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PubMed2004

Anatomic analysis of blood vessels in germinal matrix, cerebral cortex, and white matter in developing infants.

The germinal matrix (GM) located in the thick subependymal cell layer of the thalamostriate groove is a major site of cerebral hemorrhage in premature infants. Comparing the morphology of vasculature among GM, gray and white matter of the brain may help in understanding the pathogenesis of GM hemorrhage and also of periventricular leukomalacia. The objective of the present study was to determine the morphology of blood vessels in the GM, gray matter, and white matter and to examine maturational changes in the morphology of these vessels as a function of gestational age. We measured vessel density, percentage of blood vessel area, mean surface area, length, breadth, perimeter, radius, and shape of blood vessels in coronal sections of the GM, gray matter, and white matter in postmortem human brain samples for 17 fetuses and premature infants of gestational age 16-40 wk and 2 adults. We performed immunohistochemical staining using anti-laminin primary antibody, confocal microscopy to acquire images, and analysis using Metamorph version 6.1. Vessel density and the percentage of blood vessel area increased as a function of gestational age in the GM, gray matter, and white matter (p < 0.001 each). The blood vessel density and the percentage of blood vessel area were largest in the GM followed by gray matter and then white matter in all of the gestational age categories (p < 0.001 for all comparisons). Increased vascularity of the GM compared with gray and white matter may play a role in GM hemorrhage, whereas a relatively low vascularity of white matter may increase the propensity for the occurrence of periventricular leukomalacia in premature infants

Cerebral Cortex↗
PubMed1999

Three-dimensional structure of the micro-blood vessels in thyroid tumors analyzed by immunohistochemistry coupled with image analysis.

The structure of micro-blood vessels, one of the most important factors influencing the tumor growth and tumor metastasis among histological types of thyroid malignancy, was analyzed immunochemically by staining tissues for platelet endothelial cell adhesion molecule-1 (PECAM-1). Human thyroid tumor tissue obtained at surgery, consisting of 18 cases of papillary carcinoma, 9 cases of follicular carcinoma, and 9 cases of anaplastic carcinoma were fixed in formalin solution, and paraffin sections were made. They were stained for PECAM-1 using the avidin-biotin complex (ABC) technique. The volume of the blood vessels and their three-dimensional (3D) structure were analyzed using an image analyzer. The volume ratios of blood vessels in thyroid tissues were: normal tissues, 1.10%; papillary carcinoma, 3.01%; follicular carcinoma, 8.13%; and anaplastic carcinoma, 0.91%. Ratios in malignant tumors were larger than in normal tissues, except for anaplastic carcinoma. The typical 3D structure of micro-blood vessels was histopathologically varied: branching tree-like blood vessels in papillary carcinomas; vessels of varied diameter surrounding follicle structure in follicular carcinomas; and simple and immature vessels in anaplastic carcinomas. The volume and 3D structure of micro-blood vessels in thyroid malignant tumors differed from those in normal tissues, and varied according to histological classification.

Adenocarcinoma, Follicular↗
PubMed1998

[Major blood vessel excision and reconstruction in the treatment of retroperitoneal neoplasms].

OBJECTIVE: To summarize the experience in the treatment of retroperitoneal tumors involving major blood vessels. METHODS: Twenty five cases with retroperitoneal tumors involving major blood vessels were treated by excision of the tumor and the major blood vessel involved followed by vascular reconstruction. RESULTS: After a careful preoperative evaluation and necessary preparation, the tumor together with the involved blood vessels in all patients are successfully resected and the severed major blood vessels reconstructed. There was no operative death. CONCLUSION: Retroperitoneal neoplasm involving major blood vessels is not a contraindication for surgical resection. The tumor and the involved vessel can be removed en bloc followed by vascular reconstruction. The risk of local tumor recurrence can thus be minimized and better survival achieved.

Adolescent↗
PubMed2003

Tissue engineering of blood vessels with endothelial cells differentiated from mouse embryonic stem cells.

Endothelial cells (TEC3 cells) derived from mouse embryonic stem (ES) cells were used as seed cells to construct blood vessels. Tissue engineered blood vessels were made by seeding 8 106 smooth muscle cells (SMCs) obtained from rabbit arteries onto a sheet of nonwoven polyglycolic acid (PGA) fibers, which was used as a biodegradable polymer scaffold. After being cultured in DMEM medium for 7 days in vitro, SMCs grew well on the PGA fibers, and the cell-PGA sheet was then wrapped around a silicon tube, and implanted subcutaneously into nude mice. After 6~8 weeks, the silicon tube was replaced with another silicon tube in smaller diameter, and then the TEC3 cells (endothelial cells differentiated from mouse ES cells) were injected inside the engineered vessel tube as the test group. In the control group only culture medium was injected. Five days later, the engineered vessels were harvested for gross observation, histological and immunohistochemical analysis. The preliminary results demonstrated that the SMC-PGA construct could form a tubular structure in 6~8 weeks and PGA fibers were completely degraded. Histological and immunohistochemical analysis of the newly formed tissue revealed a typical blood vessel structure, including a lining of endothelial cells (ECs) on the lumimal surface and the presence of SMC and collagen in the wall. No EC lining was found in the tubes of control group. Therefore, the ECs differentiated from mouse ES cells can serve as seed cells for endothelium lining in tissue engineered blood vessels.

Animals↗
PubMed1995

Is the clustering of beta-amyloid (A beta) deposits in the frontal cortex of Alzheimer patients determined by blood vessels?

The clustering pattern of diffuse, primitive and classic beta-amyloid (A beta) deposits was studied in the upper laminae of the frontal cortex of 9 patients with sporadic Alzheimer's disease (AD). A beta stained tissue was counterstained with collagen type IV antiserum to determine whether the clusters of A beta deposits were related to blood vessels. In all patients, A beta deposits and blood vessels were clustered, with in many patients, a regular periodicity of clusters along the cortex parallel to the pia. The classic A beta deposit clusters coincided with those of the larger blood vessels in all patients and with clusters of smaller blood vessels in 4 patients. Diffuse deposit clusters were related to blood vessels in 3 patients. Primitive deposit clusters were either unrelated to or negatively correlated with the blood vessels in six patients. Hence, A beta deposit subtypes differ in their relationship to blood vessels. The data suggest a direct and specific role for the larger blood vessels in the formation of amyloid cores in AD.

Aged↗
PubMed1999

Validity of viscoelastic models of blood vessel wall.

Quantitative description of biomechanical behaviour of the blood vessel wall is needed for understanding normal and pathologic functions of the vascular system. In this study we investigated the stress relaxation of blood vessels. Strips were cut from the vessel wall and they were stretched in a stepwise manner until they tore. The mechanical stress (approximately 10(5)-10(6) Pa) induced in the strips was determined. This showed an initial steep rise and then a slow, near exponential decay (stress relaxation) after each step of stretch. For the mathematical description we used two technical models (the Maxwell and the Kelvin model--they are built of two elastic elements and of one viscous element), as well as a one-dimensional continuum mechanical model. The moduli of the models were identified with a curve fitting method. Our aim was to compare these models in order to elucidate, which one describes the rheological behaviour of the blood vessel more correctly. The results of our analysis show that the corresponding moduli diverge from each other in the Maxwell and Kelvin models: that is, they depend on the mode of the assumed connection between the mechanical units. In contrast, moduli of the continuous model are unambiguous. We conclude that the continuous model properly describes the stress relaxation of the vascular wall. Its advantage over the technical models is that moduli describing the viscoelastic behaviour of the tissue do not depend on the not wholly well-known structure of the wall components.

Algorithms↗
PubMed1991

[The effect of nasal sensory nerve on the enhanced nasal blood vessel permeability caused by histamine].

The rats' nasal blood vessel permeability caused by histamine was significantly lower in the groups pretreated with dicaine or maxillary neurectomy than in the histamine control group. The rats' nasal blood vessel permeability also enhanced with the central side of maxillary nerve stimulated electrically. The latter effect could be blocked by pretreating with atropine. Combining with other experimental results, we suggest that the nasal sensory nerve joins the processes of the nasal blood vessel permeability enhancement caused by histamine.

Animals↗
PubMed2002

Multiparameter fluorescence mapping of nonprotein sulfhydryl status in relation to blood vessels and hypoxia in cervical carcinoma xenografts.

PURPOSE: Aberrant architecture of the tumor vasculature and temporal fluctuations in blood flow can result in tumor hypoxia. The aim of this study was to classify tumor hypoxia based on distance to blood vessels, and to characterize its biologic significance by determining levels of nonprotein sulfhydryls (NPSH) in hypoxic regions located proximally and distally to tumor blood vessels. METHODS AND MATERIALS: A dual fluorescence method was developed for the spatial colocalization of the vasculature and hypoxia in frozen sections from SiHa cervical carcinoma xenografts. A parallel section was stained with the sulfhydryl stain mercury orange. Composite fluorescence images were generated by imaging and tiling individual fields of view into 2D image arrays. Image arithmetic techniques were combined with feature-based image segmentation to characterize expression of NPSH as a function of the hypoxic tumor microenvironment. RESULTS: NPSH levels were higher in hypoxic areas of the SiHa xenografts (15.1 +/- 0.5 vs. 13.5 +/- 0.5 integrated optical density [IOD], p < 0.03). When tumor hypoxia was classified by distance to the nearest visible blood vessel, significantly higher NPSH levels were found in hypoxic regions close to blood vessels than in regions at a distance from blood vessels. CONCLUSION: The results of this study indicate differential expression of NPSH levels in regions of hypoxia that are proximal or distal to blood vessels in SiHa tumors.

Animals↗
PubMed1992

Reactivity of small blood vessels in hypertension: relation with structural changes. State of the art lecture.

Small blood vessels, particularly small arteries of 150-300 microns in lumen diameter and larger arterioles of 50-150 microns in lumen diameter, are the most important location of the arterial bed that undergoes changes resulting in the increased peripheral resistance that characterizes elevated blood pressure. This article reviews these morphological and functional alterations of small blood vessels. Study of mesenteric small arteries with a lumen diameter of 220-260 microns revealed consistently a reduced external and lumen diameter in renal and deoxycorticosterone acetate-salt hypertensive rats early in the evolution of hypertension. The media of the vessel wall was significantly thickened in the hypertensive rats, and the media/lumen ratio was increased. Although the tension that developed in response to different vasoconstrictors was not elevated or was even decreased in hypertensive rats, exaggerated transmural pressures resulted in the isolated blood vessels as a consequence of the law of Laplace because of the narrowed lumen. Similar findings were obtained in small resistance arteries from subcutaneous gluteal biopsies of hypertensive humans. In arterioles, on the other hand, decreases in the density of blood vessels (rarefaction) and in vasomotion amplitude may play a more important role than reductions in lumen diameter. As a consequence of the design of small resistance blood vessels and as a result of functional and structural alterations, which may be primary to or a consequence of high blood pressure, the pressor effect of vasoconstrictors is amplified and interacts with other factors to contribute to the maintenance of elevated blood pressure even if the intrinsic response of vascular smooth muscle to these agents is not exaggerated.

Humans↗
PubMed2005

Wavelength dependence of the apparent diameter of retinal blood vessels.

Imaging of retinal blood vessels may assist in the diagnosis and monitoring of diseases such as glaucoma, diabetic retinopathy, and hypertension. However, close examination reveals that the contrast and apparent diameter of vessels are dependent on the wavelength of the illuminating light. In this study multispectral images of large arteries and veins within enucleated swine eyes are obtained with a modified fundus camera by use of intravitreal illumination. The diameters of selected vessels are measured as a function of wavelength by cross-sectional analysis. A fixed scale with spectrally independent dimension is placed above the retina to isolate the chromatic effects of the imaging system and eye. Significant apparent differences between arterial and venous diameters are found, with larger diameters observed at shorter wavelengths. These differences are due primarily to spectral absorption in the cylindrical blood column.

Algorithms↗
PubMed2004

MaxiK channel roles in blood vessel relaxations induced by endothelium-derived relaxing factors and their molecular mechanisms.

The endothelium of blood vessels plays a crucial role in the regulation of blood flow by controlling mechanical functions of underlying vascular smooth muscle. The regulation by the endothelium of vascular smooth muscle relaxation and contraction is mainly achieved via the release of vasoactive substances upon stimulation with neurohumoural substances and physical stimuli. Nitric oxide (NO) and prostaglandin I2 (prostacyclin, PGI2) are representative endothelium-derived chemicals that exhibit powerful blood vessel relaxation. NO action involves activation of soluble guanylyl cyclase and PGI2 action is initiated by the stimulation of a cell-surface receptor (IP receptor, IPR) that is coupled with Gs-protein-adenylyl cyclase cascade. Many studies on the mechanisms by which NO and PGI2 elicit blood vessel relaxation have highlighted a role of the large conductance, Ca2+-activated K+ (MaxiK, BKCa) channel in smooth muscle as their common downstream effector. Furthermore, their molecular mechanisms have been unravelled to include new routes different from the conventionally approved intracellular pathways. MaxiK channel might also serve as a target for endothelium-derived hyperpolarizing factor (EDHF), the non-NO, non-PGI2 endothelium-derived relaxing factor in some blood vessels. In this brief article, we review how MaxiK channel serves as an endothelium-vascular smooth muscle transducer to communicate the chemical signals generated in the endothelium to control blood vessel mechanical functions and discuss their molecular mechanisms.

Animals↗
PubMed1998

Ultrastructure of blood vessel regression in involution of foreign-body granuloma.

The diversity of endothelial cell deletion in regressing blood vessels during involution of granulation tissue was investigated in foreign-body granulomas induced by a collagen sponge implanted into the dorsum of the rat. Small blood vessel density counts were performed to determine the degree of blood vessel regression in the involution of granulation tissue in foreign-body granuloma. The density of these small blood vessels significantly decreased between 100 and 130 days after sponge implantation. The detachment of endothelial cells from their underlying basement membrane and the consequent protrusion into and/or out of the lumen in the vascular network of granulation tissue was observed by electron microscopy. Based on the pattern of manifestation in the endothelium and the characteristic deformation of nuclei, the detached endothelial cells were classified into two groups: 1) the endothelial cell apoptosis group and 2) the endothelial cell degeneration group. The essential difference between the two groups was easily distinguishable as the nucleus of the former group displayed chromatin condensation and margination as the hallmark of early apoptotic changes, while the nucleus of the latter group displayed a pinch structure and intranuclear pocket formation. However, the process by which the detached endothelial cells were shed into the vascular lumen and eventually eliminated from circulation was the same in both groups. The occurrence of both groups increased on the 90th day after sponge implantation and reached a maximum on the 110th day, indicating that the appearance of the groups was synchronized. These results suggest that the two major processes of apoptosis and degeneration of endothelial cells occur during endothelial cell deletion as a mechanism contributing to blood vessel regression.

Animals↗
PubMed1996

Expression of integrin alpha v beta 3 in small blood vessels of glioblastoma tumors.

Angiogenesis, which promotes tumor proliferation and invasiveness, is mediated by integrin-dependent cell adhesion mechanisms and requires expression of integrin alpha v beta 3. To determine whether integrin alpha v beta 3 is expressed in the small blood vessel hyperplasia characteristic of glioblastoma tumors, we explored the mRNA and protein expression of integrin alpha v, beta 3, beta 5, and beta 1 subunits in small blood vessels in gliomas of various grades and nontumorous brain biopsies. Antisense beta 3 and beta 5 riboprobes hybridized to small blood vessels (endothelial and adjacent mesenchymal cells) in 11 of 11 glioblastomas and 2 of 4 anaplastic astrocytomas, but failed to hybridize to small blood vessels in 12 non-neoplastic specimens and 4 low-grade astrocytomas. In contrast, antisense alpha v and beta 1 riboprobes hybridized to small blood vessels in all of the biopsies. The expression of integrin alpha v beta 3 protein in these vessels was determined by immunohistochemical analysis using anti-integrin subunit-specific antibodies. The findings were similar to those obtained using in situ hybridization: beta 3 subunit protein was detected on small blood vessels in 9 of 12 glioblastoma and 2 of 4 anaplastic astrocytomas, whereas it was not detected in small blood vessels of 10 non-neoplastic brains and 4 low-grade astrocytomas. In contrast, the alpha v and beta 1 subunit proteins were detected in small blood vessels in all of the brain biopsies, whereas the beta 5 subunit protein could not be detected. These data suggest that integrin alpha v beta 3 is expressed in small blood vessels of glioblastoma tumors.

Adult↗
PubMed2004

VE-cadherin is not required for the formation of nascent blood vessels but acts to prevent their disassembly.

We investigated the role of vascular endothelial (VE)-cadherin in blood vessel morphogenesis and established a temporal correlation linking the failure in vessel morphogenesis in VE-cadherin null embryos to a specific step in vasculogenesis. We showed that the sequence in which blood vessels failed followed the order in which they had formed (ie, those forming first--yolk sac, allantoic and endocardial vessels--were the first to display morphologic abnormalities). We next showed that in place of normal reticulated networks of blood vessels, clusters of platelet endothelial cell adhesion molecule-positive (PECAM+) cells formed within cultured allantois explants from VE-cadherin null embryos. Similarly, a function-blocking VE-cadherin antibody, BV13, caused PECAM+ cell clusters to form in cultured allantois explants from normal mice. Finally, we demonstrated that formation of PECAM+ cell clusters in response to BV13 was not due to a disruption in the formation of nascent vessels but was due to the actual disassembly of nascent vessels. Based on these findings, we conclude that the events of de novo blood vessel formation up to the point at which a vascular epithelium forms (ie, nascent vessels with lumens) are not dependent on VE-cadherin and that VE-cadherin, whose expression is up-regulated following vascular epithelialization, is required to prevent the disassembly of nascent blood vessels.

Animals↗
PubMed2005

[A microangiography technique to quantify fasciocutaneous blood vessels in small laboratory animals].

PURPOSE: A microangiographic technique is described, which allows visualization of small blood vessels with a diameter of approximately 20 microm and quantification of fasciocutaneous blood vessels by means of digital computer analysis in very small laboratory animals. METHOD: The left carotid artery of 45 nu/nu mice was cannulated (26 gauge) and a mixture of gelatine, barium sulfate and green ink was injected according to standardized protocol. Fasciocutaneous blood vessels were visualized by digital mammography and analyzed for vessel length and vessel surface area as standardized units (pixel) by computer program. RESULTS: With the described microangiography method fasciocutaneous blood vessels can be clearly visualized. Regions of interest (ROIs) can be defined and the containing vascular network quantified. Identical ROIs showed a high reproducibility for measured unit (pixel) < 6.5 +/- 2.4 %. By the use of digital image, processing the quantification of vessels was reliable, reproducible and fast. CONCLUSION: Combining microsurgical techniques, pharmacological knowledge and modern computer imaging analysis systems, we were able to visualize and quantify blood vessels with a diameter of approximately 20 microm even in small laboratory animals.

Angiography↗
PubMed2005

Laser-induced thermal injury to dermal blood vessels: analysis of wavelength (585 nm vs. 595 nm), cryogen spray cooling, and wound healing effects.

BACKGROUND AND OBJECTIVES: Successful laser treatment of cutaneous hyper-vascular lesions requires appropriate laser irradiation parameters for selective photothermolysis of ectatic dermal blood vessels as well as appropriate cooling parameters for epidermal protection based on an individual patient basis. Using the rabbit ear as an in vivo model for dermal vasculature, we investigated the influences of laser wavelength (585 nm vs. 595 nm) and cryogen spray cooling with various spurt durations on the laser-induced thermal injury to dermal blood vessels. Wound healing response was also evaluated in 2 hours and 4 days. STUDY DESIGN/MATERIALS AND METHODS: Flashlamp-pumped pulsed dye laser ScleroPlus (operated at the wavelength of 585 or 595 nm) was used for the comparison between the influences of two wavelengths (585 nm vs. 595 nm). R134-a cryogen spurts with the durations from 50 to 300 milliseconds were sprayed onto the sites to be irradiated and terminated 20 milliseconds before the onset of the laser pulses. In vivo rabbit ear was used as the model for cutaneous hyper-vascular lesions. Totally 10 New Zealand Albino white rabbits were experimented and in each rabbit ear six to seven sites were irradiated. Five animals were sacrificed 2 hours after the irradiation, and the remaining five sacrificed 4 days after the irradiation. Thermal injury to the blood vessel was assessed by hematoxylin and eosin stained histological sections and confirmed by an apoptosis assay. RESULTS: When the radiant exposures were above 10 J/cm2, 595 nm wavelength induced equivalent or more severe thermal injury to dermal blood vessels than 585 nm. Cryogen spray cooling with the spurt durations above 100 milliseconds resulted in increased depth of the most superficial thermal injury to dermal blood vessels than without cooling, indicating that superficial blood vessels were non-specifically cooled by the cryogen spurts applied at these parameters. Laser-induced thermal injury was significantly healed in the rabbit ear vasculature at 4 days post irradiation. CONCLUSIONS: Given sufficient radiant exposure, 595 nm wavelength can induce equivalent or more severe vascular injury compared with 585 nm. Cryogen spray cooling with the spurt durations above 100 ms may impair the photocoagulation of superficial blood vessels. Irreversible thermal injury to blood vessel can be achieved only when the basement membrane of blood vessel wall is irreversibly damaged.

Aerosols↗
PubMed2004

Effect of atropine on denervated rabbit ear blood vessels.

Surgical denervation of rabbit ear blood vessel beds was combined with the isolated perfused rabbit ear technique to investigate the mechanism of atropine's vasodilator action. Intramuscular injection of atropine 0.2 mg/kg dilated the denervated blood vessels in the rabbit ear like innervated ones in vivo. Atropine at the maximal concentration (Cmax) of 3 x 10(-6) to 3 x 10(-4) M did not increase effluent flow of the isolated perfused denervated rabbit ear under constant perfusion pressure, but chlorpromazine at a Cmax of 10(-6) M and acetylcholine (ACh) at 2.5 x 10(-7) M significantly increased it and noradrenaline (NA) at 10(-7) M significantly decreased it. Atropine at Cmax of 3 x 10(-7) M did not affect, but at 3 x 10(-6) M it abolished the increase of the effluent flow induced by ACh 2.5 x 10(-7) M. Atropine at 3 x 10(-7) M did not affect it, but at 10(-6), 3 x 10(-6), and 10(-5) it significantly alleviated the decrease of effluent flow induced by NA 10(-7) M. Because the increase of effluent flow of rabbit ear under constant perfusion pressure reflects vasodilation of the ear to some extent, the study suggests that atropine has no direct vasodilator action; its vasodilator action is not attributed to blockade of M-cholinoreceptors located on the vascular wall; however, the alpha1-adrenoceptor might be a target site mediating atropine's vasodilator action in vivo.

Animals↗