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PubMed1979

Studies on the enzymatic blood-brain barrier: quantitative measurements of DOPA decarboxylase in the wall of microvessels as related to the parenchyma in various CNS regions.

The presence of DOPA decarboxylase in cerebral microvessels (capillaries and venules) impedes the passage of circulating amine precursors into the brain. The relative amount of DOPA decarboxylase in this trapping mechanism as compared to the parenchyma per se was estimated in various CNS regions, measuring the formation of dopamine from L-DOPA in vitro or in vivo in two experimental models on rats and rabbits: (1) On the basis of the treatment with a peripheral decarboxylase inhibitor (carbidopa, which inhibits also microvascular DOPA decarboxylase in the CNS) it could be calculated that the enzyme in the microvessels of the caudate nucleus (rich in catecholamine nerve terminals), cerebellum (poor in catecholamine nerves), and spinal cord comprised 25, 91 and 79 per cent, respectively, of the total enzyme activity. (2) Measurement of dopamine formation in the spinal cord following transection at the midthoracic level (which causes degeneration of the catecholamine neurons caudal to the lesion since they are all descending) indicated that a similar fraction as found in the carbidopa model, 71%, of the total tissue decarboxylase activity resided in the microvessel walls. The results show that a considerable portion of tissue decarboxylase in the CNS is present in the microvessel walls, where it represents part of an enzymatic blood-brain barrier mechanism.

Animals↗

PubMed2003

Enhancement of microvessel tortuosity in the vastus lateralis muscle of old men in response to endurance training.

Muscle microvascularization is usually quantified in transverse sections, in absolute terms (capillaries around fibres, CAF, or capillary-to-fibre ratio, C/F) or as CAF related to fibre area (CAF/area, CAFA). The capillary-to-fibre perimeter exchange ratio (CFPE) has been introduced in order to assess the role of the capillary-to-fibre interface in resistance to O(2) diffusion. The ratio between the length of capillaries in contact with fibres and fibre perimeter (LC/PF) has also been used as an index for capillary tortuosity. The possibility of change in capillary tortuosity with endurance training was not considered in previous studies. Consequently, this study investigated the effect of 14 weeks of endurance training on muscle microvascularization, including microvessel tortuosity, in 11 elderly men (8th decade). Microvessels were analysed using the CD31 antibody. Together with the significant increase in peak oxygen exchange and citrate synthase activity, there was a significant increase in C/F. While CFPE and CAFA remained unchanged, an important finding was the clear increase in LC/PF (56%; P < 0.001) for a same sarcomere length. We also found a strong correlation between oxidative enzyme activity and LC/PF both before and after training. These results indicate that endurance training induces significant remodelling in the microvessel network in elderly men and that an increase in the degree of microvessel tortuosity would be an important mechanism of adaptation to endurance training.

Aged↗

PubMed2004

An electrodiffusion-filtration model for effects of endothelial surface glycocalyx on microvessel permeability to macromolecules.

Endothelial surface glycocalyx plays an important role in the regulation of microvessel permeability by possibly changing its charge and configuration. To investigate the mechanisms by which surface properties of the endothelial cells control the changes in microvessel permeability, we extended the electrodiffusion model developed by Fu et al. [Am. J. Physiol. 284, H1240-1250 (2003)], which is for the interendothelial cleft with a negatively charged surface glycocalyx layer, to include the filtration due to hydrostatic and oncotic pressures across the microvessel wall as well as the electrical potential across the glycocalyx layer On the basis of the hypotheses proposed by Curry [Microcirculation 1(1): 11-26 (1994)], the predictions from this electrodiffusion-filtration model provide a good agreement with experimental data for permeability of negatively charged a-lactalbumin summarized in Curry [Microcirculation 1(1), 11-26 (1994)] under various conditions. In addition, we applied this new model to describe the transport of negatively charged macromolecules, bovine serum albumin (BSA), across venular microvessels in frog mesentery. According to the model, the convective component of the albumin transport is greatly diminished by the presence of a negatively charged glycocalyx under both normal and increased permeability conditions.

Animals↗

PubMed2005

Determination of microvessel permeability and tissue diffusion coefficient of solutes by laser scanning confocal microscopy.

Interstitium contains a matrix of fibrous molecules that creates considerable resistance to water and solutes in series with the microvessel wall. On the basis of our preliminary studies, by using laser-scanning confocal microscopy and a theoretical model for interstitial transport, we determined both microvessel solute permeability (P) and solute tissue diffusion coefficient (D) of alpha-lactalbumin (Stokes radius 2.01 nm) from the rate of tissue solute accumulation and the radial concentration gradient around individually perfused microvessel in frog mesentery. P(alpha-lactalbumin) is 1.7 +/- 0.7(SD) x 10(-6) cm/s (n = 6). D(t)/D(free) for alpha-lactalbumin is 27% +/- 5% (SD) (n = 6). This value of D(t)/D(free) is comparable to that for small solute sodium fluorescein (Stokes radius 0.45 nm), while p(alpha-lactalbumin) is only 3.4% of p(sodium fluorescein). Our results suggest that frog mesenteric tissue is much less selective to solutes than the microvessel wall.

Animals↗

PubMed2006

Dynamic MR imaging of breast lesions: correlation with microvessel distribution pattern and histologic characteristics of prognosis.

PURPOSE: To evaluate the association of dynamic enhancement parameters of benign and malignant breast lesions at magnetic resonance (MR) imaging with microvessel distribution and histologic prognostic tumor characteristics. MATERIALS AND METHODS: Regional review board approval and informed consent were obtained. Surgical resection specimens of breast lesions (32 benign, 86 malignant) in 118 patients (age range, 28-86 years; mean, 58 years) who had undergone dynamic T1-weighted MR imaging of both breasts were included in the study. Different MR enhancement parameters and microvessel density (MVD) distribution were determined. In malignant lesions, TNM stage, tumor grade, proliferative activity, and hormone receptor expression were determined. Spearman correlation coefficients; Wilcoxon, Fisher exact, Kruskal Wallis, and chi(2) tests; and logistic regression analysis were used for evaluation. RESULTS: Malignant lesions exhibited a higher ratio of microvessels in tumor periphery versus tumor center than did benign lesions (P < .0005). High vessel ratios (P = .001) and low central vessel numbers (P = .007) were associated with high tumor grade. In malignant lesions, initial enhancement ratios of periphery to center of lesion correlated with the corresponding microvessel ratios (r = 0.61). Yet, a high peripheral MVD was not associated with strong peripheral enhancement (r = -0.09). High enhancement ratios, washout rates, and early enhancement peaks were associated with unfavorable, albeit not significant, prognostic indicators. Visible rim enhancement was the most accurate prognostic enhancement criterion for estrogen receptor status (P = .007), tumor grade (P = .06), and lymph node status (P = .046). Washout was the best discriminating criterion for proliferative activity. CONCLUSION: The different enhancement behaviors of malignant and benign breast lesions cannot be explained by MVD alone; however, a low MVD in the center of carcinoma is reflected quantitatively by a high enhancement ratio and qualitatively by rim enhancement, with an implication of adverse prognosis.

Adult↗

PubMed1987

Glucose and fatty acid metabolism in normal and diabetic rabbit cerebral microvessels.

Rabbit cerebral microvessels were used to study fatty acid metabolism and its utilization relative to glucose. Microvessels were incubated with either [6-14C]glucose or [1-14C]oleic acid and the incorporation of radioactivity into 14CO2, lactate, triglyceride, cholesterol ester, and phospholipid was determined. The inclusion of 5.5 mM glucose in the incubation mixture reduced oleate oxidation by 50% and increased esterification into both phospholipid and triglyceride. Glucose oxidation to CO2 was reduced by oleate addition, whereas lactate production was unaffected. 2'-Tetradecylglycidic acid, an inhibitor of carnitine acyltransferase I, blocked oleic acid oxidation in the presence and absence of glucose. It did not effect fatty acid esterification when glucose was absent and eliminated the inhibition of oleate on glucose oxidation. Glucose oxidation to 14CO2 was markedly suppressed in microvessels from alloxan-treated diabetic rabbits but lactate formation was unchanged. Fatty acid oxidation to CO2 and incorporation into triglyceride, phospholipid, and cholesterol ester remained unchanged in the diabetic state. The experiments show that both fatty acid and glucose can be used as a fuel source by the cerebral microvessels, and the interactions found between fatty acid and glucose metabolism are similar to the fatty acid-glucose cycle, described previously.

Alloxan↗

PubMed1987

Stimulation of proteoglycans by IGF I and II in microvessel and large vessel endothelial cells.

Endothelial cells were cultured from bovine capillaries and pulmonary arteries, and the effect of insulinlike growth factor (IGF) I and II (multiplication-stimulating activity) and insulin on the synthesis of proteoglycans was determined. IGF I and II stimulated 35SO4 incorporation into proteoglycans in a dose-dependent manner in both microvessel and pulmonary artery endothelial cells with maximum threefold increases. In pulmonary artery cells, the IGFs caused a general stimulation of all classes of glycosaminoglycan-containing proteoglycans. In microvessel endothelial cells, the IGFs appeared to preferentially increase heparan sulfate-containing proteoglycans. Insulin, at concentrations up to 10(-6) M, had no effect on the synthesis of proteoglycans in either microvessel or pulmonary arterial endothelial cells. Thus, the IGFs stimulate the synthesis of proteoglycans in both microvessel and large vessel endothelial cells, a property that is not mimicked by insulin. Because vascular endothelial cells are bathed by IGFs in vivo, such IGF-mediated functions are likely to be significant in both the normal physiology of vascular endothelium and in disease states such as diabetes mellitus.

Animals↗

PubMed1988

Effects of hypoglycemia and diabetes on fuel metabolism by rat brain microvessels.

Glucose and beta-hydroxybutyrate metabolism were compared in isolated cerebral microvessels from chronically diabetic and hypoglycemic rats. As noted previously, glucose oxidation and conversion to lactate are diminished in rats with streptozotocin-induced diabetes. The decrease in glucose metabolism did not result from selective damage to diabetic vessels during isolation, since the ATP level and the ATP/ADP ratio were similar to those of nondiabetic rats, and O2 consumption was increased. In addition, cerebral microvessel oxidation of beta-hydroxybutyrate was enhanced by diabetes. By contrast, microvessels from rats made chronically hypoglycemic by insulinoma engrafting 30 days earlier had a more than twofold increase in glucose oxidation and conversion to lactate, whereas their oxidation of beta-hydroxybutyrate was diminished by 50%. Unlike the insulinoma rats, no consistent increase in glucose metabolism was observed in microvessels from rats made hypoglycemic either by acute insulin administration or by a 4-day infusion of insulin. These results indicate that diabetes, and under some circumstances chronic hypoglycemia, markedly alters fuel metabolism in the cerebral microvasculature.

3-Hydroxybutyric Acid↗

PubMed2005

Chronic angiotensin II AT1 receptor blockade increases cerebral cortical microvessel density.

Angiotensin II is known to stimulate angiogenesis in the peripheral circulation through activation of the angiotensin II type 1 (AT1) receptor. This study investigated the effect of angiotensin receptor blockade on cerebral cortical microvessel density. Rats (6-7 wk old, n = 5-17) were instrumented with femoral arterial and venous indwelling catheters for arterial blood pressure measurement and drug administration. Rats were treated for 3 or 14 days with the AT1 receptor blocker losartan (50 mg/day in drinking water) or vehicle. Brains were sectioned and immunostained for CD31, and microvessel density was measured. Treatment with losartan for 3 or 14 days resulted in a slight decrease in mean arterial blood pressure (3 days, 92 +/- 1 mmHg; and 14 days, 99 +/- 2 mmHg) compared with vehicle (109 +/- 3 and 125 +/- 4 mmHg, respectively). A furosemide + captopril 14-day treatment group was added to control for the blood pressure change (96 +/- 3 mmHg). Microvessel density increased in groups treated with losartan for 14 days (429 +/- 13 vessels/mm2) compared with vehicle (383 +/- 11 vessels/mm2) but did not change with furosemide + captopril (364 +/- 7 vessels/mm2). Thus AT1 receptor blockade for 14 days resulted in increased cerebral microvessel density in a blood pressure-independent manner.

Angiotensin II Type 1 Receptor Blockers↗

PubMed1980

Reninlike enzymatic activity in the cerebral microvessels of the rat.

Extrarenal renin has been a subject of considerable interest. Chiefly, studies have focused on brain and vascular renin activity in large arteries. A method now exists for the isolation from the cerebrum of microvascular tissues consisting of arterioles, capillaries and venules. The present study has demonstrated reninlike enzymatic activity within the cerebral microvasculature of the rat that is distinct from plasma renin activity. Maximal activity was observed at pH 4.5 with no measurable activity at pH 7.4. Activity with homologous renin substrate was only 13% of that measured with hog substrate whereas a 400-fold increase in reninlike specific activity was observed when microvessel homogenates were incubated with synthetic tetradecapeptide renin substrate. Bilateral nephrectomy did not affect microvascular reninlike activity. Pepstatin 15 nM, abolished reninlike activity in microvessel homogenates. Mean specific microvessel reninlike activity was 1.15 +/- 0.20 pg angiotensin I . microgram protein-1 . h-1 in control animals. Neither sodium depletion nor DOC-saline administrations caused a significant change in microvascular reninlike activity. It is suggested that the reninlike activity observed in microvessels is an acid protease, perhaps cathepsin D derived from lysosomes.

Angiotensin I↗

PubMed1987

Microvessel hematocrit: measurement and implications for capillary oxygen transport.

Microvascular preparations of the hamster cheek pouch and cremaster muscle were used to establish the relationship among three measures of red cell distribution: 1) the systemic hematocrit defined as the volume percentage of red cells sampled from a toe clip; 2) the tube hematocrit defined as the instantaneous volume fraction of red cells in a microvessel segment of measured length and diameter; and 3) the discharge hematocrit defined as the volume percentage of red cells that flowed into micropipettes inserted into microvessels. The results show the tube hematocrit is low and highly variable in the presence of a nearly constant systemic hematocrit. The discharge hematocrit, in contrast, consistently approximated systemic values in blood taken from arterioles or venules with diameters of 6-98 micron. Indeed, the mean ratio of the discharge to the systemic hematocrit did not differ from unity (P greater than 0.25). The observed similarity between the discharge and systemic hematocrit indicates that red cells are distributed uniformly across capillary networks. Differences between the absolute value and variance of the tube hematocrit compared with the discharge hematocrit imply that the anatomical volume of a microvessel can differ from the volume available to cells and plasma within a microvessel. Thus moment-to-moment variation in the tube hematocrit or capillary red cell spacing may be indicative of a change in the effective capillary flow cross section and not solely on the inflow hematocrit.

Animals↗

PubMed1995

Quantitative evaluation of flow dynamics of erythrocytes in microvessels: influence of erythrocyte aggregation.

Effects of erythrocyte aggregation on the flow dynamics of erythrocytes in microvessels were examined quantitatively by perfusing human erythrocytes suspended in isotonic medium containing various concentrations of dextran (70,400 avg mol wt, Dx-70) into a part of the microvascular bed isolated from rabbit mesentery. Thickness of the marginal cell-free layer was measured with an image analyzer, total flow resistance was determined on the basis of the perfusion pressure-volume flow relationship, and homogeneity of erythrocyte flow was evaluated by the power spectrum obtained by the fast Fourier transform of the light intensity change monitored on single microvessels. With increasing dextran concentration, suspension viscosity of erythrocytes at high shear rates increased linearly and thickness of the cell-free layer increased in a sigmoidal fashion. Flow resistance increased relatively little over the range of dextran concentrations in which the cell-free layer increased most rapidly. Furthermore, the flow pattern of erythrocytes in microvessels became inhomogeneous. In conclusion, the present study shows that Dx-70-induced erythrocyte aggregation results in increased flow resistance in the circulatory system, even through the widening of the cell-free layer tends to reduce the resistance and also results in inhomogeneous flow of erythrocytes in microvessels.

Animals↗

PubMed1996

Modeling and simulation of illumination effects for evaluation of microvessels of the conjunctiva.

We present the development of a comprehensive model that was undertaken to determine the relationships between the components of an image and the light intensity values present in the image of the microvessels of translucent tissues such as the bulbar conjunctiva. Experiments were conducted during the modeling process by use of a cylindrical microvessel embedded in a diffuse medium (phantom) on a reflecting background to affirm model components and simulations. The three-dimensional model was reduced to a single illumination plane with four regions of interest and modeled as Lambertian radiators and surfaces. The modeling showed that the top of the cylinder and its immediate vicinity are diffuse reflectors of light from the source plus light reflected from the background. The limbus of the cylinder is a diffuse reflector of the source and background illumination and a specular reflector of background reflections that achieve a high grazing angle with the cylinder. The immediate vicinity of the cylinder receives direct illumination from the source, but the light is partially obscured by the cylinder. The region beyond the shadow of the cylinder is a diffuse reflector of the overhead light. The diffuse medium additionally reflects the source and also attenuates the illumination reaching the other compo- rents of the scene. The direct and reflected illumination at each region of the model was calculated by use of specific geometric relationships. To verify those calculations, we analyzed a video simulation for the effects of different illumination conditions and their contributing elements. Intensity values were calculated from the relative reflectivity data determined from the video signals. The illumination values at the points along the line at the meridian of the cylinder were due to its reflectivity and also that of the medium. Similarly, the values of points distant from the shadow of the cylinder were due to the reflectivity of the background and the medium. The excellent agreement between the model and the phantom provides a foundation for the detection and precise measurement of microvessel dimensions within a diffuse medium. The additional ability to compute relative depth, from a single view, also permits discrimination between neighboring microvessels in complex images.

Computer Simulation↗

PubMed1996

Vascular endothelial growth factor increases hydraulic conductivity of isolated perfused microvessels.

These experiments report the first direct measurement of microvessel permeability coefficients after exposure to vascular endothelial growth factor (VEGF). The Landis technique was extended to enable measurement of the resistance of the microvessel wall to water flow, hydraulic conductivity (Lp), on the same microvessel in the frog mesentery during the initial exposure to VEGF (acute) and 24 and 72 h after initial exposure (chronic). Control measurements of Lp showed no change either acutely or chronically. Exposure to 1 nM VEGF rapidly and transiently increased microvessel Lp within 30 s (to 7.8-fold greater than baseline values) and returned to control within 2 min. The baseline Lp was fivefold greater after 24 h than the initial baseline as a result of VEGF perfusion and returned to its original value after 72 h. These experiments confirm the hypothesis that VEGF acts both acutely (over a period of a few minutes) and chronically (over a few hours) to increase microvascular permeability.

Animals↗

PubMed1997

Effect of nitric oxide synthase inhibitors on endothelial [Ca2+]i and microvessel permeability.

To investigate the mechanism whereby nitric oxide (NO) signaling pathways regulate microvessel permeability in vivo, we measured changes in microvessel hydraulic conductivity (Lp) and endothelial cytoplasmic calcium concentration ([Ca2+]i) in response to calcium ionophore, ionomycin (5 microM), and ATP (10 microM) before and after the use of NO synthase (NOS) inhibitors in single perfused frog mesenteric venular microvessels. Ionomycin induced a transient increase in endothelial [Ca2+]i and an associated increase in Lp. The NOS inhibitors N omega-nitro-L-arginine methyl ester (10 and 300 microM) and N omega-monomethyl-L-arginine (L-NMMA; 10, 50, and 100 microM) significantly attenuated the peak increase in Lp induced by ionomycin. A similar inhibitory effect was also observed with the increase in Lp mediated by ATP. In contrast, D-NMMA, a biologically inactive isomer of L-NMMA, showed no effect on ionomycin-induced increase in Lp L-Arginine (3 mM) reversed the inhibitory effect of L-NMMA (10 microM) on Lp. However, the NOS inhibitors did not alter the magnitude and time course of the biphasic increase in endothelial [Ca2+]i induced by both ionomycin and ATP. These data suggest that 1) calcium-dependent NO release is a necessary step to increase microvessel permeability, and 2) the action of NOS inhibitors in attenuating the permeability increase in response to ionomycin and ATP occurs down-stream from calcium entry and does not involve modification of the initial increase in endothelial [Ca2+]i.

Adenosine Triphosphate↗

PubMed2001

EET homologs potently dilate coronary microvessels and activate BK(Ca) channels.

Epoxyeicosatrienoic acids (EETs) are released from endothelial cells and potently dilate small arteries by hyperpolarizing vascular myocytes. In the present study, we investigated the structural specificity of EETs in dilating canine and porcine coronary microvessels (50-140 microm ID) and activating large-conductance Ca2+-activated K+ (BK(Ca)) channels. The potencies and efficacies of EET regioisomers and enantiomers were compared with those of two EET homologs: epoxyeicosaquatraenoic acids (EEQs), which are made from eicosapentaenoic acid by the same cytochrome P-450 epoxygenase that generates EETs from arachidonic acid, and epoxydocosatetraenoic acids (EDTs), which are EETs that are two carbons longer. With EC50 values of 3-120 pM but without regio- or stereoselectivity, EETs potently dilated canine and porcine microvessels. Surprisingly, the EEQs and EDTs had comparable potencies and efficacies in dilating microvessels. Moreover, 50 nM 13,14-EDT activated the BK(Ca) channels with the same efficacy as either 11,12-EET enantiomer at 50 nM. We conclude that coronary microvessels and BK(Ca) channels possess low structural specificity for EETs and suggest that EEQs and EDTs may thereby also be endothelium-derived hyperpolarizing factors.

8,11,14-Eicosatrienoic Acid↗

PubMed1998

A serum-free in vitro model of renal microvessel development.

The differentiation and organization of the embryonic renal vasculature is a crucial event in renal development. To study this process, we developed a serum-free in vitro model of renal microvessel development. Mouse embryonic kidney explants, when embedded specifically in type I collagen, demonstrate outgrowth of microvascular structures when stimulated by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA, 10-50 ng/ml). Other polypeptide growth factors stimulated little, if any, microvessel outgrowth from the explants. Similar outgrowths were not observed when other embryonic tissue explants were used. The number of microvessels observed depended on the gestational age of the explants. We hypothesize that TPA induces the in situ differentiation of metanephric mesenchymal cells into endothelial cell precursors and that specific matrix proteins and cell-matrix interactions are necessary for the organization of these precursors into microvessels. Our model will allow us to examine in detail the responsiveness of metanephric kidney cells to both growth factors and extracellular matrix molecules and to understand how they influence renal endothelial cell differentiation.

Animals↗

PubMed1989

Differential adhesion of metastatic rat mammary carcinoma cells to organ-derived microvessel endothelial cells and subendothelial matrix.

The in vitro adhesion rates of rat 13762NF mammary adenocarcinoma cell clones of different spontaneous metastatic potentials to cloned microvessel endothelial cell monolayers and their subendothelial extracellular matrix were investigated. In this system, high rates of adhesion of the cloned tumor cell lines to syngeneic target (lung) organ-derived subendothelial matrix correlated with spontaneous metastatic potential, whereas adhesion to the lung microvessel endothelial cell apical surfaces occurred at lower rates and was not highly significantly different among the tumor cell lines. Adhesion rates to bovine aortic large vessel, and human brain and human meningeal microvessel endothelial cell monolayers were, in general, lower than those found with syngeneic lung microvessel endothelial cells, and did not correlate with spontaneous metastatic potential. Growth of endothelial cells in fetal bovine serum or platelet-poor horse serum did not affect the results, suggesting that in this system metastasis-associated organ-adhesive specificity is determined at the level of the subendothelial matrix.

Adenocarcinoma↗