin and vitronectin, produced an even higher permeability (4.5-fold) in venules than GRGDdSP or GPenGRGDSPCA alone, and the effect was blunted in vessels preincubated with both fibronectin and vitronectin. The results indicate the importance of integrin-matrix interaction in the physiological regulation of microvascular permeability. It is likely that both fibronectin and vitronectin binding to integrins contribute to the maintenance of endothelial barrier function in venules.

Animals↗
PubMed1975

Vascular endothelium-leukocyte interaction; sticking shear force in venules.

To determine the shear force acting on a white blood cell sticking to the endothelium of a blood vessel, the flow field about a single white blood cell in a venule was determined by hign-speed motion picture photomicrography. The force acting on the white blood cell was then calculated according to the principles of fluid mechanics. In this paper, the calculation was made using an experimentally determined dimensionless shear force coefficient obtained from a kinematically and dynamically similar model. The large physical model of the hemodynamic system could be easily instrumented, and the shear force acting on the model cell and the flow field around it were measured. The data were then used to calculate a shear force coefficient. On the basis of dynamic similarity, this shear force coefficient was applied to the white blood cell in the venule. The shear force coefficient was strongly influenced by the hematocrit, so in vivo hematocrits were measured from electron micrographs. It was found that in the venules of the rabbit omentum a white blood cell sticking to the endothelial wall was subjected to a shear force in the range of 4 times 10--5 dynes to 234 times 10--5 dynes; the exact value depended on the size and motion of the white blood cell, the size of the blood vessel, the velocity of the blood flow, and the local hematocrit, which varied between 20% and 40% in venules of about 40 mum in diameter. The contact area between the white blood cell and the endothelial cell was estimated, and the shear stress was found to range between 50 dynes/cm-2 and 1060 dynes/cm-2. The normal stress of interaction between the white blood cell and the endothelium had a maximum value that was of the same order of magnitude as the shear stress. The accumulated relative error of the experimental procedure was about 49%. The instantaneous shear force was a random function of time because of random fluctuations of the hematocrit.

Adhesiveness↗
PubMed1991

Dilatation of high endothelial venules in compartments of rat lymph nodes with abundant cortical mast cells.

Previous work has shown that the method of killing animals and of fixation of lymph nodes determines the appearance of high endothelial venules. Routine procedures produce a narrowing of the high endothelial venules whilst in situ fixation of lymph nodes results in their dilatation. More recently, routine procedures have demonstrated that lymph nodes from athymic and some euthymic ageing rats have occasional compartments in which the high endothelial venules are dilated in association with an increased population of cortical mast cells. These observations suggest that mast cell products may influence the physiological state of the high endothelial venules and affect the recruitment of blood lymphocytes.

Animals↗
PubMed1986

Evidence for endothelial cell-mediated regulation of macromolecular permeability by postcapillary venules.

Local application of inflammatory mediators to the hamster cheek pouch produces an immediate increase in the number of leaking postcapillary venules as observed by intravital light microscopy. Leaks are illuminated by using fluorescein-labeled dextran given i.v. before mediator challenge. All mediators that have been tested produce a similar pattern of vascular leakage exclusively from postcapillary venules. Mediators can be characterized by their effects on vascular permeability and whether they produce dilation (bradykinin, prostaglandins [PGs]) or constriction (leukotrienes [LTs]) of arterioles. The rank order potency for vascular leakage is LTs greater than bradykinin greater than histamine greater than PGs. A linear regression for the relation between dose of mediator and number of leaky venules has been shown for several mediators, e.g., bradykinin, histamine, and LTs. Inhibition of mediator-induced vascular leakage is produced by a wide variety of substances subsequent to a direct effect on the venular endothelial cell. Morphological, physiological, and pharmacological findings are consistent, and provide evidence for the regulation of macromolecular permeability by the endothelial cells in the postcapillary venules.

Adrenergic beta-Agonists↗