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Microvascular Networks (microvascular + network)
Selected AbstractsSelf-Healing Chemistry: Delivery of Two-Part Self-Healing Chemistry via Microvascular Networks (Adv. Funct.ADVANCED FUNCTIONAL MATERIALS, Issue 9 2009Mater. Microvascular self-healing of a brittle coating is accomplished by supplying fluid healing agents from an underlying network of microchannels. Dual independent networks filled with a two-part healing chemistry (epoxy resin and curing agent) that repeatedly heal damage in the coating up to 16 consecutive times are reported by K. S. Toohey et al. on page 1399. [source] Delivery of Two-Part Self-Healing Chemistry via Microvascular NetworksADVANCED FUNCTIONAL MATERIALS, Issue 9 2009Kathleen S. Toohey Abstract Multiple healing cycles of a single crack in a brittle polymer coating are achieved by microvascular delivery of a two-part, epoxy-based self-healing chemistry. Epoxy resin and amine-based curing agents are transported to the crack plane through two sets of independent vascular networks embedded within a ductile polymer substrate beneath the coating. The two reactive components remain isolated and stable in the vascular networks until crack formation occurs in the coating under a mechanical load. Both healing components are wicked by capillary forces into the crack plane, where they react and effectively bond the crack faces closed. Healing efficiencies of over 60% are achieved for up to 16 intermittent healing cycles of a single crack, which represents a significant improvement over systems in which a single monomeric healing agent is delivered. [source] Self-Healing Materials with Interpenetrating Microvascular NetworksADVANCED MATERIALS, Issue 41 2009Christopher J. Hansen Interpenetrating microvascular networks are embedded in an epoxy substrate via direct-write assembly. Each network is filled with one component of a two-part epoxy resin. This novel epoxy coating/substrate architecture enables repeated healing of at least 30 cycles of mechanical damage in the coating by independently supplying both healing agents to the damaged region(s). [source] Effect of Aging on the Structure and Function of Skeletal Muscle Microvascular NetworksMICROCIRCULATION, Issue 4 2006SHAWN E. BEARDEN ABSTRACT Humans are active creatures, yet physical activity and activity tolerance decline over the life span. One prevailing theme in the literature to account for a portion of the reduced activity tolerance with aging is the observation that the capacity to augment blood flow to skeletal muscle may be impaired with advancing age. This dysfunction may be due to adaptations in the structure or function of their microvascular networks, which collectively determine blood flow resistance. The intent of this review is to present the current knowledge of structure and function of microvascular networks from skeletal muscle with special regard to how these may adapt to, or persist through, the aging process. Skeletal muscles are supplied by an intricate branching network of arterioles and venules. The consistency of findings among available studies suggests that the overall arteriolar and venular network branching topology establishes early in development and varies little, if at all, over the life span. Microvascular networks are not a series of functionally isolated segmental branches. Rather, these networks transmit and communicate vasomotor signals along their lengths and among their branches. Current evidence suggests that aging is associated with a decrement in the capacity of upstream vessels to respond to downstream vasodilation and signals transmitted cell-to-cell along the vascular wall. [source] Fractal and Fourier analysis of the hepatic sinusoidal network in normal and cirrhotic rat liverJOURNAL OF ANATOMY, Issue 2 2005Eugenio Gaudio Abstract The organization of the hepatic microvascular network has been widely studied in recent years, especially with regard to cirrhosis. This research has enabled us to recognize the distinctive vascular patterns in the cirrhotic liver, compared with the normal liver, which may explain the cause of liver dysfunction and failure. The aim of this study was to compare normal and cirrhotic rat livers by means of a quantitative mathematical approach based on fractal and Fourier analyses performed on photomicrographs and therefore on discriminant analysis. Vascular corrosion casts of livers belonging to the following three experimental groups were studied by scanning electron microscopy: normal rats, CCl4 -induced cirrhotic rats and cirrhotic rats after ligation of the bile duct. Photomicrographs were taken at a standard magnification; these images were used for the mathematical analysis. Our experimental design found that use of these different analyses reaches an efficiency of over 94%. Our analyses demonstrated a higher complexity of the normal hepatic sinusoidal network in comparison with the cirrhotic network. In particular, the morphological changes were more marked in the animals with bile duct-ligation cirrhosis compared with animals with CCl4 -induced cirrhosis. The present findings based on fractal and Fourier analysis could increase our understanding of the pathophysiological alterations of the liver, and may have a diagnostic value in future clinical research. [source] Vascular response to laser photothermolysis as a function of pulse duration, vessel type, and diameter: Implications for port wine stain laser therapyLASERS IN SURGERY AND MEDICINE, Issue 2 2002Sol Kimel PhD Abstract Background and Objective Treatment of port wine stains (PWS) by photothermolysis can be improved by optimizing laser parameters on an individual patient basis. We have studied the critical role of pulse duration (tp) on the treatment efficacy. Study Design/Materials and Methods The V-beam laser (Candela) allowed changing tp over user-specified discrete values between 1.5 and 40 milliseconds by delivering a series of 100 microsecond spikes. For the 1.5 and 3 millisecond pulses, three spikes were observed at intervals tp/2 and for tp,,,6 milliseconds, four spikes separated by tp/3. The ScleroPlus laser (Candela) has a smooth output over its fixed 1.5 milliseconds duration. Blood vessels in the chick chorioallantoic membrane (CAM) were irradiated at fixed wavelength (595 nm), spot size (7 mm), radiant exposure (15 Jcm,2), and at variable tp. The CAM contains an extensive microvascular network ranging from capillaries with diameter D,<,30 ,m to blood vessels of D,,,120 ,m. The CAM assay allows real-time video documentation, and observation of blood flow in pre-capillary arterioles (A) and post-capillary venules (V). Vessel injury was graded from recorded videotapes. Mathematical modeling was developed to interpret results of vessel injury when varying tp and D. A modified thermal relaxation time was introduced to calculate vessel wall temperature following laser exposure. Results Arterioles. For increasing tp, overall damage was found to decrease. For fixed tp, damage decreased with vessel size. Venules. For all D, damage was smaller than for corresponding arterioles. There was no dependence of damage on tp. For given tp, no variation of damage with D was observed. Photothermolysis due to spiked (V-beam) vs. smooth (Scleroplus) delivery of laser energy at fixed tp (1.5 milliseconds), showed similar vessel injuries for al values of D (P>0.05). Conclusions The difference between initial arteriole and venule damage could be explained by the threefold higher absorption coefficient at 595 nm in (oxygen-poor!) arterioles. In human patients, PWS consist of ectatic venules (characterized by higher absorption), so that these considerations favor the use of 595-nm irradiation for laser photothermolysis. For optimal treatment of PWS it is proposed that tp be between 0.1 and 1.5 milliseconds. This is based on a modified relaxation time ,d,, defined as the time required for heat conduction into the full thickness of the vessel wall, which is assumed to have a thickness ,D ,,0.1D. The corresponding ,d, will be a factor of about six smaller than given in the literature. For vessels with D between 30 and 300 ,m, ,d, ranges from 0.1 to 1.5 milliseconds. Lasers Surg. Med. 30:160,169, 2002. © 2002 Wiley-Liss, Inc. [source] Inhibition of Canonical Wnt Signaling Increases Microvascular Hemorrhaging and Venular Remodeling in Adult RatsMICROCIRCULATION, Issue 5 2010JASON T. GLAW Microcirculation (2010) 17, 348,357. doi: 10.1111/j.1549-8719.2010.00036.x Abstract Objective:, The canonical Wnt signaling pathway, heavily studied in development and cancer, has recently been implicated in microvascular growth with the use of developmental and in vitro models. To date, however, no study exists showing the effects of perturbing the canonical Wnt pathway in a complete microvascular network undergoing physiological remodeling in vivo. Our objective was to investigate the effects of canonical Wnt inhibition on the microvascular remodeling of adult rats. Methods:, Canonical Wnt inhibitor DKK-1, Wnt inhibitor sFRP-1, BSA or saline was superfused onto the exteriorized mesenteric windows of 300 g adult female Sprague-Dawley rats for 20 minutes. Three days following surgery, mesenteric windows were imaged intravitally and harvested for immunofluorescence staining with smooth muscle alpha-actin and BRDU. Results:, We observed prominent differences in the response of the mesenteric microvasculature amongst the various treatment groups. Significant increases in hemorrhage area, vascular density, and draining vessel diameter were observed in windows treated with Wnt inhibitors as compared to control-treated windows. Additionally, confocal imaging analysis showed significant increases in proliferating cells as well as evidence of proliferating smooth muscle cells along venules. Conclusions:, Together, our results suggest that canonical Wnt inhibition plays an important role in microvascular remodeling, specifically venular remodeling. [source] The bronchial circulation,worth a closer look: A review of the relationship between the bronchial vasculature and airway inflammationPEDIATRIC PULMONOLOGY, Issue 1 2010Angela McCullagh MBBS Abstract Until recently, the bronchial circulation has been relatively ignored in the research and clinical arenas, perhaps because of its small volume and seeming dispensability relative to the pulmonary circulation. Although the bronchial circulation only receives around 1% of the cardiac output in health, it serves functions that are critical to maintaining airway and lung function. The bronchial circulation also plays an important role in many lung and airway diseases; through its ability to increase in size, the bronchial circulation is able to provide lung parenchymal perfusion when the pulmonary circulation is compromised, and more recently the role of the bronchial circulation in the pathogenesis of inflammatory airway disease has been explored. Due to the anatomic variability and small volume of the bronchial circulation, much of the research to date has necessitated the use of animal models and invasive procedures. More recently, non-invasive techniques for measuring bronchial blood flow in the mucosal microvascular network have been developed and offer a new avenue for the study of this circulation in humans. In conjunction with molecular research, measurement of airway blood flow (Qaw) may help elucidate the role of the bronchial circulation in inflammatory airway disease and become a useful tool for monitoring therapy. Pediatr Pulmonol. 2010; 45:1,13. © 2009 Wiley-Liss, Inc. [source] Thrombectomy during PCI for acute myocardial infarctionCATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 7 2008Are the randomized controlled trial data relevant to the patients who really need this technique? Abstract Macro and microembolization during percutaneous coronary intervention (PCI) in ST elevation acute myocardial infarction (STEAMI) is frequent and may result in obstruction of the microvascular network with subsequent reduction in efficacy of reperfusion. Numerous mechanistic studies have shown that the presence and size of the culprit thrombus is the most powerful predictor of incidence of embolization and slow flow/no reflow. Techniques that have been used to reduce the incidence of these events include thrombectomy devices and embolic protection devices. Although numerous prospective randomized clinical trials have been performed to evaluate the role of thrombectomy devices in patients with STEAMI, the results of these trials are conflicting and they speak to both sides of the controversy. The Achilles heal of the majority of these trials is the premise that thrombectomy devices should be routinely used in all patients presenting with STEAMI even irrespective of the presence and size of the thrombus. Such a hypothesis is naively optimistic and it ignores the basic knowledge available to us regarding the relationship between thrombus burden and embolization. Nonetheless, clinicians are faced every day with the reality of making difficult decisions on how to best treat patients presenting with STEAMI and large thrombus burden. The current available "evidence-based medicine" cannot and should not be generalized to these patients because only a minority of these patients was included in these randomized clinical trials. In these patients, thrombectomy devices should be strongly considered as an integral part of the armamentarium available to reduce thrombus burden prior to definitive treatment. Whether a future clinical trial will provide a definitive answer in terms of clinical outcome difference is doubtful because such a trial will need to include large number of selected patients with STEAMI who both have large amount of myocardium at jeopardy and large thrombus burden, a difficult and possibly undoable study. © 2008 Wiley-Liss, Inc. [source] LARGE-SCALE SIMULATION OF THE HUMAN ARTERIAL TREECLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2 2009L Grinberg SUMMARY 1Full-scale simulations of the virtual physiological human (VPH) will require significant advances in modelling, multiscale mathematics, scientific computing and further advances in medical imaging. Herein, we review some of the main issues that need to be resolved in order to make three-dimensional (3D) simulations of blood flow in the human arterial tree feasible in the near future. 2A straightforward approach is computationally prohibitive even on the emerging petaflop supercomputers, so a three-level hierarchical approach based on vessel size is required, consisting of: (i) a macrovascular network (MaN); (ii) a mesovascular network (MeN); and (iii) a microvascular network (MiN). We present recent simulations of MaN obtained by solving the 3D Navier,Stokes equations on arterial networks with tens of arteries and bifurcations and accounting for the neglected dynamics through proper boundary conditions. 3A multiscale simulation coupling MaN,MeN,MiN and running on hundreds of thousands of processors on petaflop computers will require no more than a few CPU hours per cardiac cycle within the next 5 years. The rapidly growing capacity of supercomputing centres opens up the possibility of simulation studies of cardiovascular diseases, drug delivery, perfusion in the brain and other pathologies. [source] Self-Healing Materials with Interpenetrating Microvascular NetworksADVANCED MATERIALS, Issue 41 2009Christopher J. Hansen Interpenetrating microvascular networks are embedded in an epoxy substrate via direct-write assembly. Each network is filled with one component of a two-part epoxy resin. This novel epoxy coating/substrate architecture enables repeated healing of at least 30 cycles of mechanical damage in the coating by independently supplying both healing agents to the damaged region(s). [source] Collateral Capillary Arterialization following Arteriolar Ligation in Murine Skeletal MuscleMICROCIRCULATION, Issue 5 2010FEILIM MAC GABHANN Microcirculation (2010) 17, 333,347. doi: 10.1111/j.1549-8719.2010.00034.x Abstract Objective:, Chronic and acute ischemic diseases,peripheral artery disease, coronary artery disease, stroke,result in tissue damage unless blood flow is maintained or restored in a timely manner. Mice of different strains recover from arteriolar ligation (by increasing collateral blood flow) at different speeds. We quantify the spatio-temporal patterns of microvascular network remodeling following arteriolar ligation in different mouse strains to better understand inter-individual variability. Methods:, Whole-muscle spinotrapezius microvascular networks of mouse strains C57Bl/6, Balb/c and CD1 were imaged using confocal microscopy following ligation of feeding arterioles. Results:, Baseline arteriolar structures of C57Bl/6 and Balb/c mice feature heavily ramified arcades and unconnected dendritic trees, respectively. This network angioarchitecture identifies ischemia-protected and ischemia-vulnerable tissues; unlike C57Bl/6, downstream capillary perfusion in Balb/c spinotrapezius is lost following ligation. Perfusion recovery requires arterialization (expansion and investment of mural cells) of a subset of capillaries forming a new low-resistance collateral pathway between arteriolar trees. Outbred CD1 exhibit either Balb/c-like or C57Bl/6-like spinotrapezius angioarchitecture, predictive of response to arteriolar ligation. Conclusions:, This collateral capillary arterialization process may explain the reported longer time required for blood flow recovery in Balb/c hindlimb ischemia, as low-resistance blood flow pathways along capillary conduits must be formed ("arterialization") before reperfusion. [source] A Separate Role for ICAM-1 and Fluid Shear in Regulating Leukocyte Interactions with Straight Regions of Venular Wall and Venular ConvergencesMICROCIRCULATION, Issue 6 2009RONEN SUMAGIN ABSTRACT Objective: Variation in expression of adhesion molecules plays a key role in regulating leukocyte behavior, but the contribution of fluid shear to these interactions cannot be ignored. Here, we dissected the effects of each of these factors on leukocyte behavior in different venular regions. Materials and Methods: Leukocyte behavior was quantified in blood-perfused microvascular networks in anesthetized mouse cremaster muscle, using intravital confocal microscopy. ICAM-1 expression and fluid shear rate were quantified by using ICAM-1 fluorescent labeling, fluorescent particle tracking, and computational fluid dynamics. Results: Tumor necrosis factor alpha induced an increase in ICAM-1 expression and abolished the differences observed among control venules of different sizes. Consequently, leukocyte adhesion was increased to a similar level across all vessel sizes [5.1±0.46 leukocytes/100 ,m vs. 2.1±0.47 (control)], but remained significantly higher in venular convergences (7.8±0.4). Leukocyte transmigration occurred primarily in the smallest venules and venular convergences (23.9±5.1 and 31.9±2.7 leukocytes/10,000 ,m2 tissue, respectively). In venular convergences, the two inlet vessels are predicted to create a region of low velocity, increasing leukocyte adhesion probability. Conclusions: In straight regions of different-sized venules, the variability in ICAM-1 expression accounts for the differences in leukocyte behavior; in converging regions, fluid shear potentially has a greater effect on leukocyte endothelial cell interactions. [source] Effect of Aging on the Structure and Function of Skeletal Muscle Microvascular NetworksMICROCIRCULATION, Issue 4 2006SHAWN E. BEARDEN ABSTRACT Humans are active creatures, yet physical activity and activity tolerance decline over the life span. One prevailing theme in the literature to account for a portion of the reduced activity tolerance with aging is the observation that the capacity to augment blood flow to skeletal muscle may be impaired with advancing age. This dysfunction may be due to adaptations in the structure or function of their microvascular networks, which collectively determine blood flow resistance. The intent of this review is to present the current knowledge of structure and function of microvascular networks from skeletal muscle with special regard to how these may adapt to, or persist through, the aging process. Skeletal muscles are supplied by an intricate branching network of arterioles and venules. The consistency of findings among available studies suggests that the overall arteriolar and venular network branching topology establishes early in development and varies little, if at all, over the life span. Microvascular networks are not a series of functionally isolated segmental branches. Rather, these networks transmit and communicate vasomotor signals along their lengths and among their branches. Current evidence suggests that aging is associated with a decrement in the capacity of upstream vessels to respond to downstream vasodilation and signals transmitted cell-to-cell along the vascular wall. [source] Regulation of Blood Flow in the MicrocirculationMICROCIRCULATION, Issue 1 2005STEVEN S. SEGAL ABSTRACT The regulation of blood flow has rich history of investigation and is exemplified in exercising skeletal muscle by a concerted interaction between striated muscle fibers and their microvascular supply. This review considers blood flow control in light of the regulation of capillary perfusion by and among terminal arterioles, the distribution of blood flow in arteriolar networks according to metabolic and hemodynamic feedback from active muscle fibers, and the balance between peak muscle blood flow and arterial blood pressure by sympathetic nerve activity. As metabolic demand increases, the locus of regulating oxygen delivery to muscle fibers "ascends" from terminal arterioles, through intermediate distributing arterioles, and into the proximal arterioles and feed arteries, which govern total flow into a muscle. At multiple levels, venules are positioned to provide feedback to nearby arterioles regarding the metabolic state of the tissue through the convection and production of vasodilator stimuli. Electrical signals initiated on smooth muscle and endothelial cells can travel rapidly for millimeters through cell-to-cell conduction via gap junction channels, rapidly coordinating vasodilator responses that govern the distribution and magnitude of blood flow to active muscle fibers. Sympathetic constriction of proximal arterioles and feed arteries can restrict functional hyperemia while dilation prevails in distal arterioles to promote oxygen extraction. With vasomotor tone reflecting myogenic contraction of smooth muscle cells modulated by flow-induced vasodilator production by endothelium, the initiation of functional vasodilation and its modulation by shear stress and sympathetic innervation dictate how and where blood flow is distributed in microvascular networks. A remarkable ensemble of signaling pathways underlie the integration of smooth muscle and endothelial cell function in microvascular networks. These pathways are being defined with new insight as novel approaches are applied to understanding the cellular and molecular mechanisms of blood flow control. [source] Volumetric flow mapping for microvascular networks by bimodality imaging with light microscope and laser doppler imagerMICROSCOPY RESEARCH AND TECHNIQUE, Issue 3 2004Ying Sun Abstract A method was developed to produce a composite image of microvascular networks with grayscales proportional to volumetric flows. Velocities in arterioles and venules were assessed with a high-resolution laser Doppler imager (LDI). The vascular structures were quantified from the micrograph with a computerized vessel detection algorithm. After registering the detected vascular network with the LDI scan, volumetric flows were calculated along the centerlines of the vessels. In vivo data were obtained from the hamster cheek pouch in 6 studies. Flow continuity of the flow map was evaluated by comparing the main flow (Q) with the sum of branch flows (Qs), averaging over the respective vessel segments incident to each bifurcation. The method was reproducible across the 6 studies with the correlation coefficient (r) between Qs and Q ranging from 0.913 to 0.986. In all, over 20,000 flow estimates from 360 vessel segments (24,160 ,m in diameter) at 166 bifurcations were analyzed. With flow normalized between 0 and 1, the linear regression yielded: Qs = 1.03 Q + 0.006; r = 0.952, n = 166, P < 0.0005. The bimodality imaging method exploits a large amount of velocity and diameter data, and therefore should be useful for studying heterogeneous flows in the microvasculature. Microsc. Res. Tech. 65:130,138, 2004. © 2004 Wiley-Liss, Inc. [source] Lymphatic/Blood Endothelial Cell Connections at the Capillary Level in Adult Rat MesenteryTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 10 2010Jennifer L. Robichaux Abstract Analyses of microvascular networks with traditional tracer filling techniques suggest that the blood and lymphatic systems are distinct without direct communications, yet involvement of common growth factors during angiogenesis and lymphangiogenesis suggest that interactions at the capillary level are possible. To investigate the structural basis for lymphatic/blood endothelial cell connections during normal physiological growth, the objective of this study was to characterize the spatial relations between lymphatic and blood capillaries in adult rat mesenteric tissue. Using immunohistochemical methods, adult male Wistar rat mesenteric tissues were labeled with antibodies against PECAM (an endothelial marker) and LYVE-1, Prox-1, or Podoplanin (lymphatic endothelial markers) or NG2 (a pericyte marker). Positive PECAM labeling identified apparent lymphatic/blood endothelial cell connections at the capillary level characterized by direct contact or direct alignment with one another. In PECAM labeled networks, a subset of the lymphatic and blood capillary blind ends were connected with each other. Intravital imaging of FITC-Albumin injected through the femoral vein did not identify lymphatic vessels. At contact sites, lymphatic endothelial markers did not extend along blood capillary segments. However, PECAM positive lymphatic sprouts, structurally similar to blood capillary sprouts, lacked observable lymphatic marker labeling. These observations suggest that nonlumenal lymphatic/blood endothelial cell interactions exist in unstimulated adult microvascular networks and highlight the potential for lymphatic/blood endothelial cell plasticity. Anat Rec 293:1629,1638, 2010. © 2010 Wiley-Liss, Inc. [source] | ||||||||||||||||