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Byline: Santhi Samy Modeliar (1), Marie-Antoinette Sevestre (2), Bertrand Cagny (1), Michel Slama (1,3) Keywords: Ultrasonography; Internal jugular vein; Femoral vein; Dynamic manoeuvres; Cross-sectional area Abstract: Objective To determine: (1) the proportion of small ( Design Prospective study. Setting Twelve-bed adult medical intensive care unit. Patients and participants Sixty patients (62a-+-a- 19 years, SAPS II score 36a-+-a-17). Interventions Ultrasound examinations of the IJV and FV in supine, Trendelenburg (T) and reverse Trendelenburg (Ti) positions. Measurements and results Maximum diameter and cross-sectional area (CSA) were measured. Venous catheter placement would have been difficult (diametera- Conclusions Ultrasonography should be performed before at least central venous catheter placement to detect the presence of deep vein thrombosis or vessels less than 5a-mm in diameter. Some positions increase veins' diameter at least internally, T position increasing IJV size and Ti position increasing FV size. Author Affiliation: (1) Unite de reanimation, service de nephrologie, CHU sud, 80054 Cedex 1, Amiens, France (2) Laboratoire d'explorations fonctionnelles vasculaires, service de chirurgie vasculaire et thoracique, CHU sud, Amiens, France (3) Unite INSERM, ERI 12, Amiens, France Article History: Registration Date: 11/09/2007 Received Date: 06/12/2005 Accepted Date: 31/07/2007 Online Date: 10/10/2007

The details of the upstream signaling pathways from nitric oxide production in vascular endothelial growth factor (VEGF) induced venular hyperpermeability were studied in pigs. The apparent permeability coefficient of albumin and endothelial cystosolic calcium were measured in intact perfused porcine coronary venules using fluorescence microscopy. Results suggest that VEGF induces venular hyperpermeability through KDR receptor-mediated activation of phospholipase C.

Rats sensitized to egg albumin were used in the investigation of the mesenteric venule response to mast cell activation. Intravital microscopy was used to monitor venular response, mast cell degranulation, changes in vascular permeability, adhesion of leukocytes and platelet aggregation. Inhibitory studies were also conducted to probe the mechanisms and mediators responsible for venular responses.

Vasculogenic and angiogenic developments of blood vessels are influenced by transmembrane ligand ephrin-B2 and its receptor. In the process of neovascularization, the transmembrane ligand ephrin-B2 and its receptor Eph-B4 disrupt arterial endothelial cells and venous endothelial cells respectively. Thus, the apparent distinctions of arteries and veins in the early stages of angiogenesis and onwards can be attributed to ephrin-B2 and its receptor.

Two protocols were used in the investigation of the sympathetic nervous system regulation of venous function in the rainbow trout. Various cardiovascular parameters were monitored in the course of the experiments which also included agonists and receptor blocking studies. Results reveal that the venous system in rainbow trout is responsive to epinephrine. It responds by mobilizing blood from unstressed to stressed compartments and by decreasing compliance.

The impact of equal doses of arterial and portal vein insulin on glucose production in the liver was investigated. Eleven conscious mongrel dogs were used as experimental models to test whether insulin infusion would suppress hepatic glucose production (HGP). Results showed that a combined increase in peripheral and portal vein insulin doses indeed reduced net hepatic glucose production in the dogs. Tracer-determined glucose production, however, was not affected.

The experimental and analytical methods presented in the companion paper [1] are used here to study the effects of cryopreservation on the in vitro biaxial random-elastic mechanical properties of canine saphenous veins. The properties of specimens tested in their physiological range of loadings immediately after thawing were not significantly different from their properties before cryopreservation. However, they stiffened significantly in the few hours following thawing. This effect was not observed for aging fresh specimens, nor for cyanide-poisoned specimens, indicating that the static tone of the venous smooth muscle may be affected by cryopreservation and thawing, but the elastin and collagen fibers are most likely unaffected.

The effects of inflammation on the binding pattern of different lectins to the vasculature of venules were analyzed in models of substance P-induced plasma leakage in the rat trachea light microscopy. Analysis of the selective binding of plant lectins to endothelial cell borders in inflamed venules of rat trachea indicated the presence of finger-like processes and endothelial gaps. The formation of endothelial gaps was caused by the deposition of dense reaction products in regions without cell retraction or endothelial gaps.

The mechanism by which the natriuretic peptide (CNP) promotes smooth muscle relaxation was investigated using femoral veins isolated from mongrel dogs. The veins were treated with endothelin, phenylephrine, and metabolic inhibitors prior to exposure to CNP. KCl and endothelin-1 attenuated the response to CNP, but the metabolic inhibitors inhibited relaxations to CNP. These results indicate that response to CNP is mediated by activation of potassium channels.

Alpha-adrenoceptors (ARs) have been shown to play an important role in the constriction of large arteries. However, little is known about the subtypes of alpha-ARs that participate in this event. Herein, different subtypes of alpha-ARs that mediate constriction of arterioles and venules in rat skeletal muscle were characterized. Alpha1A-, alpha1B-, alpha1D-, alpha2B-, and alpha2D-ARs were identified. Alpha1D- and alpha2D-ARs predominantly mediated constriction of arterioles while alpha1B- and alpha2D-ARs mediated constriction of venules.

Monos, Emil, Viktor Berczi, and Gyorgy Nadasy. Local Control of Veins: Biomechanical, Metabolic, and Humoral Aspects. Physiol. Rev. 75: 611-666, 1995. -- The incidence of vein diseases (varicosity, thrombophlebitis, phlebosclerosis, [...]

Two-dimensional microvascular tissue preparations have been extensively used to study blood flow in the microcirculation, and, most recently, the mechanism of thermal equilibration between thermally significant countercurrent artery-vein pairs. In this paper, an approximate three-dimensional solution for the heat transfer from a periodic array of blood vessels in a tissue preparation of uniform thickness with surface convection is constructed using a newly derived fundamental solution for a Green's function for this flow geometry. This approximate solution is exact when the ratio K' of the blood to tissue conductivity is unity and a highly accurate approximation when K[prime] [is not equal to] 1. This basic solution is applied to develop a model for the heat transfer from a countercurrent artery-vein pair in an exteriorized rat cremaster muscle preparation. The numerical results provide important new insight into the design of microvascular experiments in which the axial variation of the thermal equilibration in micro vessels can be measured for the first time. The solutions also provide new insight into the design of fluted fins and microchips that are convectively cooled by internal pores.

Endogenous nitric oxide regulates oxidative changes in cells and arteriolar and venular microvascular endothelium and also prevents leukocyte margination in venules. An iron-catalyzed oxidative process catalyzes intracellular hyperoxide generation in microvascular endothelium. This is enhanced by endogenous NO suppression and the hyperoxide release regulates leukocyte recruitment.

The production of NO and subsequent stimulation of guanylate cyclase and cGMP formation mediates macromolecular extravasation from post capillary venules in response to histamines. Microvascular permeability is increased by the histamine-induced NO biosynthetic pathway due to formation of venular leaky sites. L-arginine stimulates the formation of venular leaky sites for increased permeability.

Spontaneous luminal flow-induced inhibition of contractions of venules were studied using isolated bat wing specimens. The observed net effect of luminal flow was a decrease in the product of cross-sectional area multiplied by frequency and a mean diameter increase. These indicate the ability of luminal flow to regulate contractions in bat wing venules through the release of an endothelium-derived hyperpolarizing factor.

The hydraulic conductivity (Lp) of pulmonary venules during ischemia were studied in excised rat and canine lungs using a split-drop technique. Data gathered indicate that Lp response were significantly greater in ischemic venules compared to nonischemic vessels. Ischemic deterioration of the pulmonary endothelial barrier was, therefore, concluded to be independent of blood reperfusion.

The effect of ablation of the area surrounding the anteroventral third cerebral ventricle on vascular capacitance was investigated in rats. Vascular compliance was calculated from hemodynamic parameters measured utilizing labeled serum albumin. Results show that the meancirculatory filling pressure-blood volume curve was displaced towards the volume coordinate indicating a reduction in venous tone. This is explained by the absence of nervous control over vein constriction in the experimental subjects.

The dorsal handvein compliance technique was used to investigate if clonidine also induce endothelium-derived relaxation factor (EDRF) release and to determine if EDRF is responsible for the diminution of the vasoconstrictive effect of clonidine among humans. Results indicate that alpha2 adrenaline receptor-induced EDRF released is not associated with clonidine administration. Further, clonidine was demonstrated to be a partial alpha-1 adrenaline receptor agonist.

Byline: Sachidanand. Bharati, Tumul. Chowdhury, Harsh. Sapra Sir, Catheterisation of the internal jugular vein (IJV) is commonly practiced for central venous access in intensive care unit (ICU); however, may cause [...]

The aim of this study was to quantitate the density of nerve terminals as well as their synaptic vesicle population in the adventitia of saphenous (SV and SA) and brachial veins and arteries (BV and BA) obtained from rats maintained in a horizontal control or a tilted position. Adult animals were kept individually in tube-like cages in a 45 [degrees] head-up position. After 2 wk, both tilted and control animals were anesthetized, and the whole body was perfused with fixative solution at physiological pressure. Vessels segments were then excised for electron microscopy and immunohistochemistry. The nerve terminal density (NTD) of SA was 8.20 [+ or -] 1.46 nerve terminals/100 [micro] [m.sup.2] cross section of adventitia and that of SV was 4.53 [+ or -] 0.61 nerve terminals/100 [micro] [m.sup.2] cross section of adventitia in control rats. Tilting caused a significant increase in NTD of both SA (70%) and SV (52%). The synaptic microvesicle density (SyVD) was larger in SA than SV in control rats (30.48 [+ or -] 4.41 vs. 13.38 [+ or -] 2.61 synaptic vesicles/10 terminal sections), but tilting resulted in more pronounced changes in SyVD of SV (95%) than SA (54%). No significant changes in NTD and SyVD of BA were found after tilt (-3.6% relative to 4.99 [+ or -] 0.33 compared with 0.4% relative to 24.89 [+ or -] 3.7, respectively). Whereas NTD of BV exhibited a tendency to increase (3.73 [+ or -] 0.86 vs. 2.31 [+ or -] 0.29 nerve terminals/100 [micro] [m.sup.2] cross section of adventitia), SyVD did not change significantly (18.96 [+ or -] 2.74 vs. 22.85 [+ or -] 3.17 synaptic vesicles/10 terminal sections). A large number of nerve terminals of all vessels were tyrosine hydroxylase immunoreactive (containing norepinephrine). These findings support the hypothesis that long-term gravitational load causes adaptive morphological and functional remodeling of sympathetic innervation in blood vessels of the extremities. innervation of extremity arteries; innervation of extremity veins; neural remodeling; tilting head up; vascular adaptation to gravity

Axial migration of red blood cells in small glass tubes can cause blood viscosity to be effectively independent of shear rate. However, this phase separation may not occur to the same degree in the venous network due to infusion of cells and aggregates at branch points. To investigate this hypothesis, we followed trajectories of fluorescently labeled red blood cells in the venular network of the rat spinotrapezius muscle at normal and reduced flow with and without red blood cell aggregation. Cells traveling near the wall of an unbranched venular segment migrated ~1% of the longitudinal path length without aggregation and migrated slightly more with aggregation. Venular segment length between branch points averaged three to five times the diameter. Cells in the main vessel were shifted centrally by up to 20% of diameter at branch points, reducing the migration rate of cells near the opposite wall to [is less than] 1% even in the presence of aggregation. We conclude that formation of a cell-free marginal layer in the venular network is attenuated due to the time dependence of axial migration and the frequent branching of the network. venous resistance; radial migration; red blood cell aggregation; in vivo fluorescence microscopy; venous network topology

Previous studies in skeletal muscle of the dog and cat have shown that venous vascular resistance changes inversely with blood flow and may be due mainly to red blood cell aggregation, a phenomenon present in these species. To determine whether red blood cell axial migration and sedimentation contribute to this effect, we viewed either vertically or horizontally oriented venules of the rat spinotrapezius muscle with a horizontally oriented microscope during acute arterial pressure reduction. With normal (nonaggregating) rat blood, reduction of arterial pressure did not significantly change the relative diameter of the red blood cell column with respect to the venular wall. After induction of red blood cell aggregation in the rat by infusion of Dextran 500, red blood cell column diameter decreased up to 35% at low pseudoshear rates (below ~5 [s.sup.-1]); the magnitude was independent of venular orientation. In vertically oriented venules, the plasma layer was symmetrical, whereas in horizontally oriented venules, the plasma layer formed near the upper wall. We conclude that, although red blood cell axial migration and sedimentation develop in vivo, they occur only for larger flow reductions than are needed to elicit changes in venous resistance. venous resistance; low shear flow; in vivo blood rheology; blood sludging; red blood cell core

Protein tyrosine phosphatase-dependent proteolysis of focal adhesion complexes in endothelial cell apoptosis. Am J Physiol Lung Cell Mol Physiol 280: L342-L353, 2001.--Adenosine and/or homocysteine causes endothelial cell apoptosis, a mechanism requiring protein tyrosine phosphatase (PTPase) activity. We investigated the role of focal adhesion contact disruption in adenosine-homocysteine endothelial cell apoptosis. Analysis of focal adhesion kinase (FAK), paxillin, and vinculin demonstrated disruption of focal adhesion complexes after 4 h of treatment with adenosine-homocysteine followed by caspase-induced proteolysis of FAK, paxillin, and [p130.sup.CAS]. No significant changes were noted in tyrosine phosphorylation of FAK or paxillin. Pretreatment with the caspase inhibitor Z-Val-Ala-Asp-fluoromethylketone prevented adenosine-homocysteine-induced DNA fragmentation and FAK, paxillin, and [p130.sup.CAS] proteolysis. Asp-Glu-Val-Asp-ase activity was detectable in endothelial cells after 4 h of treatment with adenosine-homocysteine. The PTPase inhibitor sodium orthovanadate did not prevent endothelial cell retraction or FAK, paxillin, or vinculin redistribution. Sodium orthovanadate did block adenosine-homocysteine-induced FAK paxillin, and [p130.sup.CAS] proteolysis and Asp-Glu-Val-Asp-ase activity. Thus disruption of focal adhesion contacts and caspase-induced degradation of focal adhesion contact proteins occurs in adenosine-homocysteine endothelial cell apoptosis. Focal adhesion contact disruption induced by adenosine-homocysteine is independent of PTPase or caspase activation. These studies demonstrate that disruption of focal adhesion contacts is an early, but not an irrevocable, event in endothelial cell apoptosis. cell biology; structural biology; vascular biology

Effect of erythrocyte aggregation on velocity profiles in venules. Am J Physiol Heart Circ Physiol 280: H222-H236, 2001.--A recent whole organ study in cat skeletal muscle showed that the increase in venous resistance seen at reduced arterial pressures is nearly abolished when the muscle is perfused with a nonaggregating red blood cell suspension. To explore a possible underlying mechanism, we tested the hypothesis that red blood cell aggregation alters flow patterns in vivo and leads to blunted red blood cell velocity profiles at reduced shear rates. With the use of fluorescently labeled red blood cells in tracer quantities and a video system equipped with a gated image intensifier, we obtained velocity profiles in venous microvessels (45-75 [micro]m) of rat spinotrapezius muscle at centerline velocities between 0.3 and 14 mm/s (pseudoshear rates 3-120 [s.sup.-1]) under normal (nonaggregating) conditions and after induction of red blood cell aggregation with Dextran 500. Profiles are nearly parabolic (Poiseuille flow) over this flow ra-te range in the absence of aggregation. When aggregation is present, profiles are parabolic at high shear rates and become significantly blunted at pseudoshear rates of 40 [s.sup.-1] and below. These results indicate a possible mechanism for increased venous resistance at reduced flow. venous resistance; blood constitutive equation; in vivo blood viscosity; in vivo fluorescence microscopy; wall shear stress

Pearson, Mark J., and Herbert H. Lipowsky. Influence of erythrocyte aggregation on leukocyte margination in postcapillary venules of rat mesentery. Am J Physiol Heart Circ Physiol 279: H1460-H1471, 2000.--The role of erythrocyte (red blood cell; RBC) aggregation in affecting leukocyte (white blood cell; WBC) margination in postcapillary venules of the mesentery (rat) was explored by direct intravital microscopy. Optical techniques were refined and applied to relate the light-scattering properties of RBCs to obtain a quantitative index of aggregate size (G), which, under idealized conditions, represents the number of RBCs per aggregate. WBC margination, defined as the radial migration of WBCs to the venular wall and their subsequent rolling along the endothelium, was measured as the percentage of the potentially maximal WBC volumetric flux within the microvessel lumen ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII]). In normal blood, [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] increased exponentially fourfold, and G increased from 1 to 1.15 as wall shear rates ([Gamma]) were reduced from a steady-state value of ~600 to [is less than] 100 [s.sup.-1] by proximal occlusion with a blunt microprobe. Enhancement of aggregation by infusion (iv) of dextran 500 (428 kDa), to attain a systemic concentration of 3 g/100 ml, resulted in a four- and sevenfold increase in G and [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII], respectively, as [Gamma] was reduced below 100 [s.sup.-1]. Inhibition of RBC aggregation by infusion of dextran 40 (37.5 kDa) caused [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] to fall to one-half of its steady-state level for [Gamma] [is less than] 100 [s.sup.-1]. Thus it appears that the well-known increase of WBC margination with reductions in [Gamma] is strongly dependent on the occurrence of RBC aggregation. Increasing the extent of RBC aggregation during reductions in [Gamma] also increased the firm adhesion of WBCs to the endothelium because of an enhanced probability of contact between leukocytes and the postcapillary venular wall. erythrocyte sequestration; dextran; Wistar-Furth rats; leukocyte-endothelium adhesion

Rocheleau, B., C. Ethier, R. Houle, P. M. Huet, and M. Bilodeau. Hepatic artery buffer response following left portal vein ligation: its role in liver tissue homeostasis. Am. J. Physiol. 277 (Gastrointest. Liver Physiol. 40): G1000-G1007, 1999.--Occlusion of a lobar portal vein is known to induce atrophy of downstream liver lobes and hypertrophy of contralateral lobes. Changes in portal flow are known to be compensated by changes in hepatic arterial flow, thus defining the hepatic artery buffer response (HABR). To understand the role of liver flow in liver atrophy, we measured portal flow and hepatic artery flow after different degrees of left portal vein stenosis (LPVS). Surgery was performed to obtain 0, 43, 48, 59, 68, 72, 78, and 100% LPVS. Systemic and splanchnic blood flows were measured at 4 h or 7 days after surgery using radiolabeled microspheres. At 4 h, LPVS produced no changes in systemic hemodynamics. Increasing degrees of LPVS produced a significant decrease in left portal flow (P [is less than] 0.0001) and a fully compensatory increase in right portal flow (P [is less than] 0.0001) without significantly affecting total portal flow. Left hepatic artery flow increased by 210% (P = 0.002), and right hepatic artery flow decreased by 67% (P = 0.05) after full LPVS. There was a significant inverse correlation between portal and arterial flow changes induced by different degrees of LPVS in the left ([r.sup.2] = 0.61) and right ([r.sup.2] = 0.41) lobes. Despite this HABR, we observed a reduction in left liver flow (-45%; P = 0.01) and an increase in right liver flow (+230%; P = 0.01) with 100% LPVS. At 7 days, a significant decrease in the weight of left liver lobes (-75%; P [is less than] 0.0001) and a compensatory increase in the weight of the right lobes (+210%; P [is less than] 0.0001) were observed with 100% LPVS. Left and right liver flows were similar to results measured at 4 h, and HABR was still present. However, when expressed per gram of liver, liver flows were identical to results obtained with sham animals. Reduction in lobar portal flow is accompanied by an increase in ipsilateral hepatic artery flow and a compensatory increase in portal flow to the rest of the liver. In a given lobe, when compensatory HABR is overcome, liver weight changes occur so that at the end total liver flow per gram of liver tissue is restored. This suggests that in normal conditions liver flow is a major regulator of liver volume. liver flow; liver atrophy; liver regeneration