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PubMed1987

Hypoxia does not alter angiotensin converting enzyme activity in hamster pulmonary microvessels.

Studies were initiated to investigate the effects of hypoxia on the conversion of angiotensin I (AI) to angiotensin II (AII) in microvessels of the lung. Using the technique of allografting neonatal lung tissue into the cheek pouch of normal hamsters, the microvessels of the lung, pulmonary arterioles, and venules could be visualized and manipulated by direct in vivo microscopy. The microvessels of the lung were studied 7-10 days after allografting by anesthetizing the hamster with pentobarbital (6.0 mg/100 g body weight i.p.) and then preparing the lung tissue for observation. The tissue was suffused with a Ringer's bicarbonate solution bubbled with a normal (20% O2-5% CO2-75% N2) or a low (95% N2-5% CO2) oxygen mixture. After equilibration, a pulmonary arteriole or venule was selected for observation, and the vessel geometry was recorded. Then, a micropipette containing either AI or AII was positioned alongside the vessel, and the agent was delivered continuously for 2 minutes. Lumen diameter was recorded continually for 8-10 minutes. This procedure was repeated until both angiotensins were tested on pulmonary arterioles and venules under conditions of a normal and low oxygen environment. This protocol was repeated on cheek pouch microvessels that did not contain pulmonary allografts. Both AI and AII produced rapid decreases in the lumen diameters of all microvessels tested. This vasoconstriction was greater for AII, and the oxygen environment did not alter the response. Conversion of AI to AII was not altered by the oxygen environment, and the relative conversion was similar in the microvessels of the lung and cheek pouch.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗

PubMed1995

Hemodilution accelerates the passage of plasma (not red cells) through cerebral microvessels in rats.

BACKGROUND AND PURPOSE: Hemodilution lowers the total circulatory red cell mass and blood viscosity and thereby may alter the time of passage of red cells and plasma through cerebral microvessels. This study was designed to clarify this question. METHODS: Adult Wistar-Kyoto rats, aged approximately 32 weeks, were divided into hemodilution and control groups. Local cerebral blood flow and microvascular red cell and plasma volumes in 14 brain structures were measured with the use of [14C]iodoantipyrine, 55Fe-labeled red cells, and [14C]inulin, respectively. RESULTS: In the control group, the hematocrit in cerebral microvessels ranged from 0.29 to 0.45 with a mean of 0.36, which was 71% of the systemic hematocrit (0.51). The mean transit times of blood, red cells, and plasma through microvessels were 0.62 to 1.77 seconds (mean, 0.92 second), 0.44 to 1.15 seconds (mean, 0.65 second), and 0.78 to 2.5 seconds (mean, 1.25 seconds), respectively. In the hemodilution group, the mean hematocrit in microvessels was 0.28, which was 89% of the systemic hematocrit (0.32). Local cerebral blood flow was approximately 59% higher (P < .01) than that of the control animals. The rate of oxygen delivered to the brain was slightly increased (9%) after hemodilution. Blood volume in cerebral microvessels was similar to that of the control group. Mean transit time of blood was 0.62 second (68% of the control), transit time of red cells was 0.53 second (85% of the control), and transit time of plasma was 0.67 second (54% of the control). CONCLUSIONS: These findings indicate that isovolemic hemodilution accelerates the plasma (not red cell) flow velocity in cerebral microvessels.

Animals↗

PubMed1999

Chronic estrogen treatment increases levels of endothelial nitric oxide synthase protein in rat cerebral microvessels.

BACKGROUND AND PURPOSE: A number of studies indicate that the female gonadal hormone, estrogen, confers protection against cerebrovascular disorders such as stroke. One postulated mechanism for these effects of estrogen is an action on the enzyme endothelial nitric oxide synthase (eNOS), which produces the vasodilatory molecule NO. We have investigated the hypothesis that estrogen increases expression of eNOS in cerebral microvessels of male and female rats. METHODS: We measured levels of eNOS protein by Western blot in cerebral microvessels isolated from 7 groups of animals: females, ovariectomized females, ovariectomized females treated with estrogen, males, castrated males, castrated males treated with estrogen, and castrated males treated with testosterone. RESULTS: Ovariectomized female rats treated with estrogen had 17. 4-fold greater levels of eNOS protein in cerebral microvessels than ovariectomized females, and intact females had 16.6-fold greater levels than ovariectomized females (P<0.01). In intact females, cerebral microvessel eNOS protein levels were 9.2-fold higher than those of intact males (P<0.05). Levels of eNOS protein in castrated males, castrated males treated with testosterone, and males were not different from each other. Estrogen treatment of castrated animals resulted in an 18.8-fold increase in cerebral microvessel eNOS protein (P<0.05). CONCLUSIONS: Chronic estrogen treatment increases levels of eNOS protein in cerebral microvessels of male and female rats. This increase in eNOS protein correlates with our previous functional findings indicating that estrogen exposure increases NO modulation of cerebrovascular reactivity in both male and female animals. Upregulation of eNOS expression may contribute to the neuroprotective effect of estrogen.

Animals↗

PubMed1990

Renin release and gene expression in intact rat kidney microvessels and single cells.

To investigate whether newborn kidney microvessels and isolated single microvascular cells have the capacity to release renin and/or alter the expression of the renin gene in response to adenylate cyclase stimulation, newborn kidney microvessels were isolated and purified (95%) using an iron perfusion/enzymatic digestion technique. Incubation of microvessels with either vehicle (control; C) or 10(-5) M forskolin (F) in media resulted in an increase in microvessel cAMP (0.67 +/- 0.13 vs. 22 +/- 4.6 pmol/min per mg protein) (P less than 0.005) and renin released into the culture media (1,026 +/- 98 vs. 1,552 +/- 159 pg angiotensin I/h per mg protein) (P = 0.008) (C vs. F). Renin mRNA levels in the newborn kidney microvessels increased 1.6-fold with forskolin treatment. Renin release by isolated, single microvascular cells (with or without forskolin) was assessed using the reverse hemolytic plaque assay. Forskolin administration resulted in an increase in the number of renin-secreting cells without changes in the amount of renin secreted by individual cells. In conclusion, newborn kidney microvessels and isolated renin-releasing microvascular cells possess a functionally active adenylate cyclase whose short-term stimulation results in accumulation of cAMP, a significant increase in renin release, and an enhancement of renin gene expression. The increase in renin release is due to recruitment of microvascular cells secreting renin. Recruitment of hormone-secreting cells in response to stimuli may prove to be a mechanism of general biological importance shared by many endocrine cell types.

Animals↗

PubMed2000

A new approach to three-dimensional reconstructed imaging of hormone-secreting cells and their microvessel environments in rat pituitary glands by confocal laser scanning microscopy.

There has been considerable interest in the relationship between hormone- secreting endocrine cells and their microvessels in human pituitary gland. However, microcirculatory networks have rarely been studied in three dimensions (3D). This study was designed to visualize and to reveal the relationship between hormone-secreting endocrine cells and their microvessel environment in 3D, using rat pituitary glands under various (hyper/hypo) experimental conditions by confocal laser scanning microscopy (CLSM). Female adult Wistar rats were used after bilateral adrenalectomy or ACTH administration for 2 weeks. Clear 3D reconstructed images of ACTH cells, the microvessel network and counterstained nuclei were obtained at a maximal focus depth of 1 mm by CLSM without any background noise. In the hyperfunctional state, slender cytoplasmic processes of hypertrophic stellate ACTH cells frequently extended to the microvessels. In the hypofunctional state, ACTH cells appeared atrophic and round with scanty cytoplasm, and cytoplasmic adhesions to microvessel network patterns were inconspicuous. Therefore, 3D reconstructed imaging by CLSM is a useful technique with which to investigate the microvessel environment of hormone-secreting cells and has the potential to reveal dynamic hormone-secreting pathways.

Adrenalectomy↗

PubMed1998

Expression of leptin receptor isoforms in rat brain microvessels.

Leptin acts on specific brain regions to affect body weight regulation. As leptin is made by white adipose tissue, it is thought that leptin must cross the blood-brain barrier or the blood-cerebrospinal fluid barrier to reach key sites of action within the brain. High expression of a short form leptin receptor has been reported in the choroid plexus. However, whether one or more of the known leptin receptor isoforms is expressed in brain capillaries is unknown. To identify and quantitate leptin receptor isoforms in rat brain microvessels, we applied quantitative RT-PCR to RNA from purified rat brain microvessels in parallel with in situ hybridization. The results show that the amount of short form leptin receptor messenger RNA (mRNA) in brain microvessels is extremely high, exceeding that in choroid plexus. In contrast, low levels of this mRNA were detected in the cerebellum, hypothalamus, and meninges. The long form leptin receptor mRNA is only present at low levels in the microvessels, but surprisingly, its level in cerebellum is 5 times higher than that in the hypothalamus. In situ hybridization experiments confirmed strong expression of short leptin receptors in microvessels, choroid plexus, and leptomeninges. The distribution and type of leptin receptor mRNA isoforms in brain microvessels are consistent with the possibility that receptor-mediated transport of leptin across the blood-brain barrier is mediated by the short leptin receptor isoform.

Animals↗

PubMed2001

Clinical significance of microvessel density in multiple myeloma patients.

To investigate the role of angiogenesis in multiple myeloma (MM), bone marrow biopsy from 75 adults with newly diagnosed, untreated MM were evaluated. Microvessels were scored in at least 3 areas ( x 200 fields) of the highest microvessel density in representative sections of each bone marrow specimen using immunohistochemistry for CD34. Prognostic variables were also evaluated for the overall survival. Microvessel counts were significantly higher in patients with MM (n=69.42+/-9.67), compared with control (n=26.81+/-2.85). Microvessel density had a weak correlation with percentage of bone marrow plasma cells. By univariate analysis, age, beta2-microglobulin, serum albumin, serum creatinine, serum calcium, hemoglobin, platelet count, and bone marrow plasma cell percentage were correlated with survival. By multivariate analysis, age, serum albumin, serum creatinine, hemoglobin, platelet count and bone marrow plasma cell percentage were correlated with overall survival, whereas microvessel density was not. In summary, microvessel density in bone marrow of MM is significantly increased compared to control, but was not correlated with overall survival. Further studies regarding angiogeneic molecules are needed to determine the functional role of angiogenesis in MM.

Adult↗

PubMedDate not supplied

IgE deposition in brain microvessels and on parasitized erythrocytes from cerebral malaria patients.

Postmortem brain tissues of 21 cerebral malaria cases were obtained in Myanmar and Vietnam. The tissues were examined by light microscopy and by an immunohistochemical method. Brain microvessels (capillaries and venules) were examined for the presence of immunoglobulins IgE and IgG, Plasmodium falciparum antigen, and parasitized erythrocytes (PRBC). Deposition of IgE, IgG, and P. falciparum antigen was observed in the microvessels from all specimens examined. Sequestered PRBC in the microvessels were positive for IgG in all 21 cases and for IgE in six cases. In the latter cases, the percentage of microvessels with sequestered PRBC was > 50%, with the frequency of IgE-positive cells ranging from 42% to 52%. In contrast, in five cases that were only weakly positive for IgE, the percentage of microvessels with sequestered PRBC was remarkably low (< 1%). These data indicate that the degree of deposition of IgE in microvessels and on PRBC from cerebral malaria patients correlated with that of PRBC sequestration. As IgE-containing immune complexes are known to induce local overproduction of tumor necrosis factor-alpha (TNF-alpha), a major pathogenic factor in cerebral malaria, IgE may contribute to the pathogenesis of this severe disease.

Adolescent↗

PubMedDate not supplied

Relationship between microvessel quantification and inducibility of endogenous tumor necrosis factor in colorectal adenocarcinoma.

BACKGROUND: Although we have reported that the inducibility of endogenous tumor necrosis factor (en-TNF) by tumor cells is an independent prognostic factor in Dukes stage C colorectal cancer patients, the mechanism by which the patients having high inducibility of en-TNF show better prognosis is still unclear. We hypothesize that the inducibility of en-TNF by colorectal tumor cells affects the prognosis of patients through the modulation of angiogenesis. Thus, the aim of this study is to clarify the relationship between inducibility of en-TNF and tumor vascularity in colorectal cancer. PATIENTS AND METHODS: Histological sections from 62 Dukes stage C colorectal cancer patients who received curative operation were immunostained for CD34 antigen. Microvessels were counted in the photograph of x200 fields (0.298 mm2). The average count of five most vascular areas was determined as a microvessel density of each case. RESULTS: Two of 62 cases were excluded from the analysis, because of insufficient staining. A total of 60 patients were dichotomized by a median vessel count of 34 into two groups: 30 patients with lower microvessel density (Low MVD group) and 30 patients with higher microvessel density (High MVD group). There was no significance in the distribution of all clinicopathological factors among these two groups. Regarding en-TNF inducibility, no difference was shown between the two groups. The five year survival rate of Low MVD group and High MVD group were 58.7% and 68.0%, respectively. And, the 5 year relapse-free survival rate of Low MVD group and High MVD group were 59.7% and 52.2%, respectively. No significant difference was demonstrated between Low MVD group and High MVD group. CONCLUSION: Intratumoral microvessel density did not influence on the prognosis of colorectal cancer patients in Dukes stage C after curative operation. The inducibility of en-TNF showed no correlation with intratumoral microvessel density in Dukes stage C patients after curative operation.

Adenocarcinoma↗

PubMedDate not supplied

[Errors in measurement of section areas and perimeters of microvessels from their profiles in sections for light and electron microscopy].

The error of measuring the section areas and perimeters of microvessels was estimated, which is due to a deviation of the section plane from the direction perpendicular to the longitudinal axis of microvessels. The estimates of the microvessel nonperpendicular sectioning error correspond to the case of three-dimensional isotropic distribution of microvessels without their own eccentricity. Only those microvessel profiles are selected for morphometry that meet the condition theta min < or = b/c < or = 1.00, where b is the minor and c is the major radii of microvessel profile on a section, and theta min is the tolerance for profile nonperpendicularity.

Animals↗

PubMed2001

The chemokine receptor CCR2 mediates the binding and internalization of monocyte chemoattractant protein-1 along brain microvessels.

Previous results from this laboratory revealed the presence of high-affinity saturable binding sites for monocyte chemoattractant protein-1 (MCP-1) along human brain microvessels (Andjelkovic et al., 1999; Andjelkovic and Pachter, 2000), which suggested that CC chemokine receptor 2 (CCR2), the recognized receptor for this chemokine, was expressed by the brain microvascular endothelium. To test the role of CCR2 directly in mediating MCP-1 interactions with the brain microvasculature, we assessed MCP-1 binding activity in murine brain microvessels isolated from wild-type mice and from CCR2 (-/-) mice engineered to lack this receptor. Results demonstrate that MCP-1 binding is greatly attenuated in microvessels prepared from CCR2 (-/-) mice compared with wild-type controls. Moreover, microvessels from wild-type mice exhibited MCP-1-induced downmodulation in MCP-1 binding and a recovery of binding activity that was not dependent on de novo protein synthesis. Furthermore, MCP-1 was shown to be internalized within wild-type microvessels, but not within microvessels obtained from CCR2 (-/-) mice, additionally demonstrating that CCR2 is obligatory for MCP-1 endocytosis. Last, internalization of MCP-1, but not transferrin, was observed to be inhibited by disruption of caveolae. Internalized MCP-1 also colocalized at some sites with caveolin-1, a major protein of caveolae, implying that this chemokine is endocytosed, in part, via nonclathrin-coated vesicles. These results prompt consideration that MCP-1 signals may be relayed across the blood-brain barrier by highly specialized interactions of this chemokine with its cognate receptor, CCR2, along brain microvascular endothelial cells.

Animals↗

PubMed2003

[Microvessel density and endothelial area in assessment of angiogenesis in patients with laryngeal cancer].

The growth of solid tumours and the process of metastasis are dependent on the formation of new blood vessels. Indeed, the intensity of angiogenesis has been shown to be increase in various human tumours. The main aim of this work was the assessment of angiogenesis intensity (AI) in patients with laryngeal cancer using two methods: microvessels density (MVD) and microvessels area (MVA). The group of 151 patients with laryngeal cancer, surgically treated with minimum 5 years observation, was multi-variously analysed. Paraffin--embedded tissue sections from each case were stained with a monoclonal antibody raised against FVIII and CD34 antigens. Intensity of angiogenesis (IA) was measured as microvessels density (MVD) and microvessels area (MVA) by mean of computer image analysis. There were statistically significant correlation between IA measured as MVD using CD34 and tumour size and nodal metastasis. IA described as MVA correlated with: staging, tumour size, nodal recurrences and metastasis. IA measured as MVD after using anti-FVIII correlated with tumour size and nodal metastasis. MVA correlated with staging and nodal recurrences. Overall survival was related to IA measured as MVD using anti-CD34 and anti-FVIII. Disease-free survival was related to IA measured as MVD using anti-VIII. Intensity of angiogenesis has prognostic value in patients with laryngeal cancer. Both methods: microvessels density and microvessels area seems to have similar value in assessment of angiogenesis intensity.

Adult↗

PubMed1992

Microvessel and astroglial cell densities in the mouse hippocampus.

In order to study the factors responsible for glucose uptake in the mouse hippocampus, microvessel and astroglial cell densities were measured and compared in each laminal region. Microvessel density was examined on histologically prepared sections after injection of Indian ink and measured by means of an image analyser. Astroglial cell density was determined after the cells were stained immunohistochemically. Microvessel and astroglial cell densities were determined in 10 different hippocampal structures. Microvessel and astroglial cell densities were strongly correlated in all layers except the pyramidal cell layers. The highest density of perfused microvessels was found in the stratum lacunosum-moleculare, compared with other regions, and the lowest values were found in the stratum lucidum and dentate granular cell layer. Among pyramidal cell layers, microvessel density in sector CA3a was significantly higher than that in CA1.

Animals↗

PubMedDate not supplied

Immunohistochemical microvessel count is not a reliable prognostic predictor in colorectal carcinoma.

BACKGROUND/AIMS: Immunohistochemical microvessel count for angiogenesis is associated with the growth and metastasis of various solid tumors, but its role in colorectal carcinoma remains controversial. This study aimed to determine its role in predicting the relapse and survival of colorectal carcinomas after curative surgery. METHODOLOGY: Representative paraffin-embedded sections of invasive colorectal cancers from 104 patients were studied by immunohistochemical staining using polyclonal anti-factor VIII antibody. Two investigators examined the microvessel count in the hot spot area of tumor using a 400x field in a blind fashion. RESULTS: There was no correlation between microvessel count and tumor size, location of carcinoma, tumor cell differentiation and nodal status. The microvessel count appeared to be lower among advanced-stage cancers as compared with early-stage cancers (pN0 vs. pN1+ pN2: 56 +/- 25. vs. 50 +/- 20; Dukes A + B vs. C + D: 56 +/- 25 vs. 49 +/- 18). In node-negative patients, the value of microvessel count greater than or equal to 75 seemed to correlate with longer disease-free survival and overall survival. CONCLUSIONS: Based on these results, immunohistochemical microvessel count seemed to decrease as colorectal cancer progressed and was not a reliable prognostic predictor in colorectal carcinoma.

Adult↗

PubMed2005

[Microvessel counts and the expressions of chemotactic factors in the pathological scar tissues].

OBJECTIVE: To explore the microvessel counts and the expressions of interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein-1 ( MIP-1) alpha mRNA in the pathological scar tissues. METHODS: Immunohistochemical method of avidin-biotin complex was used for microvessel counts on the routinely formalin-fixed and paraffin-embedded sections of specimens of hypertrophic scars, keloids, normal skin, and surgical scar, and in situ hybridization for the expressions of IL-8, MCP-1, MIP-1alpha mRNA. RESULTS: The microvessel counts as well as the positive rates and the scorings of IL-8, MCP-1, and MIP-1alpha mRNA were significantly higher in pathological scars than those in the normal skin and surgical scar (all P < 0.05). The microvessel counts were significantly higher in the positive cases of IL-8, MCP-1 and MIP-1alpha mRNA than those in the negative ones (P < 0.05). The close positive correlations were found among the microvessel counts and the expressive scorings of 3 factors (P < 0.05). The close positive correlations were also found among the expressive scorings of IL-8, MCP-1, and MIP-1alpha mRNA in pathological scars. Microvessel counts were significantly higher in hypertrophic scars with the course less than 1 year than those with the course more than 1 year. CONCLUSION: IL-8, MCP-1 and MIP-1alpha play important roles in promoting the neovascularization of pathological scars.

Adolescent↗

PubMed1983

Aldose reductase activity in retinal and cerebral microvessels and cultured vascular cells.

Isolated microvessels (primarily capillaries) from bovine retina and cerebral cortex, as well as cultured bovine retinal capillary pericytes and porcine and canine retinal capillary endothelial cells contain apparent aldose reductase activity. This conclusion is based on the ability of these cultured cells and vessel fragments to reduce DL-glyceraldehyde in preference to D-glucuronate at low (0.1 mM) substrate concentrations, in the presence of NADPH, and in the accumulation of high levels of sorbitol or galactitol when retinal pericytes and endothelial cells are cultured in media enriched in glucose or galactose. The quantitative similarities of these activities in bovine retinal and cerebral microvessels, as well as the quantitatively similar ability of these two sets of microvessels to oxidize 14C-labeled glucose with the label either in the C-1 or the C-6 position, suggests that aldose reductase may not be a major causal factor in diabetic retinopathy. This conclusion is suggested because, while these metabolic activities are similar in bovine retinal and cerebral microvessels, only the retinal microvasculature suffers major anatomic and functional damage in diabetes. This conclusion must be viewed with caution, however, because other metabolic pathways that we have not investigated may be altered by an excess of sugar alcohols, and be present in differing activities in retinal and cerebral microvessels; species differences may exist; and similar experiments have not been conducted using human microvessels.

Aldehyde Reductase↗

PubMed1993

Immunohistochemical study of intimal microvessels in coronary atherosclerosis.

Two hundred ninety-nine human coronary artery paraffin-embedded tissue blocks were examined for intimal microvessel invasion by probing for factor VIII-associated antigen with indirect immunofluorescence and high resolution confocal microscopy. The results obtained confirm that intimal microvessels originate in the adventitia and show that the richness of intimal microvessels is strongly positively correlated with intimal thickness and negatively correlated with relative lumen size. A number of plasma constituents were examined in serial sections. Comparison of immunofluorescence distribution patterns of these components with intimal microvessel distribution patterns reveals that intimal microvessels leak plasma albumin into artery walls, exude fibrinogen, and are associated with the build-up of plasma cells within atherosclerotic lesions. Therefore, intimal microvessels are demonstrated to play important roles in the development of atherosclerosis.

Antibodies↗

PubMedDate not supplied

Interrelationships between microvessel density, expression of VEGF and resistance to doxorubicin of non-small lung cell carcinoma.

It has been shown that hypoxia can induce resistance to a number of antineoplastic agents. Since vessel density may be considered as an indirect measure of the oxygenation of tumours, in this study we analysed the relationship between tumour vascularity or vascular endothelial growth factor (VEGF) expression and drug resistance. Tumour specimens of 152 non-small cell lung carcinomas (NSCLC) of previously untreated patients were analysed for microvessel density by staining with factor VIII (von Willebrand factor) antibody and for expression of vascular endothelial growth factor (VEGF) using an anti-VEGF-antibody. Both proteins were determined by immunohistochemistry and the expression was compared with the resistance to doxorubicin measured in vitro. Microvessel density was significantly reduced in resistant tumours when compared with sensitive tumours. Of the 98 tumours with low microvessel density 83 (85%) were resistant; whereas of the 54 tumours with high microvessel density only 34 (63%) were resistant (p = 0.004). Expression of VEGF was significantly lower in resistant than in sensitive lung carcinomas. Of the 102 tumors with low expression of VEGF, 87 (85%) were resistant; whereas of the 50 tumors with high expression only 30 (60%) were resistant (p = 0.0009). Corresponding results were obtained when the analysis was restricted to squamous cell lung carcinomas or adenocarcinomas of the lung. Analysis of microvessel density or VEGF expression and clinical data (stage, histology, metastasis) revealed no significant interrelationships. These data show clearly that poor microvessel density (vascularisation) and reduced expression of VEGF are linked with resistance to doxorubicin.

Adult↗