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PubMedDate not supplied

Microvessel density in brain tumors.

Sections from formalin fixed paraffin embedded tumor tissue from 165 patients with brain tumors including 62 meningiomas, 80 supratentorial astrocytomas (19 astrocytomas-grade I/II, 20 anaplastic astrocytomas-grade III, 41 glioblastomas-grade IV), 7 cerebellar astrocytomas-grade I/II, one gliosarcoma, 7 oligodendrogliomas, 3 ependymomas and 5 medulloblastomas were immunostained for factor VIII-related antigen in order to highlight microvessel endothelial cells. Microvessel count (MVC; the highest number of microvessels in three areas of highest vascular density at X200 magnification) was determined and correlated with histological grade of tumors and patients' sex and age. The mean MVC was 27.9 in meningiomas. Astrocytic tumors, particularly malignant astrocytomas (grade III, IV), were highly vascular. The mean MVC as regards the supratentorial astrocytic neoplasms was 14.5 in astrocytomas (grade I/II), 42.3 in anaplastic astrocytomas (grade III) and 50.2 in glioblastomas (grade IV). All cerebellar astrocytomas studied, even though well differentiated (grade I/II), were highly vascularised tumors (MVC: 41.1. A comparison of the mean MVC vlaues showed that there was a statistically significant difference between supratentorial astrocytomas (Grade I-II) and cerebellar astrocytomas (Grade I-II) (p = 0.0004), anaplastic astrocytomas (Grade I-II) (p = 0.00004) and glioblastomas (p = 0.00001). There was no significant difference between cerebellar astrocytomas and anaplastic astrocytomas (p = 0.8) and glioblastomas (p = 0.4). Astrocytic neoplasms showed statistically significant higher mean MVC from meningiomas (p = 0.002). The mean MVC was 14.1 in oligodendrogliomas, 22.7 in ependymomas and 19.6 in medulloblastomas. In one gliosarcoma that was studied the MVC was 40. The MVC appeared to be independent of the age and sex of patients. This study supports the importance of microvessel density as a measure of angiogenesis, as well as a further morphologic feature in the classification of brain tumors. The determination of microvessel density may become useful in the planning and monitoring of anti-angiogenesis therapies of these tumors.

Adult↗

PubMed1998

Microvessel density in prostate cancer: prognostic and therapeutic utility.

Microvessel density is a promising prognostic factor in management of patients with prostate cancer. Unlike cancer cell-based factors, microvessel density is a host stromal factor that has apparently limited heterogeneity within a cancer. Its predictive value for pathological stage has been demonstrated in most but not all reports. Further, recent studies reveal that microvessel density may be predictive of cancer recurrence and perhaps survival in some patients. Inhibition of angiogenesis may be an effective chemopreventive approach, particularly for men at high risk of prostate cancer. The patient described in the case study may benefit from microvessel density determination. Manual or computer-assisted counting of microvessels in the diagnostic needle biopsy specimen would provide a value that could be compared with published findings to predict pathological stage and outcome, particularly in combination with Gleason score and serum prostate-specific antigen concentration. The probability of extraprostatic extension may be sufficiently high that a urologist may choose not to operate on the patient. Similarly, the probability of recurrence after surgery or radiation may be sufficiently high to warrant adjuvant therapy.

Antineoplastic Agents↗

PubMed2006

Microvessel density and p53 in detecting cervical cancer by FDG PET in cases of suspected recurrence.

PURPOSE: Cervical cancer is the second most frequently diagnosed cancer in women worldwide. About one-third of patients experience recurrent disease. A better chance of survival might be achieved by the early detection of recurrent cervical cancer. [(18)F]fluoro-2-deoxy-D-glucose (FDG) PET could be a promising imaging modality for this purpose, given that FDG PET has high diagnostic efficacy. Ideally, pre-selection of patients should be performed before considering FDG PET. The purpose of this study was to investigate parameters of primary cervical cancer associated with recurrence as a basis for pre-selection of patients in whom FDG PET should be performed. METHODS: Thirty-eight cervical cancer patients, clinically suspected of having recurrent disease, underwent FDG PET. Tissue from primary tumours and nine histologically confirmed metastases was analysed for biomarkers possibly related to glucose metabolism and prognosis (vascular endothelial growth factor, CD31 for microvessel density, glucose transporter-1, hexokinases I, II and III, Ki67, p53, hypoxia-inducible factor 1alpha, and degree of infiltration by lymphocytes and macrophages). RESULTS: Based on clinical outcome, sensitivity and specificity of FDG PET were 96% and 100%, respectively. Cox regression revealed microvessel density and p53 (tumour suppressor protein) to be the two most important biomarkers for prediction of recurrence (hazard ratios 2.54 and 2.28, respectively). By combining these two biomarkers in a parallel test, sensitivity and specificity in predicting recurrence were 87% and 71%, respectively. Leave-one-out cross-validation demonstrated predictive validity of a model based on microvessel density and p53. CONCLUSION: In this first study of its kind, we have demonstrated that microvessel density and p53 profiles could be important in pre-selecting cervical cancer patients for detection of recurrence by FDG PET.

Adult↗

PubMed2005

[Role of microvessel density on human middle ear cholesteatoma].

OBJECTIVE: To explore the role of microvessel density in acquired middle ear cholesteatoma, to analyze it playing the possible role in proliferative ability of cholesteatoma epidermis. METHODS: The specimens from 15 cases acquired middle ear cholesteatoma patients having typical perforation in the posterior fold (the adjacent skin around perforation and the normal deep external ear skin) were examined by immunohistochemical ABC method. The microvessel density was analyzed by computer, and was compared with 20 cases non-cholesteatoma otitis media's the adjacent skin around perforation. RESULTS: Counts of microvessel and relative area of all microvessels per image in the adjacent skin around perforation were 14.395 +/- 2.000 and (9.927 +/- 2.600)%, respectively. These were significantly higher than the normal deep external ear skin's with the average of 6.218 +/- 0.949 and (5.076 +/- 0.807)% in 15 cases acquired middle ear cholesteatoma patients (P < 0.001). The adjacent skin around perforation of cholesteatoma was also significantly higher than non-cholesteatoma's with the average of 6.163 +/- 1.051 and (5.785 +/- 1.428)% (P < 0.001). CONCLUSIONS: The adjacent skin around perforation in human middle ear cholesteatoma had a relatively hyperproliferative ability.

Adolescent↗

PubMed1997

Effect of hypoxia on the proliferation of retinal microvessel endothelial cells in culture.

BACKGROUND: To determine if hypoxia stimulates the proliferation of retinal microvessel endothelial cells in culture. METHODS: Bovine retinal microvessel endothelial cells were cultured in normoxic (95% air, 5% CO2) and hypoxic (2% O2, 5% CO2, 93% N2) conditions. Endothelial cells were identified by acetylated LDL and Factor VIII-related antigen immunocytochemical staining. Cells from passages three to eight were used in these experiments. Proliferation assays included cell counts by hemocytometer and autoradiographic analysis of incorporated 3H-thymidine (3H-TdR). RESULTS: At day 4, cell counts of endothelial cells in hypoxia showed a 133% increase over those grown in normoxic conditions (N = 25, P < 0.01). Cell counts per day for 5 days were 121-181% greater in hypoxia. Autoradiography of endothelial cells exposed to 3H-TdR and counted every 12 hours for 60 hours exhibited labeling indices 112-118% higher in hypoxic conditions (P < 0.0001). Endothelial cells cultured under hypoxic conditions were smaller and spindle-shaped, whereas those grown under normoxic conditions were larger and more polygonal. CONCLUSIONS: Hypoxia increases DNA synthesis and stimulates proliferation of retinal microvessel endothelial cells in vitro and induces alterations in morphology. These results may be relevant to microvessel angiogenesis, which occurs in vivo under ischemic conditions.

Animals↗

PubMed1995

Hyperthermia induces ultrastructural changes in mouse pial microvessels.

BACKGROUND: Pial microvessels' responses to local hyperthermia revealed the development of in vivo spontaneous thrombosis. The cellular and subcellular changes which contribute to such events remained unexplored. Therefore, the effect of regional hyperthermia (43 degrees C) on mouse pial microvessels was studied at the ultrastructural level. METHODS: A simple cranial window assembly, including an artificial cerebrospinal fluid delivery and heating system to ensure a precise brain regional temperature, was used. The animal core body temperature was maintained at 37 degrees C. Topical and transvessel bimodal fixation of microvessels was done with a phosphate buffered mixture of glutaraldehyde and paraformaldehyde, followed by a standard electron microscopy procedure. RESULTS: When the pial microvessels of control (37 degrees C) animals were examined, no evidence of cellular damage was discerned. Endothelial cells including luminal membrane were unchanged. Degranulated platelets or platelet aggregates were not seen. However, numerous platelets in association with scattered red blood cells and occasional white blood cells could be observed in a close proximity, but not adhered, to the endothelial wall of hyperthermic (43 degrees C) brains. Platelets displayed a variety of forms consistent with the onset of platelet activation. Discoid platelets containing granules and spheroid degranulated platelets and those with large pseudopodia were recognized. The venular endothelial surface revealed conspicuous endothelial change, with the presence of endothelial denudation. The site of platelet aggregation in both venules and arterioles was accompanied by focal endothelial lucency and denudation vacuole formation, luminal membrane rupture, and swelling of the nuclear envelope. CONCLUSIONS: These findings demonstrate the extent of damage to the pial microvasculature in response to a local hyperthermic exposure. The results emphasize that changes in the endothelium may represent the earliest signs of oncoming vascular pathology.

Animals↗

PubMed1992

Butanol-extractable and detergent-solubilized cell surface components from murine large cell lymphoma cells associated with adhesion to organ microvessel endothelial cells.

Metastatic variant cell lines of the murine RAW117 large cell lymphoma were used to study the cell surface components involved in syngeneic tumor cell/microvessel endothelial cell interactions. Poorly liver-metastatic parental RAW117-P cell line adhered to murine hepatic sinusoidal endothelial cell monolayers at significantly lower rates than the liver-selected, highly liver-metastatic RAW117-H10 line and both cell lines were poorly adherent to lung microvessel and bovine aorta endothelial cells. Viable, 2% 1-butanol-treated RAW117-H10 tumor cells formed fewer liver tumor nodules in experimental metastasis assays than untreated H10 cells and were significantly less adherent to murine hepatic sinusoidal endothelial cell monolayers. When 2% 1-butanol extracts of metabolically labeled or CHAPS detergent lysates of cell surface-labeled tumor cells were analyzed for their ability to bind to fixed microvessel endothelial cell monolayers, quantitative differences were found in the extractable tumor cell surface components that bound to the different organ-derived microvessel endothelial cells. Cell surface components (1-butanol extractable), of Mr approximately 85,000-90,000 and approximately 37,000-40,000 bound to hepatic sinusoidal endothelial cell monolayers to a greater extent than to murine lung microvessel endothelial or bovine aortic endothelial cell monolayers, whereas tumor cell surface components of Mr approximately 45,000, approximately 33,000, and approximately 25,000 bound similarly to endothelial cells regardless of origin. The results suggest but do not prove that tumor cell/endothelial cell adhesion involves multiple tumor cell surface components, some of which commonly bind to various endothelial cells and others for which binding may be dictated by the tissue origin and type of endothelial cell. Particular RAW117 butanol-extractable cell membrane components were associated with tumor cell-endothelial cell adhesion, and these components could be responsible, in part, for the preferential adhesion of RAW117 cells to liver sinusoidal endothelial cells and metastasis to liver.

1-Butanol↗

PubMed1988

Transport of digoxin into brain microvessels and choroid plexuses isolated from guinea pig.

To characterize the efflux system of digoxin, a cardiac glycoside, from the brain to the blood through the blood-brain barrier and blood-cerebrospinal fluid (CSF) barrier, the accumulation of digoxin by the brain microvessel or the choroid plexus isolated from guinea pig brain was investigated. The accumulation of digoxin by the brain microvessel has a saturable component (Km = 0.163 microM, Vmax = 0.142 nmol/mL of tissue/min), with a nonsaturable component [Kd = 0.203 cell-to-medium (C:M) ratio/min] that was decreased by hypothermia (Q10 = 2.9), sulfhydryl reagent, and quinidine, but not by a metabolic inhibitor [2,4-dinitrophenol (DNP)]. It was concentration- and Na+-dependent. The accumulation of digoxin by the choroid plexus was also saturable (Km = 1.9 microM, Vmax = 3.8 nmol/mL of tissue/min), and was decreased by hypothermia (Q10 = 4.4), sulfhydryl reagents, ouabain, and quinidine, but not by metabolic inhibitors (DNP, KCN); it was also concentration- and Na+-dependent. The binding of digoxin to the homogenate of choroid plexus was one-tenth of digoxin accumulation by the intact choroid plexus, suggesting that digoxin is transported into the cells and bound to the cytosol fraction. The value of (Vmax/Km + Kd) multiplied by the total tissue weight of the microvessel per guinea pig is approximately 10-fold that of Vmax/Km multiplied by the tissue weight of the choroid plexus, although (Vmax/Km + Kd) per milliliter of the microvessel is half the Vmax/Km value of the choroid plexus. These findings suggest that digoxin can be excreted from both the brain and the cerebrospinal fluid to blood by a carrier-mediated diffusion system which is inhibited by quinidine, and that a main route of digoxin efflux from the brain to the blood is not through the blood-CSF barrier, but through the blood-brain barrier.

Animals↗

PubMed2002

Vascular activities of prostaglandins and selective prostanoid receptor agonists in human retinal microvessels.

Prostanoid analogs have recently been introduced into clinical use for the management of increased intraocular pressure (IOP). This class of compounds is known to exert effects on vascular components and some endogenous parent prostaglandins have been shown to alter regional ocular blood flow and exhibit significant vasoactive properties in isolated ocular blood vessels, so the possibility exists that prostanoids could affect the ocular microcirculation either by absorption into the systemic circulation or by direct localized activity on the retinal microvasculature. Thus, the aim of this study was to examine systematically the effects of a broad variety of agonists that exhibit preferential activity at EP(1)-, EP(2)-, EP(3)-, FP-, DP-, IP-, and TP-prostanoid receptor sites on microvessel caliber in the microvasculature associated with human retinal tissues grafted into the hamster cheek pouch membrane. The selective DP-receptor agonist, BW245C and the selective TP-receptor agonist, U-46619, were the only compounds tested that exhibited significant vasoactive effects relative to baseline resting diameters in retinal microvessels. A dose-dependent increase in arteriolar caliber was elicited by BW245C over a concentration range of 10(-8)-10(-4)M at the tested 5- and 10-min timepoints. U-46619 evoked a sharp decrease in microvessel diameter within a 10(-7)-10(-4)M gamut, with the dose-response profiles at 5- and 10-min timepoints remaining essentially parallel over the tested range of concentrations. In contrast to the vasoconstriction induced by U-46619, retinal microvessel calibers were not markedly affected by AGN 192093, a thromboxane-like agonist with additional unique properties. No significant changes in human retinal arteriolar diameters relative to baseline were observed in response to a broad panel of parent and derived compounds known to be selective for EP-, FP- and IP-prostanoid receptors.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1999

Prognostic significance of epithelial-stromal vascular cuffing and microvessel density in squamous cell carcinoma of the uterine cervix.

OBJECTIVE: Tumor angiogenesis has been shown to play an important role in tumor growth and metastasis. This study examines the prognostic significance of two histological markers of angiogenesis, i.e., vascular cuffing (VC), a bead-like arrangement of microvessels closely surrounding microscopic tumor nests, and microvessel density (MVD), the number of microvessels in a unit area, in cervical squamous cell carcinoma. METHODS: One hundred twenty-two specimens from surgically resected uteri with cervical squamous cell carcinoma were histologically reviewed and immunostained for CD34. VC was graded into "none," "incomplete," and "complete." The MVD was determined by counting the microvessels with a light microscope within a x200 field area where neovascularization occurred most actively. Stromal inflammation was also split into three grades. The relationship of VC or MVD to clinicopathological prognostic factors such as FIGO stage, cervical stromal invasion, lymph-vascular space invasion, pelvic lymph node metastasis, and parametrial invasion was evaluated using univariate and multivariate analyses. RESULTS: The patients with a complete VC pattern showed a significantly worse prognosis compared to those with a pattern graded as either none or incomplete (P<0.011 and P<0.0001, respectively). The Cox regression analysis revealed the complete VC pattern, together with parametrial invasion, to be an independent prognostic indicator for overall survival. MVD and the grading of stromal inflammation showed no significant relationship with VC or overall survival. CONCLUSIONS: The complete VC pattern may therefore be a useful prognostic indicator in cervical squamous cell carcinoma.

Adult↗

PubMed1994

Remodelling of microvessels by coronary hypertension or cardiac hypertrophy in rats.

We attempted to clarify the individual effects of coronary hypertension and ventricular pressure-overload on the remodelling of coronary arterial microvessels. We examined structural vascular changes in the right ventricular free walls using two experimental rat models: 12-week ascending aortic banding, i.e. a model of coronary hypertension without ventricular pressure-overload and 12-week pulmonary artery banding, i.e. a model of ventricular pressure-overload without coronary hypertension. In vivo peak systolic left ventricular pressure and left ventricular weight to body weight ratio in the aortic banding model increased to 198 +/- 10 mmHg and by 39% above the controls, respectively. In vivo peak right ventricular pressure and right ventricular weight to body weight ratio in the pulmonary artery banding model increased to 87 +/- 7 mmHg and by 69% above the controls, respectively. The right coronary reserve measured by the Doppler method decreased in both experimental models. Aortic banding increased the medial area and perivascular collagen to lumen area ratios in the microvessels > 30 microns in lumen diameter but not in those < 30 microns. Pulmonary artery banding increased the perivascular collagen to lumen area ratio in the microvessels < 60 microns, but not in those > 60 microns. Medial thickening was not observed over the whole range of lumen diameter. These results suggest that the mechanisms responsible for the remodelling of coronary microvessels differ between non-hypertrophied hearts with coronary hypertension and hypertrophied hearts without coronary hypertension.

Animals↗

PubMed2000

Canine coronary microvessel NO production regulates oxygen consumption in ecNOS knockout mouse heart.

We have previously shown that NO production by tissues following stimulation with bradykinin or other agonists can regulate oxygen consumption in skeletal muscle, heart and kidney. From those studies and from those using agonists, which classically release NO from blood vessels and which are unable to regulate tissue oxygen consumption in heart from ecNOS knockout mice, we concluded that vascular NO production is capable of regulating tissue oxygen consumption. The goal of these studies was to directly address the concept that NO production by blood vessels can regulate tissue oxygen consumption using a classical transfer paradigm. Microvessels, capable of producing NO, were prepared from canine hearts using a sieving technique, cardiac tissue was taken from mice lacking the ability to produce NO from ecNOS (ecNOS -/- mice) and tissue oxygen consumption measured in vitro using a Clark type electrode in a sealed chamber. Bradykinin (10(-7)to 10(-4)M) had no effect on tissue oxygen consumption when administered to heart from ecNOS -/mice as expected and no effect on oxygen consumption by isolated canine coronary microvessels (0+/-5% at 10(-5)M). However when coronary microvessels were co-incubated with heart from ecNOS -/- mice, bradykinin caused a dose dependent reduction in tissue oxygen consumption reaching a maximum of 44+/-10% at 10(-4)M. The effects of bradykinin were entirely abolished by L -NAME. The calculated concentration range for NO in these studies was 2.9 to 293 n M, within estimated physiologic range for the activity of NO on cytochrome oxidase. These data indicate that coronary microvessels can regulate cardiac oxygen consumption through a NO dependent mechanism.

Animals↗

PubMed1995

Effects of human alpha-thrombin and 8bromo-cAMP on large and microvessel endothelial monolayer equivalent "pore" radii.

Previous studies have reported that endothelial cells isolated from large vessels compared with microvessels from the same or distinct organs showed considerable phenotypic and biochemical heterogeneity. In the present study we extend these findings by comparison of the effects of 8-bromo-cyclic adenosine monophosphate (8Br-cAMP), human alpha-thrombin, 8Br-cAMP followed 5 min later by thrombin or no treatment (control) on the equivalent "pore" radii (rp) of endothelial monolayers isolated from the main bovine pulmonary artery (BPAEC) compared with lung microvessels (BLMV). BLMV, isolated from a 1-cm peripheral segment of the lung, were significantly larger than those obtained from large vessels (1602 +/- 142 microns2 vs 398 +/- microns2, respectively). In addition, BLMV monolayers formed a heteroporous barrier with less size-selectivity compared with BPAEC monolayers. 8Br-cAMP caused monolayers of both cell types to close their large "pores" which completely restricted the passage of solute molecular radii > 35-60 A across these barriers, consistent with a rp of approximately 75-100 A. This effect was due to a reduction in the area available for solute exchange (Ap) and/or an increase in the path length of the transport pathway (delta X). Human alpha-thrombin produced an increase in the Ap/delta X consistent with the formation of large open areas between adjacent cells that exposed the approximately 2000 A pore radius of the filter support. Since this effect was more marked in microvessel compared with large vessel monolayers, microvessel endothelial cells appear to be more sensitive to the effects of thrombin.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1995

Effect of histamine on endothelial permeability and structure and adhesion molecules of the paracellular junctions of perfused human placental microvessels.

The microvessels of the human placenta resemble those of skeletal muscle, both in endothelial cell junctional organization and in the single passage extraction of radiolabeled tracers. Addition of histamine (100 microM) to the fetal perfusate in an isolated term lobule resulted in a rapid and sustained rise (40-80%) over a 30-min perfusion period in the single circulation extraction values of 57Co-labeled cyanocobalamin and of 51Cr-labeled EDTA, but not of 22Na. Extraction values for 125I-albumin were not increased in histamine-perfused vessels nor was any focal leakage of label observed in serial cryostat sections of lobules perfused with rhodamine-conjugated albumin. There was no electron microscopic evidence of transendothelial channels in the microvascular bed; no gaps were seen at the paracellular cleft regions or in neighboring cytoplasm in any microvessels. Tilting of sections on a goniometric stage showed a significant increase in the separation between adjoining endothelial membrane leaflets at tight junctional regions (from 4.1 to 6.1 nm) although the dimensions of the wide zones remained unchanged. Placental microvessels contain the endothelial adhesion molecules PECAM-1 and VE-cadherin in the wide regions of paracellular clefts: PECAM-1 is also localized on the luminal membrane. Histamine-stimulated microvessels showed an altered staining pattern for both of these molecules, at the expense of the cleft regions. These changes in adhesion molecule distribution and tight junctional membrane separation may be parts of a series of events which leads to increased permeability during inflammatory events.

Antigens, CD↗

PubMed2001

Mathematical analysis of hemoglobin spectrophotometry in microvessels.

Spectrophotometry of hemoglobin in microvessels is commonly performed by collecting light either from a small region around the vessel centerline or from the entire lumen of the vessel. In the latter instance, parallel rays of light may not encounter the same amount of absorbing species. Hence, a phenomenon similar to the sieve effect reported in the literature on hemoglobin spectrophotometry may be expected to occur. Although it has been observed that under such circumstances nonlinearities in calibration characteristics arise, the implications of this effect on the interpretation of the spectrophotometric mean concentration have never been addressed so far. Mathematical analysis of hemoglobin spectrophotometry in microvessels, performed in this study, reveals that for practical situations the calibration curve is indeed nonlinear. Moreover, the spectrophotometric mean oxygen saturation is an overestimate of the mean oxygen saturation during oxygenation and an underestimate of the mean oxygen saturation during deoxygenation. These deviations depend upon the manner in which the total heme concentration is distributed within the lumen. Application of the analysis to artificial microvessels showed that the observed superior oxygen transport characteristics of flowing erythrocyte suspensions and hemoglobin solution mixtures could in part be due to the assumptions underlying the procedure used to interpret the experimental results. The implications of this result on models for oxygen transport in microvessels are discussed along with possible resolutions.

Calibration↗

PubMed2002

Impact of microscope numerical aperture on microspectrophotometric measurements of hemoglobin in microvessels.

In the microspectrophotometric method to measure hemoglobin concentration and oxygen saturation in microvessels it is recommended that a low numerical aperture (NA) condenser be employed to ensure that the recorded image is a true projection of the object. However, this tenet has never been rigorously justified. In this study, the microspectrophotometric method is evaluated using the theory of three-dimensional image formation by a light microscope for a wide range of NA. The results of the calculations show that for measurements for hemoglobin concentration, the recorded image is close to the true projection only when the size of the microvessel is large compared to the degree of smearing ( proportional, variant 1/NA) but small compared to the degree of defocus ( proportional, variant NA(2)). These opposing tendencies lead to an optimum NA for which the errors are minimum. This optimum NA is a function of the size of the microvessel and the manner in which the hemoglobin concentration is distributed within the lumen. For measurements of oxygen saturation, the recorded image is the true projection as long as the measurements are made in regions near the microvessel centerline. For measurements made in regions away from the centerline, good agreement was obtained only when the distribution of oxygen saturation was uniform. Reconstruction of the axisymmetric profiles from the recorded projections showed that the errors in the projections cause the recovered profiles to deviate from the true profiles. These deviations are directly related to the extent by which the recorded projections deviate from the true projection.

Animals↗

PubMed1989

The effect of bradykinin and its fragments on the arachidonate cascade of brain microvessels.

The lipoxygenase pathway dominated the arachidonate cascade in the microvessels isolated from cerebral cortical microvessels of male rats. Bradykinin significantly reduced the lipoxygenase pathway and the synthesis of PGD2 in the microvessels of rats. The synthesis of vasoconstrictor cyclooxygenase metabolites was stimulated with Ser-Pro-Phe-Arg tetrapeptide in the cerebral capillaries while the Phe-Arg dipeptide stimulated the release of arachidonate metabolites. The arachidonate cascade was shifted to the cyclooxygenase pathway with angiotensin III in cerebral microvessels. Kallikrein stimulated the lipoxygenase pathway and the synthesis of vasoconstrictor cyclooxygenase metabolites.

Angiotensin II↗

PubMed1984

Adenylate cyclase in the microvessels of the rat brain. A histochemical study with light and electron microscopy.

The presence of adenylate cyclase (AC) in the microvessels of the rat brain was studied by a new histochemical method for light and electron microscopy. The method is based on the precipitation of strontium and the subsequent conversion of the formed strontium salt into lead phosphate. Isoproterenol and 5-guanylylimidodiphosphate were used as enzyme activators. In the light microscope, the final reaction product was detected in the choroid plexus as well as in the walls of the microvessels in the brain parenchyma. In the electron microscope, both the luminal and abluminal endothelial membrane as well as the basal lamina of the parenchymal microvessels displayed reaction product. The observations demonstrate that isoproterenol-stimulated AC is located in the endothelium of the rat brain microvessels and suggest that the enzyme may play a role in the receptor-mediated regulation of endothelial functions.

Adenylyl Cyclases↗