SEARCH · PubMed Health

Results for “Microvessels”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

PubMed1994

Expression of immunologically relevant endothelial cell activation antigens on isolated central nervous system microvessels from patients with multiple sclerosis.

Activation of the vascular endothelium is thought to be an important facet of inflammation, thrombosis, and vasculitis. Activated endothelial cells express a number of immunologically relevant surface markers not expressed by normal endothelial cells. Many of these surface antigens are thought to augment adhesion reactions and migration. Our results show that endothelial activation may play a central role in the pathogenesis of multiple sclerosis (MS). Normal human central nervous system microvessels isolated from autopsy material do not express endothelial cell activation markers, including the adhesion proteins vascular cell adhesion molecule-1 (VCAM-1) and endothelial cell leukocyte adhesion molecule-1 (E-selectin/ELAM-1). They exhibit little to no constitutive expression of immunoreactive intercellular adhesion molecule-1 (ICAM-1) or the urokinase plasminogen activator receptor. Control microvessels exhibit no major histocompatibility complex (MHC) class II antigen. MS microvessels express significant levels of MHC class II antigens, ICAM-1, VCAM-1, and urokinase plasminogen activator receptor. E-selectin was expressed by 3 of 5 MS brains tested. Histologically unaffected areas of MS brain expressed less VCAM-1, ICAM-1, and E-selectin than did microvessels from periplaque zones. However, MHC class II antigens and urokinase plasminogen activator receptor were increased in areas exhibiting little to no evidence of leukocyte infiltration. When microvessels were examined for dual expression of activation markers, we found that in periplaque areas, 50% of microvessels coexpressed HLA-DR and VCAM-1, 28% of microvessels coexpressed HLA-DR and urokinase plasminogen activator receptor, and 43% of microvessels coexpressed HLA-DR and ICAM-1.

Adolescent↗

PubMed2005

Access of tumor-derived macromolecules and cells to the blood: an electron microscopical study of structural barriers in microvessel clusters in highly malignant primary prostate carcinomas.

BACKGROUND: The neo-angiogenetic microvessels forming a major reactive stromal element in highly malignant prostate neoplasms may exhibit fine-structural features relevant to our understanding of the passage of macromolecules from tumor to blood, on the one hand, and of events facilitating the metastatic cascade, on the other hand. METHODS: Ensuring rapid, optimal fixation in buffered glutaraldehyde was a foremost concern. Thin parings from radical prostatectomy specimens of Gleason scores (GS) 5-9 were taken from the tumor and from the contralateral side of the gland, glutaraldehyde-fixed, diced to smaller than 1 mm(3), postfixed in osmium tetroxide, embedded in Epon, ultrathin-sectioned, contrasted with lead and uranyl salts, and viewed in a transmission electron microscope. RESULTS: In dysplastic tissue areas, intraductal microvessels located in gland ducts were occasionally observed, and found to be aggressively invasive and highly active in producing neo-angiogenetic sprouts. Closely spaced microvessel clusters contained almost exclusively neo-angiogenetic microvessels, which were in cell-cell contact with numerous ameboid migratory cells, some of which were likely to be tumor cells. In these microvessel clusters, all structural barriers hindering passage of tumor-derived molecules or cells to the blood were eliminated. CONCLUSION: In microvessel clusters, the ultrastructural equivalent of microvascular hotspots, tumor invasion of microvessels is facilitated, but equally microvessels are observed invading the gland duct epithelial walls. This reciprocal invasivity of tumor cells and microvascular endothelial cells generates ideal conditions for tumor products and metastatic cells to enter the blood.

Aged↗

PubMed1991

Isolation and characterization of microvessels from normal brain and brain tumors.

We describe a new technique for isolating microvessels from both brain and brain tumors. This method is relatively quick and provides a microvessel preparation free of contamination by other brain tissue. Using this method, structurally intact microvessels from normal rat brain and from a malignant rat astrocytoma were isolated and characterized with light microscopy, scanning electron microscopy and transmission electron microscopy. In contrast to microvessels derived from normal rat brain, rat astrocytoma microvessels had endothelial cells with multilayered basement membranes, extensive microvilli on the cell surfaces, and a significant increase in the number of pinocytes in the cytoplasm. Furthermore, astrocytoma microvessel endothelial cells had pleomorphic electron dense nuclei with pale perichromatin, whereas the nuclei of endothelial cells of microvessels derived from normal brain tissue were finely granular and homogeneous with characteristically electron dense perichromatin. The morphologic characteristics of the astrocytoma microvessels are similar to the histologic changes seen in astrocytoma tissue in situ, and correlate well with the known altered functions of brain tumor neovasculature.

Animals↗

PubMed1993

Quantitative receptor autoradiographic analysis for angiotensin II receptors in bovine retinal microvessels: quantitation with radioluminography.

1. Specific 125I-Sar1, Ile8-Angiotensin II (125I-Sar1, Ile8-AII) binding sites in bovine retinal microvessels were investigated using the quantitative receptor autoradiographic method with pellet sections. 2. A quantitation was made with the computerized radioluminographic imaging plate system, a newly developed and highly sensitive method. Binding characteristics of the retinal microvessels were compared with those of the cerebral microvessels and the retinal macrovessels. 3. We isolated microvessels from the bovine retina and bovine cerebral cortex using the method composed of two-size sievings and high-speed homogenization with a Polytron. The isolated microvessels were composed of capillaries, and the retinal macrovessels contained vessels with smooth muscle. 4. There were specific binding sites for 125I-Sar1, Ile8-AII which were single and of a high affinity, in both the cerebral and the retinal microvessels and the retinal macrovessels. There were no differences in affinity between the vessels, but the retinal microvessels did have a higher density of binding sites than the cerebral microvessels. 5. The method we used is simple and sensitive for detecting and characterizing 125I-Sar1, Ile8-AII binding sites in retinal capillaries. Knowledge of the existence of large numbers of specific binding sites, candidates of physiologically active angiotensin II receptors, aids with understanding the regulatory roles of angiotensin II in the blood-retinal barrier.

1-Sarcosine-8-Isoleucine Angiotensin II↗

PubMed1994

In vivo visualization of lymphatic microvessels and lymphocyte migration through rat Peyer's patches.

BACKGROUND/AIMS: In the small intestine, lymphocytes migrate through Peyer's patches. The distribution of lymphatic microvessels in rat Peyer's patches and lymphocyte traffic through them were studied. METHODS: Vital dyes were injected via a micropipette into the Peyer's patches tissue to fill lymphatic microvessels and to stain lymphocytes in lymphatic microvessels. RESULTS: Direct microscopic observation revealed a dense plexus of lymphatic microvessels in the perifollicular and interfollicular areas. Injection of the dyes into the germinal center failed to delineate lymphatic microvessels. The lymphatic microvessels in the perifollicular area were filled with lymphocytes. Most lymphocytes in the perifollicular lymphatics stayed in the lymphatic microvessels. Some lymphocytes became detached and drained into lymphatic microvessels in the interfollicular areas. Lymphocytes then moved toward the submucosal lymphatics beneath the villi around the Peyer's patches. The interfollicular lymphatics did not display contractile activity but had valves. Opening and closing of valves was synchronized with the respiration and the back and forth flow of lymphocytes. CONCLUSIONS: There are numerous lymphocytes in a dense lymphatic network in the perifollicular and interfollicular areas of Peyer's patches. This well-developed lymphatic network has the potential capacity for storage of lymphocytes and modulation of lymphocyte migration.

Animals↗

PubMed1990

Use of tracers to measure flow within single microvessels.

Most techniques for making quantitative measurements of flow within single microvessels rely on tracers which are injected upstream of the microvessel and monitored noninvasively (e.g., optical densitometry) at selected sites along the microvessel. This study examines theoretically the measurement of average flow velocity (v) within individual microvessels from tracer flow data at monitoring sites. Starting with a fundamental convection-diffusion equation, the theory considers tracers which can distribute across both plasma and red cell phases. An integral analysis indicates that v = delta zeta/delta tau, where delta zeta is the distance between monitoring sites, and delta tau is the tracer transit or "residence" time needed to traverse that distance. The residence time which arises explicitly requires measurement of the flow-weighted average tracer concentration at each monitoring site. Because noninvasive tracer measurements provide indices of the unweighted average tracer concentration, a velocity measurement error, delta(zeta), arises, delta(zeta) is quantified in relation to the axial location of the measurement site, the velocity profile, the tracer Peclet number, and the radial distribution of tracer at the vessel inlet. delta(zeta) does not vanish when tracer enters a microvessel with a radially uniform concentration profile, but does vanish past a critical distance, Lc, from the microvessel entrance. The critical distance can be estimated using Lc/d = 0.05(vd)/D (d. vessel diameter; v, average flow velocity; D, tracer diffusivity). Accordingly, tracer data can be used to quantify flow velocity within a microvessel provided the microvessel length allows for monitoring tracer flow beyond the estimated Lc value. This study serves as a necessary precursor to analyses of plasma-phase tracers used to measure microvascular plasma flow.

Blood Flow Velocity↗

PubMed1989

Increased alpha 2- and beta 2-adrenergic receptors in cerebral microvessels in Alzheimer disease.

Adrenergic receptors exist in brain microvessels which are innervated by noradrenergic locus ceruleus neurons. Biochemical and pathological studies indicate locus ceruleus degeneration in Alzheimer disease (AD), which can cause adrenergic receptor alterations in brain microvessels. To assess this, we studied adrenergic receptors in human brain microvessels from AD subjects and age-matched controls by ligand binding methods. Total beta receptors of cerebral microvessels and beta 2 receptors, the type which predominates in microvessels, were significantly increased in AD. Compared to the cerebral cortex, there was a paucity of alpha 1-adrenergic receptors in cerebral microvessels, and they did not change in AD. Binding to alpha 2 receptors in cerebral microvessels was approximately 50% of that in the cortex, and these receptors increased by approximately 60% in cerebral microvessels of AD subjects. These findings suggest adrenergic receptor 'upregulation' in response to noradrenergic deafferentation in AD, which may have functional consequences at the blood-brain barrier.

Aged↗

PubMed2006

Expression of drug transporters at the blood-brain barrier using an optimized isolated rat brain microvessel strategy.

Quantitative RT-PCR (qRT-PCR) and Western blotting studies on transporters at the blood-brain barrier (BBB) of isolated brain microvessels have produced conflicting data on their cellular distribution. A major problem is identifying cells expressing the genes of interest, since isolated brain microvessels are composed of several cell types and may be contaminated with mRNA or proteins from astrocytes and neurons. We isolated rat brain microvessels and examined microscopically samples at each step of isolation to evaluate microvessel purity. The expression of specific markers of endothelial cells (Glut-1, Flk-1), pericytes (Ng2), neurons (synaptophysin, Syn) and astrocytes (Gfap) was measured by qRT-PCR in order to select the protocol giving the least astrocyte and neuron mRNAs and the most endothelial mRNAs. We also evaluated the gene expression of drug transporters (Mdr1a, Mdr1b, Mrp1-5, Bcrp and Oatp-2) at each step to optimize their location in cells at the BBB. The Mdr1a, Mrp4, Bcrp and Oatp-2 gene profiles were similar to those of endothelium markers. The profiles of Mrp2 and Mrp3 closely resembled that of Ng2. Mrp5 and Mrp1 expression was not increased in the microvessel-enriched fraction, suggesting that they are ubiquitously expressed throughout the cortex parenchyma. We also evaluated by Western blotting the expression of P-gp, Mrp2, Gfap and Syn in the cortex and in the purest obtained microvessel fraction. Our results showed that P-gp expression strongly increased in microvessels whereas Mrp2 was not detected in any of the fraction. Surprisingly, Gfap expression increased in isolated microvessels whereas Syn was not detected. Our results showed that the strategy consisting of identifying gene expression at different steps of the protocol is useful to identify cells containing mRNA at the BBB and give overall similar results with protein expression.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1998

Increased microvessel density in mucinous compared with malignant serous and benign tumours of the ovary.

Microvessel density of benign, borderline and malignant ovarian tumours was studied immunohistochemically using antibodies to the endothelial cell markers CD31, CD34 and factor VIII-related antigen. Microvessel density was compared in tumours of different histological subtype, stage and patient outcome. CD31-immunostained sections were examined and regions of high and average microvessel density were selected. Identical regions were located on CD34- and factor VIII-related antigen-immunostained serial sections and microvessel counts obtained and converted to vessels mm(-2). CD31 and CD34 immunostaining revealed increased microvessel density in both the high and average vessel density regions of mucinous (222.4 +/- 24.8; 79.9 +/- 8.5) compared with serous (105.4 +/- 20.7; 33.3 +/- 6.8) and benign (84.4 +/- 19.4; 20.4 +/- 4.4) tumours (P < 0.001). CD31 and CD34 immunostaining also revealed increased microvessel density in early-stage mucinous tumours (234.6 +/- 28.2; 87.8 +/- 9.2) compared with that observed in both early- (72.8 +/- 15; 12.9 +/- 2.4) and late- (115.6 +/- 26.5; 29.8 +/- 8.5) stage serous tumours (P < 0.001). No differences in microvessel density in samples from patients with differing outcomes were observed (P > 0.05). Reduced factor VIII-related antigen compared with CD31 and CD34 immunostaining was observed in both borderline and malignant mucinous and serous tumours (P < 0.02) but not in benign tumours (P > 0.05). Our results contradict the putative association between increased microvessel density and poor prognosis and suggest that the level and control of angiogenesis may differ between ovarian tumour types.

Adenocarcinoma, Mucinous↗

PubMed1990

Angiotensin peptide regulation of fluid-phase endocytosis in brain microvessel endothelial cell monolayers.

An in vitro model comprised of primary cultures of brain microvessel endothelial cells was used to investigate angiotensin II (Ang II) effects on blood-brain barrier fluid-phase endocytosis. The effects of Ang II, saralasin, sarathrin, bradykinin (BK), and phorbol myristate acetate (PMA) on brain microvessel endothelial cell fluid-phase endocytosis were determined using the fluorescent marker, Lucifer yellow. Nanomolar concentrations of saralasin (a partial Ang II agonist) stimulated brain microvessel endothelial cell endocytosis by 30% whereas Ang II treatment enhanced Lucifer yellow uptake by 20%. Sarathrin (an Ang II antagonist) had no effect on Lucifer yellow uptake. Nanomolar concentrations of BK and PMA also stimulated Lucifer yellow uptake by the brain microvessel endothelial cell by 40 and 95%, respectively. Stimulatory effects of Ang II and saralasin on Lucifer yellow uptake by brain microvessel endothelial cells could be completely blocked by pretreatment with either sarathrin or indomethacin (an inhibitor of prostaglandin synthesis). In contrast, the effects of neither BK nor PMA on brain microvessel endothelial cell uptake of Lucifer yellow ere altered by indomethacin pretreatment. Results indicated that Ang II, saralasin, BK, and PMA produce similar stimulatory effects on brain microvessel endothelial cell fluid-phase endocytosis with only Ang II and saralasin, producing increases in brain microvessel endothelial cell fluid-phase endocytosis that appeared to be mediated by prostaglandins.

Angiotensin II↗

PubMed1995

Microvessels isolated from brain: localization of muscarinic sites by radioligand binding and immunofluorescent techniques.

The present investigation was carried out to determine the extent to which muscarinic acetylcholine receptors (mAChRs) in vascular and perivascular structures were colocalized with glial fibrillary acidic protein (GFAP)-positive structures. To this aim, an immunocytochemical approach on free-floating cryosections and isolated microvessels obtained from rat brain was performed to study the possible colocalization of immunostaining with the anti-mAChR protein antibody (M35) and an anti-GFAP antibody. Double-labeling experiments were carried out by fluorescent techniques. Confocal microscopic observations of GFAP and M35 immunoreactivities on free-floating sections showed a high degree of colocalization on astrocyte processes associated with large vessels or capillaries. This pattern suggests that muscarinic receptors are associated with astrocytic endfeet. Confocal microscopic observations of immunoreactivity from isolated cerebral microvessels strengthen this conclusion since double-labeling of M35 and GFAP showed that perivascular astrocytic structures remained attached to the isolated microvessels and were present on vascular segments showing M35 immunoreactivity. In another set of experiments, the specific binding of [3H]quinuclidinylbenzylate ([3H]QNB) to isolated microvessel membrane preparations from cerebral cortex, caudate nucleus, thalamus, and cerebellum showed that a constant binding yield (20% in bovine and 40% in rat) was observed for microvessels compared with the corresponding brain region. According to our immunocytochemical results, the astrocytic membrane remaining attached to microvessels may account for the majority of the muscarinic binding to isolated microvessels. [3H]QNB binding values found in isolated microvessels cannot therefore be considered as artifacts without any link with vascular function. Taken together, the present study strengthens the idea that the muscarinic receptors may be implicated in the functional relationship between glial and vascular structures.

Animals↗

PubMed2005

Angiogenic and lymphangiogenic microvessel density in breast carcinoma: correlation with clinicopathologic parameters and VEGF-family gene expression.

Angiogenesis and lymphangiogenesis are essential for breast cancer progression and are regulated by vascular endothelial growth factors (VEGF). To determine clinical and molecular correlates of these processes, we measured blood and lymphatic vascular microvessel density in 29 invasive carcinomas (22 ductal, six lobular, one papillary), using the vascular marker CD31 and the novel lymphatic marker D2-40. Microvessel density was assessed microscopically and by image cytometry, and was compared with tumor histology, grade, stage, lymph node metastasis, hormone receptors, HER2/neu status, and expression of VEGF, VEGF-C and VEGF-D by immunohistochemistry or quantitative RT-PCR. Strong correlation was observed between visual and image cytometric microvessel density using D2-40 but not CD31 (P=0.016 and 0.1521, respectively). Image cytometric CD31 microvessel density correlated with tumor size, grade, stage and lymph node metastasis (P=0.0001, 0.0107, 0.0035 and 0.0395, respectively). D2-40 microvessel density correlated with tumor stage (P=0.0123 by image cytometry) and lymph node metastasis (P=0.0558 by microscopy). Immunohistochemical VEGF signal in peritumoral blood vessels correlated with image cytometric CD31 and D2-40 microvessel density (P=0.022 and 0.0012, respectively), consistent with the role of VEGF in blood and lymphatic vascular growth. Intratumoral VEGF-C and VEGF-D expression by quantitative RT-PCR correlated with D2-40 (P=0.0291 by image cytometry) but not with CD31 microvessel density, which could suggest a selective role of VEGF-C and VEGF-D in lymphangiogenesis. CD31 and D2-40 microvessel density correlated significantly with several prognostic factors, including lymph node metastasis. Thus, measurements of angiogenesis and lymphangiogenesis may have utility for breast cancer pathology, particularly for estimation of metastatic risk.

Adult↗

PubMed2000

2.5 kDa and 5.0 kDa heparin fragments specifically inhibit microvessel sprouting and network formation in VEGF165-mediated mammalian angiogenesis.

Tumour growth is angiogenesis dependent. Thrombosis and thromboembolism are very common in cancer patients. These patients are often treated with heparin as an anti-coagulant. Many tumour angiogens, including VEGF165, and endogenous anti-angiogenesis factors bind heparin tightly. Using the non-surgical mesenteric-window angiogenesis assay, we studied in detail the systemic effect of heparin fractions with a mean MW of 2.5, 5.0 and 16.4 kDa on the microvessel sprouting and network formation in angiogenesis mediated by VEGF165 in rats. The microvessel network was assessed objectively in terms of the number and lengths of segments (the distance between two successive branching points), the number of branching points, the degree of tortuosity, the index of interconnecting loop formation, the index of intersection, as well as the number and lengths of sprouts. Compared with the saline control, the 2.5 kDa fraction significantly shortened the microvessel sprouts and the microvessel segments but increased the microvessel tortuosity in statistical terms; the 5.0 kDa fraction statistically significantly shortened the sprouts, decreased the number of segments and the number of microvessel branching points; whereas the 16.4 kDa fraction statistically significantly elongated the longest segments. Moreover, statistically significant differences were found between the three heparin fractions in terms of microvessel tortuosity (2.5 vs. 16.4 kDa), index of loop formation (5.0 vs. 2.5 + 16.4 kDa) and index of intersection (5.0 vs. 16.4 kDa). These findings demonstrate that heparin fragments size-specifically inhibit microvessel sprouting and network formation in VEGF165-mediated angiogenesis. As VEGF165 is a potent angiogen in human tumours, we suggest that heparin enriched in 2.5 kDa species and 5.0 kDa species especially should be exploited as a combined anti-coagulant and specific adjuvant anti-angiogenic agent in cancer patients who require anti-coagulant therapy.

Angiogenesis Inhibitors↗

PubMed1992

Identification of a stable fragment of the Alzheimer amyloid precursor containing the beta-protein in brain microvessels.

Altered proteolysis of the beta-amyloid precursor protein (beta APP) resulting in release of the approximately 40-residue amyloid beta-protein (A beta P) may be a seminal pathogenetic event in Alzheimer disease. Using region-specific beta APP antibodies, we searched for stable proteolytic intermediates containing the intact A beta P region in brain tissue. A 22-kDa beta APP fragment was selectively detected in microvessels purified from cerebral cortex and other brain regions. On immunoblots, the 22-kDa band is labeled by five distinct antisera to beta APP carboxyl-terminal peptides and by affinity-purified antibodies to the recombinant proteins beta APP444-592 and beta APP592-695, which flank the A beta P region. The protein is virtually undetectable in whole-brain homogenates or microvessel-free fractions of brain. The protein is extractable from microvessels in Triton X-100 and other detergents, indicating its membrane association. In comparison with cortical microvessels, microvessels purified from white matter, cerebellum, and nonneural tissues contain lower amounts of the 22-kDa protein. The protein is found in microvessels of both normal and Alzheimer disease brains and occurs in low amounts in microvessels from fresh bovine brain. The size and specific immunoreactivity of the 22-kDa protein indicate that it is a stable fragment of beta APP containing the intact A beta P. The occurrence of this potentially amyloidogenic intermediate in microvessels is consistent with a vascular or hematogenous origin for some A beta P deposits in Alzheimer disease.

Age Factors↗

PubMed1991

Effects of oxygen tension on endothelium dependent responses in canine coronary microvessels.

STUDY OBJECTIVE: The aim was to determine the direct effects of oxygen tension on endothelium dependent vasodilator responses in canine coronary microvessels. DESIGN: Coronary microvessels were isolated and studied in vitro in a no flow constant pressure state using a video dimension analysing system. Microvessels were exposed to different partial pressures of oxygen. Endothelium dependent responses to acetylcholine and A23187 calcium ionophore were obtained with and without indomethacin during hyperoxia and normoxia, and compared to responses during hypoxia. Dose-response curves were also obtained to the direct smooth muscle dilator nitroprusside during normoxia and hypoxia. The reversibility of the effects of hypoxia on the acetylcholine response was studied after return to hyperoxic conditions following hypoxia. EXPERIMENTAL MATERIAL: Coronary microvessels (58-150 micron diameter) were obtained from adult mongrel dogs of either sex. MEASUREMENTS AND MAIN RESULTS: Exposure of preconstricted microvessels to hypoxia alone [PO2 5.8(0.4)kPa] resulted in a 25.9(SEM 6.8)% relaxation that was abolished by indomethacin [0.35(2.9)% relaxation]. Acetylcholine elicited dose dependent vasodilatation, with no significant differences in sensitivity between normoxia [PO2 14.6(0.04) kPa] and hypoxia: EC50 = 0.023 v 0.027 mumol.litre-1, respectively. During hyperoxia [PO2 80.2(6.0) kPa] there was a significant increase in the EC50 value to 0.09 mumol.litre-1 (hypoxia and normoxia v hyperoxia). After inhibition of prostaglandin synthesis with indomethacin, the sensitivity to acetylcholine was significantly decreased during hypoxia (EC50 = 0.16 mumol.litre-1) when compared to normoxia and hyperoxia. Indomethacin alone did not alter the acetylcholine response during normoxia and hyperoxia. As with acetylcholine, the sensitivity of indomethacin treated microvessels to A23187 was also decreased during hypoxia when compared to hyperoxia. There was no difference in the nitroprusside response during hypoxia and hyperoxia. The decreased vasodilator response to acetylcholine after hypoxia was persistent up to 2 h after return to hyperoxic conditions. CONCLUSIONS: Hypoxia decreases vasodilatation due to endothelium dependent relaxing factor, and oxygen tension has an important influence on both receptor dependent and receptor independent endothelium dependent vasodilator responses in coronary microvessels. Hypoxia also induces a prostaglandin mediated dilatation of preconstricted coronary microvessels. The effects of hypoxia on endothelium dependent responses are persistent up to 2 h.

Acetylcholine↗

PubMed1997

Early histologic and ultrastructural changes in microvessels of periosteal callus.

OBJECTIVE: To document early histological and ultrastructural changes in periosteal fracture callus blood vessels. DESIGN: Rabbit control and fractured ribs, after healing for three, six, and twelve hours and daily for seven days, were evaluated by light and electron microscopy. RESULTS: Control periosteal microvessels were formed mainly by endothelial cells and occasionally by pericytes. Only these cells displayed basal lamina within the periosteum. Three to twelve hours postfracture, periosteal microvessels were little changed. By two days postfracture, dramatic increases in size and population of microvessel cells resulted in a smaller lumen and thicker wall. Microvessel cells, while retaining their basal lamina, had transformed to mesenchymal cells. Transformed pericytes, as evidenced by their basal lamina, had extravasated. Three to four days postfracture, additional transformed pericytes had extravasated. Within the distal periosteal callus, a close spatial relationship among transformed microvessels, extravascular mesenchymal cells (some with basal lamina), and osteoblasts was present. Four to five days postfracture, within the proximal periosteal callus, a close spatial relationship among transformed microvessels (rapidly disappearing because of continued extravasation), extravascular mesenchymal cells (some with basal lamina), and chondroblasts (some with basal lamina) was present. CONCLUSIONS: New evidence showed that after fracture, periosteal microvessel endothelial cells and pericytes increased in population and transformed to mesenchymal cells. These changes, their subsequent extravasation as mesenchymal cells, and their development into chondroblasts were verified by basal lamina evidence. New evidence also suggested that continued extravasation of transformed microvessel cells rendered the fracture callus cartilage avascular.

Animals↗

PubMed1981

Uptake of amino acids by brain microvessels isolated from rats after portacaval anastomosis.

The uptake of amino acids by microvessels isolated from brains of rats was studied. Previous studies have demonstrated alterations in blood-brain amino acid transport after portacaval shunt in rats. In order to elucidate whether such changes in the blood-brain barrier were located in the microvessels, brain microvessels were isolated from both rats with portacaval shunt and controls. Brain microvessels from rats 2 weeks after shunt operations took up significantly greater amounts of 14C-labeled neutral amino acids, but not of glutamic acid, lysine, or alpha-methylaminoisobutyric acid than microvessels from sham-operated controls. Measurement of uptake kinetics showed a higher Vmax for phenylalanine and leucine uptake and a lower Vmax for lysine uptake in microvessels from shunted rats compared with control, whereas the respective Km's of uptake were similar in both preparations. The results suggest that changes in brain microvessel transport activity account for altered brain neutral amino acid concentrations after portacaval shunt and that such changes can be studied in vitro in isolated microvessels.

Amino Acids↗

PubMed1985

Identification of the insulin receptor of cerebral microvessels.

Cerebral microvessels are known to possess receptors for insulin and have recently been shown to respond to physiological levels of this hormone. Scatchard analysis of binding data obtained with isolated cerebral microvessels gave curvilinear plots and showed that neonatal porcine cerebral microvessels have a greater number of insulin receptors per unit of protein than adult bovine cerebral microvessels. The high-affinity form of the insulin receptors of both neonatal porcine and adult bovine cerebral microvessels have similar binding constants (dissociation constant = 0.3 X 10(-9) M). Dissociation of 125I-insulin from cerebral microvessels was accelerated by the presence of unlabeled insulin in preparations from both neonatal pigs and adult cows. 125I-insulin was covalently cross-linked to its receptor in cerebral microvessels with disuccinimidyl suberate, and the hormone-receptor complex was isolated on sodium dodecyl sulfate-polyacrylamide gels. Under reducing conditions, 125I-insulin was found associated with a polypeptide with a molecular weight of 130,000, which is indistinguishable from the alpha-subunit of the liver insulin receptor. In contrast, nonvascular cerebral cortical tissue contained an insulin receptor with an alpha-subunit that was lower in molecular weight than the form isolated from cerebral cortical microvessels.

Animals↗