bluuebunny/crossref_metadata_2025_split huggingface dataset:
New Metalized Polyimide Films Structure and Physical Properties
Authors: Kudaikulova Saule K. , Iskakov Rinat , Vecherkina Elena , Zhubanov Bulat A. , Prikhodko Oleg , Kurbatov Andrey , Akhmetov Tleuken , Bazhenov Sergey , Razumovskaya Irina , Perichaud Alain , Voytekunas Vanda Yu. , Lipik Vitali , Abadie Marc J.M. 
Published: April 2008

The classical techniques of PI film metallization by either vapour deposition or electrochemical reduction of
metals involve necessary technological steps such as polymer surface modification via plasma or ion beam, electron
beam, or photolytic treatment, or surface sensitization by the conferment of catalytic properties, in order to enhance metal-
PI adhesion, which is the main problem to be overcome in all processes.
The technology presented differs by the use of another chemical approach yielding electro-conductive materials with high
reflectivity, but without damaging the films in the process. The metalized polyimide films have been prepared by heterogeneous
chemical modification of the polyimide surface and the suggested technology includes several chemical conversion
steps (hydrolysis, chelating by metal salts and reduction) requiring no complicated procedures and proceeding under
mild conditions, at room temperature and without aggressive agents. This new process allows the formulation of metal
phase while both simplifying the technology and making use of commercial PI films, such as Kapton®HN and Upilex®S.

In memoriam of Dr. Saule K. Kudaikulova
Virtually Unaltered Permeability‐Surface Area Products Imply Little Capillary Recruitment in Brain with Hypoxia
Authors: Chen J.‐L. , Wei L. , Bereczki D. , Hans F.‐J. , Otsuka T. , Acuff V. , Richardson G. , Patlak C. , Fenstermacher J. 
Published: April 2008

ABSTRACT Objective: To test the capillary recruitment hypothesis for the brain with control and hypoxic rats. Methods: Local cerebral blood flow (LCBF) was sharply raised by respiring 10% O2 (hypoxia). LCBF as well as local influx rate constants (K1) and permeability‐surface area (PS) products of 14C‐antipyrine and 14C‐3‐O‐methyl‐d‐glucose (30MG) were estimated for capillary systems in 44 brain areas. Results: With this testing, an increase in PS product would be suggestive of capillary recruitment. In all brain areas, LCBF was increased by 30–90% by hypoxia. Hypoxia modestly raised the influx of antipyrine in brain but did not appreciably alter its PS products. With hypoxia, K1's and PS products of 30MG were significantly lowered (5–25%) throughout the brain, and the blood levels of glucose were sizeably raised. The latter increase would diminish the transfer of 30MG across the blood‐brain barrier by the hexose transporter because of increased glucose competition. By applying a glucose‐concentration correction to the data, the apparent PS product of 30MG for the hypoxic group became equal to that for the controls, which agrees with the antipyrine PS product results. Conclusions: Hypoxia, thus, leads to virtually no increase in PS products and no capillary recruitment in brain, and elevates LCBF mainly, perhaps exclusively, by raising the velocity of flow through already perfused capillaries.
Changes in Perimicrovascular Protein Spatial Distribution due to Superfusate
Authors: Barber B. J. , Dutta S. , Parameswaran S. , Babbitt R. A. 
Published: April 2008

ABSTRACTObjective: To determine superfusate‐induced changes in the distribution of plasma proteins in the perimicrovascular interstitial matrix.Methods: Rats were anesthetized with sodium pentobarbital and a mesenteric loop was exteriorized. Intravital video microspectrophotometry was performed using wavelengths of 280, 320, and 700 nm. The images were analyzed to give protein and collagen spatial distributions in vascular regions of rat mesenteric tissue. Perimicrovascular protein concentrations were fitted to an exponential decay model ci + cv exp (‐x/k), where ci is distal protein concentration, ci + cv is the protein concentration proximal to the vessel, x is the distance from the vessel wall, and k is the decay constant indicating protein gradient slope.Results: Before superfusion with 0.5‐ml normal saline, ci = 1.45 ± 0.13 g/dl, ci + cv = 4.56 ± 0.23 g/dl. After the first superfusion, ci decreased (p < 0.01) to 0.53 ± 0.06 g/dl; following a second superfusion, ci decreased to 0.4 ± 0.03 g/dl; an additional final superfusion caused a further decrease to 0.33 ± 0.02 g/dl. ci + cv also decreased significantly during repeated superfusions to 2.92 ± 0.15, 2.35 ± 0.25, and 2.1 ± 0.12 g/dl, respectively.Conclusions: Superfusion produced changes in perivascular and distal interstitial matrix protein distribution. Protein concentration proximal to the microvessel remained higher than distal concentrations. This could be due to increased gel concentrations inhibiting protein mobility.
Differential Contractile Response of Cultured Microvascular Pericytes to Vasoactive Agents
Authors: Murphy Diane D. , Wagner Roger C. 
Published: April 2008

ABSTRACTObjective: Microvascular pericytes may contract in two different ways: In the first, a circumferential or radial mechanical force applied at right angles to the long axis of the vessel may constrict the underlying vessel affecting blood flow and transmural pressure. Retraction and elongation of pericyte processes may also occur tangentially and at right angles to the vessel axis and alter microvessel permeability by changing the amount of ablumenal surface covered or the openness of interendothelial junctions. In this study, cultured pericytes were utilized as a model experimental system to determine if vasoactive stimulation changes their shape in a manner consistent with this hypothesis.Methods: Pericytes cultured from isolated rate capillaries were subjected to angiotensin II and histamine. Their response was monitored by measuring the area of nonyielding substrate covered by the pericytes and the manner in which their shape changed. Shape changes were quantified by calculating the surface area: perimeter perimeter ratios.Results: Histamine significantly reduced surface area covered and the surface area: perimeter ratio. The pericyte processes retracted, resulting in elongated, spindle‐shaped cells. These effects were nullified by the H1 blocker diphenhydramine suggesting a receptor‐specific response. Angiotensin II also elicited contraction and reduced surface area, but the cells contracted laterally and longitudinally. The surface area: perimeter ratios also decreased.Conclusions: These results indicate that pericytes are capable of two types of contractile responses in culture, depending on the specific vasoactive stimulus.
Reduced Renal Microvascular Reactivity to Angiotensin II in Diabetic Rats
Authors: Inman Sharon R. , Porter James P. , Fleming John T. 
Published: April 2008

ABSTRACTObjective: Renal hyperfiltration in early diabetes is often correlated with increased renal blood flow, reflecting dilation of resistance arterioles. This loss of arteriolar tone has been associated with an impaired reactivity to angiotensin II (Ang II). This study determined if outer cortical arterioles (preglomerular and/or postglomerular) of diabetic rats exhibit a diminished reactivity to Ang II and established if renal vascular prostaglandins account for the diminished responsiveness.Methods: The constriction of renal microvessels to Ang II (applied to the kidney bath) was quantitated in hydronephrotic kidneys of diabetic rats (7‐10 days after streptozotocin treatment) and nondiabetic rats by in vivo videomicroscopy.Results: Interlobular, afferent, and efferent arterioles of diabetic rats were found to be less reactive to Ang II than arterioles of nondiabetic rats. Indomethacin, added to the bath to inhibit renal vascular prostaglandin synthesis, enhanced the interlobular and efferent arteriolar reactivity to the peptide among diabetic rats. Yet, after indomethacin treatment, the afferent and efferent arterioles of diabetic rats were still less reactive than control arterioles to Ang II.Conclusions: We conclude that the blunted reactivity of afferent and efferent arterioles to Ang II among diabetic hydronephotic kidneys cannot be fully explained by the influence of renal vascular‐derived dilator prostaglandins.
Role of Endothelium‐Derived Relaxing Factors in Arteriolar Dilation During Muscle Contraction Elicited by Electrical Field Stimulation
Authors: Saito Yuichiro , Eraslan Akin , Hester Robert L. 
Published: April 2008

ABSTRACTObjective: To determine the contribution of either endothelium‐derived nitric oxide (EDNO) or prostaglandins in the functional vasodilation of first‐order arterioles of the hamster cremaster muscle.Methods: First‐order arterioles dilated from 72 ± 3 μm to 93 ± 4 μm in response to contraction of the cremaster muscle for 1 min (n = 7). After EDNO inhibition by topical application of 10 μM Nω‐nitro‐l‐arginine methyl ester (L‐NAME), the resting diameter decreased to 66 ± 3 μm and functional dilation was attenuated to 75 ± 3 μm (P < 0.05). When the arteriolar diameter was returned to the control values by the addition of sodium nitroprusside, an NO donor, into the superfusion solution (n = 7), functional dilation was similar to that observed before EDNO inhibition (91 ± 3 μm vs. 89 ± 3 μm, P > 0.05). To evaluate whether the vasoconstrictor effect of L‐NAME on functional dilation is same as other vasoconstrictors, norepinephrine was applied on the cremaster muscle to induce a vasoconstriction (72 ± 2 to 66 ± 1 μm, n = 7) equivalent to L‐NAME.Results: Norepinephrine treatment attenuated functional dilation to 77 ± 3 μm which was to a level similar to L‐NAME treatment (P > 0.05). Inhibition of prostaglandin synthesis by topical application of indomethacin (28 μM) resulted in no significant changes in the resting diameter but functional vasodilation was attenuated from 89 ± 2 to 81 ± 3 μm (n = 7, P < 0.05).Conclusions: These results suggest that EDNO is important for the resting tone of arterioles and that prostaglandins are important in modulating the functional dilation of the first‐order arterioles in the hamster cremaster muscle.
A Circumferential Stress‐Growth Rule Predicts Arcade Arteriole Formation in a Network Model
Authors: PRICE RICHARD J. , SKALAK THOMAS C. 
Published: April 2008

ABSTRACTObjective: To test the hypothesis that terminal arteriolar remodeling that is stimulated by elevated levels of circumferential wall stress (σθ) will proceed in a network pattern that gives rise to new arcade arterioles.Methods: A network model of two interconnected skeletal muscle arterio‐capillary‐venous units that incorporated diameter‐ and hematocrit‐dependent blood viscosity was constructed. After computing the control values for wall shear stresses (τij) and σθij, a stimulus was provided by dilating the arterioles and raising input pressure. Wall shear stresses and σθij were then recomputed. The diameters of transverse arteriolar segments with σθij greater than a σθ threshold were increased by an amount that was dependent on the original diameter and the difference between σθ and the σθ threshold. Capillaries with an intraluminal pressure greater than a specified threshold were converted to terminal arterioles. Separate simulations in which remodeling was stimulated by elevated levels of τij were also performed for comparison.Results: Arterialization patterns from simulations of σθij stimulated arteriolar remodeling were representative of those seen in vivo with arterialization of back‐connection capillaries leading to arcade arteriole formation. Simulations based on similar rules for τij yielded arterio‐venous shunts, which are rarely seen in vivo, but no arcade arterioles.Conclusion: The simulations presented here are consistent with the hypothesis that arteriolar remodeling is stimulated by increased levels of circumferential wall stress and that new arcade arteriole formation is a consequence of terminal arteriolar growth.
The H2O2‐Generating Enzyme, Xanthine Oxidase, Decreases Luminal Ca2+ Content of the IP3‐Sensitive Ca2+ Store in Vascular Endothelial Cells
Authors: WESSON DONALD E. , ELLIOTT STEPHEN J. 
Published: April 2008

ABSTRACTObjective: Xanthine oxidase inhibits agonist‐stimulated Ca2+ signaling in calf pulmonary artery endothelial cells by an H2O2‐dependent mechanism. We investigated the effect of xanthine oxidase on luminal Ca2+ content of the inositol‐1,4,5‐trisphosphate (IP3)‐sensitive Ca2+ store.Methods: Luminal Ca2+ content was estimated from the net release of Ca2+ activated by 2,5‐di‐t‐butylhydroquinone (BHQ), an inhibitor of microsomal Ca2+ pumps.Results: Initially, xanthine oxidase depleted the IP3‐sensitive Ca2+ store of releasable Ca2+, but with more prolonged incubation, the enzyme also depleted non‐IP3‐sensitive stores. In addition, xanthine oxidase inhibited capacitative Ca2+ influx. Similar results were observed when thapsigargin was substituted for BHQ.Conclusions: Depletion of luminal Ca2+ content within the IP3‐sensitive Ca2+ store contributes to xanthine oxidase inhibition of Ca2+ signaling in vascular endothelial cells.
Deformation of Erythrocytes in Microvessels and Glass Capillaries: Effects of Erythrocyte Deformability
Authors: SUZUKI YOJI , TATEISHI NORIHIKO , SOUTANI MASAO , MAEDA NOBUJI 
Published: April 2008

ABSTRACTObjective: The deformation of erythrocytes in microvessels less than 15 μm in inner diameter was analyzed using a microvascular bed isolated from rabbit mesentery. The deformation was compared with that found in glass capillaries.Methods: Human erythrocytes were perfused through two media: first, a microvascular‐bed section isolated from rabbit mesentery; and second, a set of glass capillaries. Images of deformed erythrocytes were recorded on videotape under strobe light and analyzed with an image processor. The flow velocity of the erythrocytes was determined from the difference of their positions between video frames or by a dual‐spot cross‐correlation technique. Erythrocyte deformability was modified with diamide, diazene dicarboxylic acid bis[N,N‐dimethylamide], by crosslinking spectrins.Results: Symmetrical (parachute‐like or slipper‐like) deformation of erythrocytes was observed only in microvessels smaller than 13 μm in inner diameter. Erythrocytes in microvessels were less deformed than those in glass capillaries with corresponding diameters, and the marginal cell‐free layer was narrower. The deformation increased by increasing the flow velocity of erythrocytes, and the cell‐free layer became wider. Diamide‐treated cells in microvessels were less deformed than normal cells and showed slightly narrower cell‐free layers. Stronger stress in narrower microvessels induced further deformation of cells.Conclusions: Erythrocyte deformation in microvessels was essentially different from that in glass capillaries, and the effect of erythrocyte deformability on the flow dynamics of erythrocytes in microvessels was properly evaluated using an isolated microvascular bed.
Ascorbate Uptake by Microvascular Endothelial Cells of Rat Skeletal Muscle
Authors: Wilson J. X. , Dixon S. J. , Yu J. , Nees S. , Tyml K. 
Published: April 2008

ABSTRACTObjective: In several systems, exogenous ascorbate (reduced vitamin C) has been shown to protect against microvascular injury induced by reactive oxygen species. Since skeletal muscle is relatively resistant to oxidative injury, it is possible that under physiological conditions endogenous ascorbate in the muscle microvasculature affords such protection. To examine the ability of microvascular endothelium to accumulate ascorbate, we aimed (1) to develop an in vitro model of microvascular endothelial cells derived from rat hindlimb skeletal muscles and (2) to investigate the uptake and steady‐state concentration of ascorbate in these cells.Methods: Microvascular cells were enzymatically dissociated, isolated on a density gradient, and grown in serum‐supplemented medium. After passaging, they were tested for formation of tube‐like structures, coagulation factor VIII antigen expression, Griffonia simplicifolia lectin I‐isolectin B4 binding, and acetylated low‐density lipoprotein (LDL) uptake. Concentrations of reduced ascorbate were measured by high‐performance liquid chromatography (HPLC) with electrochemical detection. Transport activity was assessed on the basis of the initial rate of [14C]ascorbate uptake.Results: The cultured cells tested positively for factor VIII antigen expression, lectin binding, LDL uptake, and tube formation. Although these cells did not synthesize ascorbate de novo, they accumulated reduced vitamin C when it was added to the culture medium. The initial rate of [14C]ascorbate uptake was 0.9 μ‐mol/g cell protein 10 min when cells were incubated with 10 μM of the radiolabeled vitamin. This uptake was Na+‐dependent and was blocked by the organic anion transport inhibitor sulfinpyrazone, but was not acutely affected by glucose. Following incubation with a physiological concentration of vitamin C (100 μM L‐ascorbate), cells accumulated a high concentration of ascorbate within 6 h (approximately 16 mM at steady‐state). Steady‐state cellular ascorbate concentration was also dependent on extracellular Na+ and sensitive to sulfinpyrazone.Conclusions: Microvascular cells derived from rat hindlimb muscles demonstrated endothelial characteristics. These cells accumulated reduced vitamin C by means of Na+‐dependent ascorbate transporters, which are distinct from hexose carriers. The high endothelial ascorbate concentration at steady‐state is consistent with the role of ascorbate as a major antioxidant in the skeletal muscle microvasculature.
Enzymatic Isolation and Characterization of Single Vascular Smooth Muscle Cells from Cremasteric Arterioles
Authors: Jackson William F. , Huebner James M. , Rusch Nancy J. 
Published: April 2008

ABSTRACTObjective: The goal of the present study was to develop a method to isolate enzymatically viable arteriolar muscle cells from single cremasteric arterioles, which retain the contractile and electrophysiological phenotype of the donor microvessels.Methods: Arterioles were hand‐dissected from rat and hamster cremaster muscles and dissociated by incubation in papain and didiioerythritol for 35 min followed by incubation in collagenase, elastase, and soybean trypsin inhibitor for 10 to 25 min in solutions containing 100 μM Ca2+, 10 μM sodium nitroprusside, and 1 mg/ml albumin at 37°C.Results: Populations of single smooth muscle cells enzymatically isolated from cremasteric arterioles showed elongated fusiform morphology and intact plasmalemmal membranes as indicated by retention of calcein, by exclusion of ethidium homodimer‐1, and by high membrane resistances (11 ± 0.8 Gω, n = 36 for rat cells; 8 ± 0.6 Gω, n = 21 for hamster cells; p < 0.05). Muscle cells contracted in a concentration‐dependent fashion in response to pipette application of norepinephrine (10 nM‐100 μM). Cell shortening in response to 1 μM norepinephrine was inhibited by 10 μM phentolamine, 1 μM sodium nitroprusside, and 1 μM nifedipine or nominally Ca2+‐free media. Resting membrane potential recorded in patch‐clamped cells by perforated patch methods was −48 ± 1 mV (n = 47) for rat cells and −44 ± 2.8 mV (n = 14) for hamster cells (p > 0.05). Families of voltage‐dependent K+ currents were observed during stepwise depolarizing pulses from −60 mV to more positive potentials. Blockers of voltage‐gated and ATP‐sensitive K+ channels (4‐Aminopyridine [3 mM] and glibenclamide [1 μM], respectively) inhibited membrane K+ conductance, increased membrane resistance, and depolarized cells by 20 ± 4 mV (n = 8) and 14 ± 3 mV (n = 6), respectively.Conclusions: The present method permits isolation of smooth muscle cells from a single cremasteric arteriole. These cells seem to retain the contractile phenotype, α‐adrenergic signaling cascade, membrane potential, and K+ conductances described for the donor arteriole. Correlating the functional and electrophysiological properties of these smooth muscle cells to in situ and in vitro studies of their donor arterioles should provide a useful extension for understanding die physiology, pathophysiology, biophysics, and cell biology of the microcirculation in skeletal muscle.
Perfusion of Single Tumor Microvessels: Application to Vascular Permeability Measurement
Authors: Lichtenbeld Hera C. , Yuan Fan , Michel C. Charles , Jain Rakesh K. 
Published: April 2008

ABSTRACT Objective: To develop a new method for determining the relative importance of convection versus diffusion in macromolecular transport across tumor microvessel walls. Methods: The human colon adenocarcinoma LS174T was transplanted in the dorsal skinfold chamber in a severe combined immunodeficient (SCID) mouse. The vasculature at the tumor surface was exposed by carefully removing the glass window of the chamber. A tumor microvessel was randomly selected, which was ∼20–40 μm in diameter, embedded in the connective tissue 10–12 μm below the surface of the tumor. The vessel was cannulated with a micropipette and perfused with fluorescein isothiocyanate (FITC)‐labeled bovine serum albumin (BSA) at different perfusion pressures. The fluorescence intensity was recorded on videotapes via a video system attached to the fluorescence microscope for offline analysis. The apparent vascular permeability was determined based on the time‐dependence of fluorescence intensity and the vessel diameter. Results: The apparent vascular permeability of single vessels to FITC‐labeled BSA was quantified at perfusion pressures of 20–45 cmH2O. The pressure dependence of vascular permeability in LS174T tumors was heterogeneous. On average, there was no correlation between the apparent vascular permeability and the perfusion pressure in the range of 20–35 cmH2O (p= 0.73), even though the apparent permeability increased significantly when the pressure was increased from 20 to 45 cmH2O (p= 0.008). Conclusions: These results indicate that convection in the transvascular transport of albumin is not significant in non‐peripheral regions of solid tumors in which the pressure difference across the vessel wall is small or even negligible. In addition to the permeability studies, this preparation can be used to study cell‐cell interactions in single tumor vessels under defined flow conditions.
Myocardial Fluid Balance in Acute Hypertension
Authors: Mehlhorn Uwe , Davis Karen L. , Laine Glen A. , Geissler Hans J. , Allen Steven J. 
Published: April 2008

ABSTRACT Objectives: We hypothesized that (1) acute arterial hypertension increases myocardial microvascular fluid filtration and (2) the combination of acute arterial hypertension and coronary sinus pressure elevation may increase myocardial microvascular filtration sufficiently to estimate the osmotic reflection coefficient of the myocardial exchange vessels. Methods: In nine mechanically ventilated dogs we cannulated the prenodal major cardiac lymph trunk. With the use of central venous phenylephrine infusion, mean arterial pressure (MAP) was raised progressively to 120, 160, and 180 mm Hg. In five dogs we additionally raised coronary sinus pressure (CSP) to 20 and 40 mm Hg. At each manipulation of MAP and/or CSP, we measured indexes of myocardial lymphatic function and lymph‐to‐plasma concentration ratios for total protein (CL(TP)/CP(TP)) and albumin (CL(alb)/CP(alb)). Results: Myocardial lymph flow rate (QL; μL/min) increased exponentially (QL= 10.9 e0.014‐(MAP)) and myocardial lymph driving pressure (PL; mm Hg) increased linearly (PL= 2.30 + 0.20 MAP) following MAP increases, whereas CL(TP)/CP(TP) and CL(alb)/CP(alb) decreased from 0.67 ± 0.07 (SD) to 0.56 ± 0.10 and from 0.91 ± 0.05 to 0.75 ± 0.11, respectively. Adding CSP elevation increased QL up to 12 times control associated with further CL(TP)/CP(TP) and CL(alb)/CP(alb) decreases to 0.49 ± 0.05 and 0.59 ± 0.02, respectively. Conclusions: We conclude that hypertensive arterial pressures are, at least in part, transmitted to the myocardial microvascular exchange vessels in the intact animal leading to increased microvascular fluid filtration. However, the combination of acute arterial hypertension and coronary sinus pressure elevation is not sufficient to produce filtration independence required for myocardial osmotic reflection coefficient determination.