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Results for “Microvessels”

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At least 127 records · Page 7Linked to original sources

PubMed1998

Expression of thymidine phosphorylase in malignant ovarian tumors: correlation with microvessel density and an ultrasound-derived index of angiogenesis.

OBJECTIVE: The aim of this study was to determine whether the expression of thymidine phosphorylase by ovarian cancer cells correlates with the density of microvessels within the tumor, and with ultrasound-derived indices of blood flow. METHODS: Transvaginal ultrasonography with color Doppler imaging and pulsed Doppler spectral analysis was used to scan patients with an overt ovarian mass immediately before laparotomy. Sections of malignant tumors were analyzed for the cellular expression of thymidine phosphorylase and the intratumoral density of microvessels by immunohistochemistry using monoclonal antibodies to thymidine phosphorylase and factor VIII-related antigen, respectively. The main outcome measures were the histological classification of the tumor, the stage of the disease, whether or not the tumor cells were positive or negative for thymidine phosphorylase, the microvessel count and the peak systolic velocity (PSV). RESULTS: Forty-two tumors were studied (three of low malignant potential, 29 epithelial, four granulosa cell, two germ cell and four metastatic); 18 were stage I, six stage II, 11 stage III and three stage IV. Twenty-seven tumors (64%) were classified as thymidine phosphorylase-positive. The proportion of stage I tumors that was thymidine phosphorylase-positive (44%) was significantly lower (p = 0.022) than the corresponding value for stages II-IV (85%), but the values for microvessel count and PSV were similar. The microvessel count in thymidine phosphorylase-positive tumors was significantly higher than in thymidine phosphorylase-negative tumors (p = 0.005). Similarly, the PSV was significantly higher in thymidine phosphorylase-positive tumors (p = 0.009). There was a significant correlation between the microvessel count and the PSV (r = 0.354, p = 0.022). CONCLUSIONS: The expression of thymidine phosphorylase by malignant tumor cells is associated with an increase in microvessel density and PSV in patients with ovarian cancer.

Adolescent↗

PubMed2005

Vascular endothelial growth factor expression and microvessel parameters of colonic mucosa correlate with sensitivity to steroid in patients with ulcerative colitis.

OBJECTIVE: Vascular endothelial growth factor (VEGF) expression and microvessel parameters have not yet been quantified in the colonic mucosa of ulcerative colitis (UC). The aim of this study was to correlate the parameters with clinical responsiveness to steroid therapy. MATERIAL AND METHODS: Colorectal biopsy specimens from 39 UC patients with high sensitivity to steroid (H-UC), 9 UC patients with low sensitivity to steroid (L-UC) and 6 normal controls (NC) were examined. METHODS: Tissue sections were immunostained with anti-VEGF antibody for number of inflammatory cells (/mm(2)), VEGF-positive cell (/mm(2)) and VEGF-positive ratio (%), and with CD34 for microvessel counts (/mm(2)) and the mean microvessel diameter (microm). RESULTS: The H-UC group had a significantly larger total cell count (10,048+/-2751, p<0.0001) or VEGF-positive cells (2363+/-707, p<0.0001) than the NC group (7235+/-2088 or 1537+/-297, respectively) with no difference in VEGF-positive ratio (24.3+/-6.9 for H-UC versus 22.7+/-6.9 for NC). The L-UC group had a significantly lower VEGF-positive cell count (1420+/-701, p<0.0005) or VEGF-positive ratio (11.6+/-5.5, p<0.0005) than the H-UC group, whereas microvessel counts were almost constant regardless of the subject groups (345+/-7 0 for NC versus 346+/-99 for H-UC versus 349+/-114 for L-UC). Significant increases in microvessel diameter were seen when comparing NC (6.68+/-0.60) with H-UC (7.83+/-1.09, p<0.0001) and H-UC with L-UC (9.05+/-1.70, p<0.03). Out of the five parameters, VEGF-positive ratio and microvessel diameter had a predictive value for L-UC with an 88.9% sensitivity and 88.9% specificity. CONCLUSIONS: L-UC was characterized either as VEGF underexpression or enlarged microvessel. The disruption of the healing process or disturbance of microcirculation may be involved in low sensitivity to steroid therapy in UC.

Adrenal Cortex Hormones↗

PubMed1999

Activated microvessels express vascular endothelial growth factor and integrin alpha(v)beta3 during focal cerebral ischemia.

Both vascular endothelial growth factor (VEGF) and integrin alpha(v)beta3 play roles in angiogenesis. In noncerebral vascular systems, VEGF can induce endothelial integrin alpha(v)beta3 expression. However, it is unknown whether VEGF, like integrin alpha(v)beta3, appears in the initial response of microvessels to focal brain ischemia. Their coordinate expression in microvessels of the basal ganglia after middle cerebral artery occlusion (MCAO) in the nonhuman primate model was examined quantitatively. Cells incorporating deoxyuridine triphosphate (dUTP+) by the polymerase I reaction at 1 hour (n = 3), 2 hours (n = 3), and 7 days (n = 4) after MCAO defined the ischemic core (Ic) and peripheral regions. Both VEGF and integrin alpha(v)beta3 were expressed by activated noncapillary (7.5- to 30.0-microm diameter) microvessels in the Ic region at 1 and 2 hours after MCAO. At 7 days after MCAO, the number of VEGF+, integrin alpha(v)beta3+, or proliferating cell nuclear antigen-positive microvessels had decreased within the Ic region. The expressions of VEGF, integrin alpha(v)beta3, and proliferating cell nuclear antigen were highly correlated on the same microvessels using hierarchical log-linear statistical models. Also, VEGF and subunit alpha(v) messenger ribonucleic acids were coexpressed on selected microvessels. Here, noncapillary microvessels are activated specifically early during a focal cerebral ischemic insult and rapidly express VEGF and integrin alpha(v)beta3 together.

Animals↗

PubMed1990

Pericyte degeneration and thickening of basement membranes of cerebral microvessels in complex partial seizures: electron microscopic study of surgically removed tissue.

Complex partial seizures are associated with alterations in regional cerebral blood flow in abnormally spiking foci, as shown by positron emission tomography and single photon emission computed tomography, with an increase in flow ictally and a decrease interictally. Alterations of vasoregulation during ictal periods have also been described in animal seizure models. An electron microscopic study on human brain tissue from seven patients undergoing resections for the treatment of intractable complex partial seizures was performed to examine ultrastructural changes of the microvasculature and their locations within the microvessel wall. Biopsies were obtained intraoperatively from temporal lobe regions with electrocorticographically detected abnormal spiking and from regions without abnormality on electrocorticograms (control samples) removed as part of the therapeutic resection. A total of 539 microvessels from three regions were evaluated: spiking mesial temporal lobe, spiking lateral temporal cortex, and nonspiking (control) cortex. Evidence of pericyte degeneration (aggregates of cellular debris within the basement membrane) was noted in the majority of spiking area microvessels (76.7% in spiking mesial temporal cortex; 69.8% in spiking lateral temporal cortex) as compared with 37.8% of control microvessels (P less than 0.0005). Morphometric studies revealed a significant increase in total wall thickness, pericyte-basement membrane unit thickness, pericyte cytoplasmic density, basement membrane density, and basement membrane thickness in microvessels from spiking (mesial and lateral temporal cortex), as compared to control areas (P less than 0.01). No statistically significant difference was noted in pericyte coverage or pericyte or endothelial mitochondrial densities between microvessels in spiking and control regions. This study shows degeneration of pericytes, cells thought to play an essential role in microvascular hemodynamics, and thickening of microvessel walls in abnormally spiking brain regions in patients with intractable complex partial seizures. The pericyte degeneration and basement membrane thickening in abnormally spiking areas may explain alterations in vasoregulation, by a decrease in the microvascular compliance and in cross-capillary diffusion.

Adult↗

PubMed2000

Immunohistochemical measurement of tumor vascular endothelial growth factor in breast cancer. A more reliable predictor of tumor stage than microvessel density or serum vascular endothelial growth factor.

Microvessel density counting is commonly proposed as a method of assessing angiogenesis. However, results have been difficult to reproduce because of many methodological inconsistencies. Vascular endothelial growth factor (VEGF), an angiogenic regulator, is also a poor prognostic indicator in breast cancer, correlating in many studies with microvessel density. In this study, VEGF and microvessel density counting were examined as methods of assessing angiogenesis in breast cancer and correlated with tumor stage. A representative tumor section was stained with anti-CD34 and anti-VEGF. Microvessel density was evaluated using the manual "hot-spot" procedure and a semiquantitative image analysis system. Serum VEGF levels were available from an additional nine patients. Results were analyzed using Kendall's tau correlation. Tumor stage correlated with tumor VEGF, but not with microvessel "hot-spot" or vessel counts. There was no correlation between scores obtained from the manual or semiquantitative methods. Serum VEGF did not correlate with either tumor VEGF or tumor stage. The prognostic importance of VEGF in invasive breast cancer is associated with tumor stage. Measurement of tumor VEGF, as an indicator of angiogenesis, is more reliable prognostically than measurement of microvessel density or serum VEGF. Routine measurement of microvessel density in breast cancer is less reliable.

Adult↗

PubMed1998

Evaluation of the prognostic significance of microvessel count and tumor size in renal cell carcinoma.

BACKGROUND: We analyzed the significance of tumor microvessel count and tumor size as prognostic factors for renal cell carcinoma (RCC). METHODS: T criteria (local invasion), M criteria (distant metastasis), macrovenous invasion, histological grade, cell type, tumor size, and tumor microvessel count were investigated as prognostic factors in 62 patients with RCC. Microvessel density was evaluated by immunohistochemical staining of the endothelial cells. RESULTS: No significant correlation was found between tumor size and the other prognostic factors. Analysis of the survival rate based on tumor size revealed that patients with a small tumor tended to show a good prognosis, but no significant difference was found in the prognosis between medium-sized and large-sized tumor groups. Analysis of all patients revealed that M criteria, macrovenous invasion, cell type and microvessel count were significant factors and that in 37 patients with low-stage tumors, the only significant prognostic factor was microvessel count (P=0.003). CONCLUSION: Tumor size cannot be readily justified as a determinant of prognosis in patients with medium- or large-sized tumors. In patients with low-stage tumors, microvessel count served as the only significant determinant for prognosis. When the patients were considered as a whole, microvessel count, M criteria, macrovenous invasion and histological grade were significant prognostic factors.

Adult↗

PubMed1987

Blood-brain barrier monoamine oxidase: enzyme characterization in cerebral microvessels and other tissues from six mammalian species, including human.

We studied the enzyme monoamine oxidase (MAO) in isolated cerebral microvessels, and in mitochondria-enriched brain and liver preparations from six mammalian species, including human. We also studied MAO distribution in various tissues and in discrete brain regions of the rat. MAO was assessed by measuring the specific binding of [3H]pargyline, an irreversible MAO inhibitor, and the rates of oxidation of known MAO substrates: benzylamine, tyramine, tryptamine, and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Molecular forms of MAO were examined by using specific MAO inhibitors, and by polyacrylamide gel electrophoresis after [3H]pargyline binding. In general, the liver from all species had higher MAO levels than the brain, with minor variation among species in their brain and liver MAO content. However, there were remarkable species differences in brain microvessel MAO, with rat microvessels having one of the highest MAO activity among all tissues, whereas MAO activities in brain microvessels from humans, mice, and guinea pigs were very low. In most rat tissues, including the brain, there was a preponderance of MAO-B over MAO-A. The only exceptions were the heart and skeletal muscle. Estimates of MAO half-life in rat brain microvessels, rat brain, and rat liver indicated that microvessel MAO had a higher turnover rate. The reasons underlying the remarkable enrichment of rat cerebral microvessels with MAO-B are unknown, but it is evident that there are marked species differences in brain capillary endothelium MAO activity. The biological significance of these findings vis a vis the role of MAO as a "biochemical blood-brain barrier" that protects the brain from circulating neurotoxins and biogenic amines should be investigated.

Adult↗

PubMed1984

Diabetes-induced alterations of glucose metabolism in rat cerebral microvessels.

The effect of diabetes on the metabolism of glucose and lactate was examined in isolated rat cerebral microvessels. In rats with diabetes induced with streptozotocin, glucose oxidation to CO2 by the microvessels was decreased by 54-83% and its conversion to lactate by 21-61%. Insulin therapy for several days or starvation for 48 h both lowered blood glucose levels in the diabetic rats and restored microvessel glucose metabolism to normal. Cerebral microvessels consist principally of the capillaries that constitute the blood-brain barrier. Direct assessment of the blood-brain barrier in vivo using the brain uptake index (BUI) technique revealed a close parallel to the findings in the microvessels. Thus, hexose transport was diminished in diabetic rats and restored to normal by both insulin therapy and starvation. The oxidation of [1-14C]lactate to CO2 like that of glucose was depressed in microvessels of diabetic rats. In contrast to glucose, however, the transport of lactate across the blood-brain barrier in vivo was not altered. These findings suggest that diabetes suppresses glucose metabolism in rat cerebral microvessels and downregulates glucose transport across the blood-brain barrier. They also suggest that both of these processes are regulated by chronic alterations in blood glucose concentration rather than by insulin per se.

Animals↗

PubMed2006

Leukocyte-platelet aggregate adhesion and vascular permeability in intact microvessels: role of activated endothelial cells.

Leukocyte-platelet aggregation and aggregate adhesion have been indicated as biomarkers of the severity of tissue injury during inflammation or ischemic reperfusion. The objective of this study is to investigate the mechanisms of the aggregate adhesion and quantitatively evaluate its relationship with microvessel permeability. A combined autologous blood perfusion with single microvessel perfusion technique was employed in rat mesenteric venular microvessels. The aggregate adhesion was induced by systemic application of TNF-alpha plus local application of platelet-activating factor (PAF). Changes in permeability were determined by measurements of hydraulic conductivity (Lp) before and after aggregate adhesion in the same individually perfused microvessels. The compositions of the adherent aggregates were identified with fluorescent labeling and confocal imaging. In contrast to leukocyte adhesion as single cells resulting in no increase in microvessel permeability, aggregate adhesion induced prolonged increases in microvessel Lp (6.1 +/- 0.9 times the control, n = 9) indicated by the initial Lp measurements after 3 h of blood perfusion, which is distinct from the transient Lp increase caused by PAF-induced endothelial activation in the absence of blood. Isoproteronol (Iso) attenuated aggregate adhesion-mediated Lp increases if applied after autologous blood perfusion and prevented the aggregate adhesion if the initial endothelial activation is inhibited by applying Iso before PAF administration but showed less effect on single leukocyte adhesion. This study demonstrated that leukocyte-platelet aggregate adhesion via a mechanism different from that of single leukocyte adhesion caused a prolonged increase in microvessel permeability. Our results also indicate that the initial activation of endothelial cells by PAF plays a crucial role in the initiation of leukocyte-platelet aggregate adhesion.

Adrenergic beta-Agonists↗

PubMed1989

Adrenergic receptors on cerebral microvessels: pericyte contribution.

R224-R230, 1989.--[125I]iodocyanopindolol ([125I]ICYP) and [3H]rauwolscine were used to quantitate, respectively, the beta- and alpha 2-adrenergic receptors in freshly isolated bovine cerebral microvessels and in pericyte cultures derived from these microvessels. Morphological and immunocytochemical criteria distinguished the pericytes from endothelial cells. Competitive binding studies established the specificity of the radioligand binding. The maximal number of binding sites (Bmax) for [125I]ICYP in the pericytes constituted only 8% of that in the microvessels (3.5 +/- 1.3 vs. 44.4 +/- 6.6 fmol/mg protein). In contrast, the Bmax for [3H]rauwolscine in the pericytes was 50% of that in the microvessels (55.4 +/- 11.8 vs. 111.1 +/- 9.5 fmol/mg protein). The dissociation constants for both [125I]ICYP and [3H]rauwolscine were similar in the two preparations. No alpha 1-adrenergic receptors, as defined by the specific binding of [3H]prazosin, were identified either in the pericytes or microvessels. Overall, our results suggest that pericytes contribute minimally to the total beta-adrenoceptor number of cerebral microvessels, and thus the beta-adrenoceptors must be located predominantly on endothelial cells. However, the contribution of pericytes to the total alpha 2-adrenoceptor number of the microvessels may be substantial.

Animals↗

PubMed2006

Computer-assisted analysis of biopsy specimen microvessels predicts the outcome of esophageal cancers treated with chemoradiotherapy.

PURPOSE: A computer-assisted microvessel analysis system was developed to evaluate correlations between the architecture of biopsy specimen microvessels and the outcome for patients with esophageal cancer treated with chemoradiotherapy. EXPERIMENTAL DESIGN: Biopsy specimens from 51 patients with esophageal cancer (T(2-3), any N, M0) treated with chemoradiotherapy were immunostained with an anti-CD31 antibody and quantified using computerized image analysis. We evaluated the association of several microvessel factors with overall survival, including the ratio of total microvessel perimeter to total tumor area (TP/TA), the tumor hypoxic ratio, and the ratio of total microvessel number to total tumor area (TN/TA). Results from traditional manual microvessel density (MVD) hotspot count and computerized hotspot count were compared and the relation between hotspot MVD count and survival rate was evaluated. RESULTS: The median follow-up time was 32 months. Both univariate and multivariate analyses revealed that computer-counted hotspot MVD and TN/TA and TP/TA ratios correlated significantly with the outcome of chemoradiotherapy. Kaplan-Meier survival curves showed that patients with high computer-counted hotspot MVDs and high TN/TA and TP/TA ratios had better overall survival rate than patients with low MVDs or ratios (P = 0.025, 0.008, and 0.031, respectively). Combining computer-counted MVD or TN/TA ratio with TP/TA ratio proved more predictive than any single factor. Two researcher-counted hotspot MVDs had no significant relation with outcome. CONCLUSION: Computer-assisted tumor microvessel analysis is a powerful tool in predicting the outcome for patients with esophageal cancer treated with chemoradiotherapy because intraobserver and interobserver variability is minimized.

Adult↗

PubMed2004

Hypercholesterolemia impairs transduction of vasodilator signals derived from ischemic myocardium: myocardium-microvessel cross-talk.

OBJECTIVE: Coronary microvessels are functionally coupled to the myocardial metabolic state. In hypercholesterolemia, the coronary vascular dysfunction extends to microvascular levels. We hypothesized that the vasodilator signal transduction from ischemic heart is impaired in the coronary microvascular wall of hypercholesterolemia. METHODS AND RESULTS: Rabbits were fed with normal chow (control group) or 2% high-cholesterol diet (hypercholesterolemia group) for 8 weeks. Coronary microvessels isolated from rabbit hearts were pressurized and gently placed on a beating canine heart. Myocardial ischemia was produced in the beating heart and the diameter of the isolated microvessel was observed using an intravital microscope with a floating objective. In control group, the isolated microvessels significantly dilated 2 minutes after the onset of ischemia, and a plateau was observed at 10 minutes. In contrast, the microvessels from hypercholesterolemia group did not dilate during ischemia. Dihydroethidium fluorescence microscopy revealed an elevated superoxide level in the microvessels of hypercholesterolemia group. The application of tiron (free radical scavenger) significantly dilated the isolated microvessels only from hypercholesterolemic animals. CONCLUSIONS: We conclude that the transduction of vasodilator signals derived from ischemic myocardium is impaired in the coronary microvascular wall of hypercholesterolemia. Enhanced oxidative stress in hypercholesterolemia may alter the microvascular function.

Acetylcholine↗

PubMed1996

Regulation of nitric oxide production in human coronary microvessels and the contribution of local kinin formation.

BACKGROUND: The goal of this study was to define the regulation of nitric oxide release by coronary microvessels from the failing and nonfailing human heart and to determine the role of local kinin production in the elaboration of nitric oxide by human coronary microvascular endothelium. METHODS AND RESULTS: Ten hearts from humans with end-stage heart failure and two hearts from patients without heart failure were harvested at the time of orthotopic cardiac transplantation. Microvessels were sieved and the production of nitrite was determined by the Griess reaction. Microvessels were incubated in the presence of agonists for nitric oxide production (acetylcholine and bradykinin), which caused dose-dependent increases in nitrite, a response that was blocked by NG-nitro-L-arginine methyl ester and receptor-specific antagonists (atropine and HOE 140, respectively). In addition, the production of nitrite by microvessels from the failing heart appeared to be less than that produced by microvessels from the nonfailing heart. Incubation with norepinephrine or the alpha2-adrenergic agonist BHT 920 also caused dose-dependent increases in nitrite production, which were blocked by the B2-receptor antagonist HOE 140. This implicated local kinin synthesis as an intermediate step in the production of nitric oxide in response to alpha2-adrenoceptor stimulation. The production of nitric oxide was also prevented by the addition of serine protease inhibitors, which blocked the action of local kallikrein, again suggesting a role for local kinin synthesis. CONCLUSIONS: Our results indicate that nitric oxide is produced by human coronary microvessels, that nitric oxide production may be reduced but certainly not increased in microvessels from the failing human heart, and that there is active local kinin generation in these blood vessels.

Adult↗

PubMed1981

Sites of prostaglandin synthesis in the bovine heart and isolated bovine coronary microvessels.

Metabolically active coronary microvessels (generally less than 100 micrometers in diameter) were isolated from bovine hearts. These preparations were virtually free of contaminating myocytes and consisted of a mixture of arterioles, venules, capillaries, and collagen fibers. The prostaglandin biosynthetic capacity of isolated coronary microvessels was assessed by quantitating conversion of 14C-arachidonic acid and 14C-prostaglandin endoperoxide (PGH2) to prostaglandins. Coronary microvessels were found to exhibit low cyclooxygenase activity, i.e., minimal conversion (less than 1%) of arachidonic acid (AA) to prostaglandins when compared with either the coronary artery (3.6% conversion of AA) or coronary vein (3.3%). Isolated myofibril fractions demonstrated virtually no cyclooxygenase activity (less than 0.1%). Two enzymatic endoperoxide metabolizing activities were evident in the microvessels, prostacyclin synthetase and PGE isomerase. When compared on a microsomal protein basis, the coronary artery exhibited higher prostacyclin synthetase activity than the microvessels but was devoid of PGE isomerase activity. In contrast, whereas PGE isomerase activity was detectable in the coronary vein, the activity was lower than that of the microvessels; further, it could not be demonstrated in the other myocardial fractions. A glutathione-enhanced PGD-forming activity was present in high speed supernatants derived from the coronary artery and vein preparations, but was not present in the coronary microvessel or isolated myofibril fractions. From these studies we conclude that (1) the major source of prostaglandins released into the coronary circulation is the coronary vasculature, and (2) the resistance elements of the coronary circulation differ from the larger elements (i.e., arteries and veins) in the enzymes of the prostaglandin biosynthetic pathway present and thus in the nature and perhaps quantity of prostaglandins biosynthesized.

Animals↗

PubMed1992

A method for measuring the rate of oxygen release from single microvessels.

A system determining the rate of oxygen release from erythrocytes flowing in single microvessels was constructed with an inverted microscope by connecting 1) a scanning/grating spectrophotometer equipped with a photon-counting detector through a thin light guide, to obtain the visible absorption spectrum of a spot (5 microns in diameter) focused on a microvessel, 2) two photomultipliers (connected to a microcomputer via an analog-to-digital converter) through two light guides, to determine the flow velocity of erythrocytes by calculating the cross correlation between the light-intensity changes of two spots (3 microns in diameter, 5 microns apart from each other) focused on the microvessel, and 3) an image processor through a video camera, to estimate the diameter of microvessel from the digitized video images. The rate of oxygen release from single microvessels 7-25 microns in diameter in rat mesentery was measured under the superfusion of deoxygenated solution: 1) The maximal rate was obtained in capillaries, and the rate in arterial microvessels was larger than that in venous microvessels, when similar diameters were compared. 2) The rate was maximum at pH 7.0-7.2, and it decreased in more acidic and alkaline pH values. 3) The rate decreased with a decrease in temperature. The reliability of the measurement using the present apparatus was tested in detail.

Animals↗

PubMed2003

Influence of contrast ultrasonography with perflutren lipid microspheres on microvessel injury.

Microbubbles have been reported to enhance ultrasound (US)-related side effects in animal systems. The present study investigated the influence of contrast ultrasonography (US) with perflutren lipid microspheres, a recently developed second-generation contrast agent, on microvessels. Rat mesentery was exposed to 1.8-MHz pulsed US with intravenous injection of perflutren (0.1 or 1.0 ml/kg) or Levovist (300 mg/kg), and the microvessel bleeding and endothelial cell injury was examined. Impaired endothelial cells were identified by the fluorescence of propidium iodide. Microvessel bleeding was examined also in the rat myocardium. The interaction between 0.1 ml/kg of perflutren and US exposure did not cause microvessel bleeding, and did not increase endothelial cell injury compared with the sham operation, unless frequent, strong US exposure occurred. When the dose was increased to 1.0 ml/kg, the combination of perflutren and US exposure resulted in capillary bleeding and increased endothelial cell injury in capillaries and venules (p<0.01). However, the incidence of microvessel bleeding and endothelial cell injury did not exceed that with Levovist microbubbles. In the myocardium, microvessel bleeding was not observed under any conditions. In conclusion, perflutren lipid microspheres enhanced US-related microvessel injury as with other contrast agents at the dose of 1.0 ml/kg, but not with 0.1 ml/kg and the appropriate US setting.

Animals↗

PubMed2001

Blood flow structure related to red cell flow: determinant of blood fluidity in narrow microvessels.

The review article deals with phenomena of the blood flow structure (structuring) in narrow microvessels-capillaries and the adjacent arterioles and venules. It is particularly focused on the flow behavior of red blood cells (RBCs), namely, on their specific arrangements of mutual interaction while forming definite patterns of self-organized microvascular flow. The principal features of the blood flow structure in microvessels, including capillaries, include axial RBC flow and parietal plasma layer, velocity profile in larger microvessels, plug (or bolus) flow in narrow capillaries, and deformation and specific behavior of the RBCs in the flow. The actual blood flow structuring in microvessels seems to be a most significant factor in the development of pathological conditions, including arterial hypertension, brain and cardiac infarctions, inflammation, and many others. The blood flow structuring might become a basic concept in determining the blood rheological properties and disorders in the narrow microvessels. No solid theoretical (biorheological) basis of the blood flow structuring in microvessel has been found, but in the future it might become a foundation for a better understanding of the mechanisms of these properties under normal and pathological conditions in the narrowest microvessels 5 to 25 microm large. It is also a topic for further biorheological research directed to find the background of actual physiopathological phenomena in the microcirculation.

Animals↗

PubMed1995

Visualization of endothelial clefts and nuclei in living microvessels with combined reflectance and fluorescence confocal microscopy.

OBJECTIVE: The cellular basis for spatial heterogeneity along postcapillary venules in their response to inflammatory mediators is not understood. To study permeability regulatory processes on an individual cell basis in intact microvessels, we developed methods to delineate individual endothelial cells within living, single perfused microvessels. METHODS: Individual postcapillary microvessels in the mesenteries of frogs and hamsters were perfused with chloride-free Ringer's solutions containing AgNO3 (0.1 g per 100 ml) for 5--10 s. Vessels were immediately flushed with Ringer's solution containing serum albumin and some vessels subsequently perfused with the fluorescent nucleic acid stain YO-PRO-1 (1 microM) for 10-15 min. Vessels were imaged in situ using laser scanning confocal microscopy. A reflectance image from silver precipitate in the endothelial clefts and a fluorescence image of the nuclei were simultaneously recorded. Stacks of confocal images were merged and used to reconstruct the three-dimensional orientation of endothelial cells. Hydraulic conductivity of some frog mesenteric venular vessels, measured before and after perfusion with AgNO3, was used to assess the integrity of the vessels. RESULTS: The endothelial cell clefts were delineated with a very fine, readily imaged precipitate of silver. Hydraulic conductivity measured after AgNO3 perfusion in frog mesenteric venular microvessels was not significantly different from control. Vessels showed a slight reduction in reactivity to inflammatory stimuli. The three-dimensional pattern of endothelial cells in the living vessels was imaged. CONCLUSIONS: Combining confocal microscopy with silver staining in single perfused microvessels was shown to be an effective means to delineate the three-dimensional pattern of endothelial cells forming microvessel walls. It enables further study of the vascular structure and function relationships at the individual cell level in intact microvessels.

Animals↗