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Cell Velocity (cell + velocity)
Kinds of Cell Velocity Selected AbstractsLosartan and Ozagrel Reverse Retinal Arteriolar Constriction in Non-Obese Diabetic MiceMICROCIRCULATION, Issue 5 2008Seungjun Lee ABSTRACT Objective: Reductions in retinal blood flow are observed early in diabetes. Venules may influence arteriolar constriction and flow; therefore, we hypothesized that diabetes would induce the constriction of arterioles that are in close proximity to venules, with the constriction mediated by thromboxane and angiotensin II. Methods: Using nonobese diabetic (NOD) mice, retinal measurements were performed three weeks following the age at which glucose levels exceeded 200 mg/dL, with accompanying experiments on age-matched normoglycemic NOD mice. The measurements included retinal arteriolar diameters and red blood cell velocities and were repeated following an injection of the thromboxane synthase inhibitor, ozagrel. Mice were subdivided into equal groups and given drinking water with or without the angiotensin II receptor antagonist, losartan. Results: Retinal arterioles were constricted in hyperglycemic mice, with a significant reduction in flow. However, not all arterioles were equally affected; the vasoconstriction was limited to arterioles that were in closer proximity to venules. The arteriolar vasoconstriction (mean arteriolar diameters = 51 ± 1 vs. 61 ± 1 , m in controls; p < 0.01) was eliminated by both ozagrel (61 ± 2 , m) and losartan (63 ± 2 , m). Conclusions: Venule-dependent arteriolar vasoconstriction in NOD mice is mediated by thromboxane and/or angiotensin II. [source] Free fatty acids exert a greater effect on ocular and skin blood flow than triglycerides in healthy subjectsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 8 2004M. Bayerle-Eder Abstract Background, Free fatty acids (FFAs) and triglycerides (TGs) can cause vascular dysfunction and arteriosclerosis. Acute elevation of plasma FFA and TG concentration strongly increase ocular and skin blood flow. This study was designed to discriminate whether FFA or TG independently induce hyperperfusion by measuring regional and systemic haemodynamics. Methods, In a balanced, randomized, placebo-controlled, double-blind, three-way, crossover study nine healthy subjects received either Intralipid® (Pharmacia and Upjohn, Vienna, Austria) with heparin, Intralipid® alone or placebo control. Pulsatile choroidal blood flow was measured with laser interferometry, retinal blood flow and retinal red blood cell velocity with laser Doppler velocimetry, and skin blood flow with laser Doppler flowmetry during an euglycaemic insulin clamp. Results, A sevenfold increase of FFA during Intralipid®/heparin infusion was paralleled by enhanced choriodal, retinal, and skin blood flow by 17 ± 4%, 26 ± 5% (P < 0·001), and 47 ± 19% (P = 0·03) from baseline, respectively. In contrast, a mere threefold increase of FFA by infusion of Intralipid® alone did not affect outcome parameters, despite the presence of plasma TG levels of 250,700 mg dL,1; similar to those obtained during combined Intralipid®/heparin infusion. Systemic haemodynamics were not affected by drug infusion. Conclusions, Present findings demonstrate a concentration-dependent increase in ocular and skin blood flow by FFA independently of elevated TG plasma concentrations. As vasodilation of resistance vessels occur rapidly, FFA may play a role in the development of continued regional hyperperfusion and deteriorate microvascular function. [source] Vasopressin decreases intestinal mucosal perfusion: a clinical study on cardiac surgery patients in vasodilatory shockACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2009A. NYGREN Background: Low to moderate doses of vasopressin have been used in the treatment of cathecholamine-dependent vasodilatory shock in sepsis or after cardiac surgery. We evaluated the effects of vasopressin on jejunal mucosal perfusion, gastric-arterial pCO2 gradient and the global splanchnic oxygen demand/supply relationship in patients with vasodilatory shock after cardiac surgery. Methods: Eight mechanically ventilated patients, dependent on norepinephrine to maintain mean arterial pressure (MAP) ,60 mmHg because of septic/post-cardiotomy vasodilatory shock and multiple organ failure after cardiac surgery, were included. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h for 30-min periods. Norepinephrine was simultaneously decreased to maintain MAP at 75 mmHg. At each infusion rate of vasopressin, data on systemic hemodynamics, jejunal mucosal perfusion, jejunal mucosal hematocrit and red blood cell velocity (laser Doppler flowmetry) as well as gastric-arterial pCO2 gradient (gastric tonometry) and splanchnic oxygen and lactate extraction (hepatic vein catheter) were obtained. Results: The cardiac index, stroke volume index and systemic oxygen delivery decreased and systemic vascular resistance and systemic oxygen extraction increased significantly, while the heart rate or global oxygen consumption did not change with increasing vasopressin dose. Jejunal mucosal perfusion decreased and the arterial-gastric-mucosal pCO2 gradient increased, while splanchnic oxygen or lactate extraction or mixed venous,hepatic venous oxygen saturation gradient were not affected by increasing infusion rates of vasopressin. Conclusions: Infusion of low to moderate doses of vasopressin in patients with norepinephrine-dependent vasodilatory shock after cardiac surgery induces an intestinal and gastric mucosal vasoconstriction. [source] Roles of cell adhesion molecules nectin and nectin-like molecule-5 in the regulation of cell movement and proliferationJOURNAL OF MICROSCOPY, Issue 3 2008H. OGITA Summary In response to chemoattractants, migrating cells form protrusions, such as lamellipodia and filopodia, and structures, such as ruffles over lamellipodia, focal complexes and focal adhesions at leading edges. The formation of these leading edge structures is essential for directional cell movement. Nectin-like molecule-5 (Necl-5) interacts in cis with PDGF receptor and integrin ,v,3, and enhances the activation of signalling molecules associated with these transmembrane proteins, which results in the formation of leading edge structures and enhancement of directional cell movement. When migrating cells come into contact with each other, cell,cell adhesion is initiated, resulting in reduced cell velocity. Necl-5 first interacts in trans with nectin-3. This interaction is transient and induces down-regulation of Necl-5 expression at the cell surface, resulting in reduced cell movement. Cell proliferation is also suppressed by the down-regulation of Necl-5, because the inhibitory effect of Necl-5 on Sprouty2, a negative regulator of the Ras signalling, is diminished. PDGF receptor and integrin ,v,3, which have interacted with Necl-5, then form a complex with nectin, which initiates cell,cell adhesion and recruits cadherin to the nectin-based cell,cell adhesion sites to form stable adherens junctions. The formation of adherens junctions stops cell movement, in part through inactivation of integrin ,v,3 caused by the trans -interaction of nectin. Thus, nectin and Necl-5 play key roles in the regulation of cell movement and proliferation. [source] Inhibition of Leukocyte Adherence Enables Venular Control of Capillary Perfusion in Streptozotocin-Induced Diabetic RatsMICROCIRCULATION, Issue 8 2004KAVITHA NELLORE ABSTRACT Objective: Vasoactive molecules can diffuse from venules to dilate closely paired arterioles and enhance capillary perfusion. Venular control of capillary flow has been found to be dependent on nitric oxide (NO), which might be scavenged rapidly in diabetic microvasculature due to the presence of activated leukocytes. This study attempts to improve venular control of capillary flow using fucoidan, which inhibits venular leukocyte adhesion. Methods: Microvascular red blood cell velocity was measured in the mesentery of streptozotocin-induced diabetic rats, with and without fucoidan treatment, and in normal rats. Arteriolar pathways leading to branching capillaries were videotaped to measure the percent of the surrounding area occupied by a venule (% pairing). Microvascular wall NO was measured using fluorescent diaminofluorescein-2-diacetate in diabetic rats, with and without fucoidan treatment. Results: In normal rats, close pairing of venules to arterioles resulted in faster capillary flow. However, after 4,5 weeks of diabetes, the correlation between capillary velocity and % pairing was no longer significant. Capillary velocity and % pairing decreased , 50% in comparison to normal rats. Treatment of diabetic rats with fucoidan restored venular control of capillary flow and increased NO levels. Conclusion: Leukocyte-derived mediators that scavenge NO may lead to inadequate venular control of capillary flow in diabetes. [source] Acute remote ischemic preconditioning on a rat cremasteric muscle flap modelMICROSURGERY, Issue 6 2002Markus V. Küntscher M.D. A previous study showed, in a rat adipocutaneous flap model, that acute ischemic preconditioning (IP) can be achieved not only by preclamping of the flap pedicle, but also by a brief extremity ischemia prior to flap ischemia. The purpose of this study was to determine whether remote IP is also effective in other tissues such as muscle flaps. Twenty male Wistar rats were divided into three experimental groups. The rat cremaster flap in vivo microscopy model was used for assessment of ischemia/reperfusion injury. In the control group (CG, n = 8), a 2-hr flap ischemia was induced after preparation of the cremaster muscle. In the "classic" IP group (cIP, n = 6), a brief flap ischemia of 10 min was induced by preclamping the pedicle, followed by 30 min of reperfusion. A 10-min ischemia of the contralateral hindlimb was induced in the remote IP group (rIP, n = 6). The limb was then reperfused for 30 min. Flap ischemia and the further experiment were performed as in the CG. In vivo microscopy was performed after 1 hr of flap reperfusion in each animal. A significantly higher red blood cell velocity in the first-order arterioles and capillaries, a higher capillary flow, and a decreased number of leukocytes adhering to the endothelium of the postcapillary venules were observed in both preconditioned groups by comparison to the control group (P < 0.05). The differences within the preconditioned groups were not significant for these parameters. Our data show that ischemic preconditioning and improvement of flap microcirculation can be achieved not only by preclamping of the flap pedicle, but also by induction of an ischemia/reperfusion event in a body area distant from the flap prior to elevation. These findings indicate that remote IP is a systemic phenomenon, leading to an enhancement of flap survival. Our data suggest that remote IP could be performed simultaneously with flap elevation in the clinical setting without prolongation of the operation and without invasive means. © 2002 Wiley-Liss, Inc. MICROSURGERY 22:221,226 2002 [source] Acute remote ischemic preconditioning II: The role of nitric oxideMICROSURGERY, Issue 6 2002Markus V. Küntscher M.D. The purpose of this study was to determine whether nitric oxide (NO) plays a role in the mechanism of acute "classic" as well as acute remote ischemic preconditioning (IP). Thirty-two male Wistar rats were divided into five experimental groups. The rat cremaster flap in vivo microscopy model was used for assessment of ischemia/reperfusion injury. In the control group (CG, n = 8), a 2-hr flap ischemia was induced after preparation of the cremaster muscle. The animals of group NO (n = 6) received 500 nmol/kg of the NO-donor spermine/nitric oxide complex (Sper/NO) intravenously 30 min prior to ischemia. The group LN + P (L-NAME + preclamping, n = 6) received 10 mg/kg N,-nitro-L-arginine methyl ester (L-NAME) intravenously before preclamping of the flap pedicle (10-min cycle length, 30-min reperfusion). L-NAME (10 mg/kg) was administered in group LN + T (L-NAME + tourniquet, n = 6) before ischemia of the right hindlimb was induced, using a tourniquet for 10 min after flap elevation. The limb was then reperfused for 30 min. Thereafter, flap ischemia was induced in each group as in group CG. In vivo microscopy was performed after 1 hr of flap reperfusion in each animal. Group NO demonstrated a significantly higher red blood cell velocity (RBV) in the first-order arterioles and capillaries, a higher capillary flow, and a decreased number of leukocytes adhering to the endothelium (stickers) of the postcapillary venules by comparison to all other groups (P < 0.05). The average capillary RBV and capillary flow were still higher in the CG than in the groups receiving L-NAME (P < 0.05). The data show that NO plays an important role in the mechanism of both acute "classic" as well as acute remote IP, since the administration of a NO-donor previous to ischemia simulates the effect of IP, whereas the nonspecific blocking of NO synthesis by L-NAME abolishes the protective effect of flap preconditioning. © 2002 Wiley-Liss, Inc. MICROSURGERY 22:227-231 2002 [source] Blunting of rapid onset vasodilatation and blood flow restriction in arterioles of exercising skeletal muscle with ageing in male miceTHE JOURNAL OF PHYSIOLOGY, Issue 12 2010Dwayne N. Jackson Exercise capacity and skeletal muscle blood flow are diminished with ageing but little is known of underlying changes in microvascular haemodynamics. Further, it is not clear how the sympathetic nervous system affects the microcirculation of skeletal muscle with ageing or whether sex differences prevail in the regulation of arteriolar diameter in response to muscle contractions. In the gluteus maximus muscle of C57BL/6 mice, we tested the hypothesis that ageing would impair ,rapid onset vasodilatation' (ROV) in distributing arterioles (second-order, 2A) of old (20-month) males (OM) and females (OF) relative to young (3-month) males (YM) and females (YF). Neither resting (,17 ,m) nor maximum (,30 ,m) 2A diameters differed between groups. In response to single tetanic contractions at 100 Hz (duration, 100,1000 ms), ROV responses were blunted by half in OM relative to OF, YM or YF. With no effect in YM, blockade of ,-adrenoreceptors with phentolamine (1 ,m) restored ROV in OM. Topical noradrenaline (1 nm) blunted ROV in YM and YF to levels seen in OM and further suppressed ROV in OM (P < 0.05). To evaluate arteriolar blood flow, red blood cell velocity was measured in 2A of OM and YM; respective heart rates (353 ± 22 vs. 378 ± 15 beats min,1) and carotid arterial blood pressures (76 ± 3 vs. 76 ± 1 mmHg) were not different. Blood flows at rest (0.6 ± 0.1 vs. 1.6 ± 0.2 nl s,1) and during maximum dilatation (2.0 ± 0.8 vs. 5.4 ± 0.8 nl s,1) with sodium nitroprusside (10 ,m) were attenuated >60% (P < 0.05) in OM. Blood flow at peak ROV was blunted by 75,80% in OM vs. YM (P < 0.05). In response to 30 s of rhythmic contractions at 2, 4 and 8 Hz, progressive dilatations did not differ with age or sex. Nevertheless, resting and peak blood flows in YM were 2- to 3-fold greater (P < 0.05) than OM. We suggest that ageing blunts ROV and restricts blood flow to skeletal muscle of OM through subtle activation of ,-adrenoreceptors in microvascular resistance networks. [source] Local heat-shock priming-induced improvement in microvascular perfusion in osteomyocutaneous flaps is mediated by heat-shock protein 32BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 3 2001Dr M. Rücker Background: Stress conditioning is thought to improve microvascular free flap survival but the mechanisms of protection are not clear. The aim of this study was to determine whether local induction of heat-shock protein (HSP) 32 improves microvascular perfusion in transferred osteomyocutaneous flaps. Methods: The hindlimb harvest region of osteomyocutaneous flaps in Wistar rats was subjected to stress conditioning by local heating (30 min, 42·5°C) 24 h before microvascular flap transfer. In a second group of animals, after heat-shock priming, the action of HSP-32 was inhibited by tin protoporphyrin IX. Animals with unconditioned flaps served as controls. After transfer, the microcirculation of the muscle, cutaneous, subcutaneous and periosteal tissue of the flap was analysed quantitatively for 6 h using intravital fluorescence microscopy. Results: Immunohistochemistry revealed that HSP-32 was detectable only after priming and not in unconditioned flaps. Priming did not alter functional capillary density or capillary red blood cell velocity compared with that in unconditioned flaps. However, heat-shock priming induced significant capillary dilatation (P < 0·05) and thus a substantial increase in capillary blood flow volume (P < 0·05) in all tissues of the transferred flaps. Inhibition of HSP-32 by tin protoporphyrin IX completely abolished the priming-induced improvement in capillary perfusion, as indicated by the lack of increased capillary diameters and volumetric blood flow. Conclusion: The present study demonstrated that stress conditioning by local heat-shock priming improves nutritive perfusion in osteomyocutaneous flaps by capillary dilatation, probably mediated through the vasoactive action of HSP-32. © 2001 British Journal of Surgery Society Ltd [source] Effect of systemic moxaverine on ocular blood flow in humansACTA OPHTHALMOLOGICA, Issue 7 2009Hemma Resch Abstract. Purpose:, A number of common eye diseases are associated with ocular perfusion abnormalities. The present study aimed to investigate whether systemically administered moxaverine improves ocular blood flow. Methods:, Sixteen healthy volunteers were studied in this randomized, double-masked, placebo-controlled, two-way crossover study. Moxaverine in a dose of 150 mg was administered i.v. Ocular haemodynamic parameters were measured before and after drug administration. Retinal arterial and venous diameters were measured with a retinal vessel analyser. Retinal blood velocity was assessed using laser Doppler velocimetry and choroidal and optic nerve head blood flow was measured with laser Doppler flowmetry. Results:, Moxaverine increased choroidal blood flow (22.6 ± 27.9%), an effect which was significant versus placebo (p = 0.015). Red blood cell velocity in retinal veins tended to increase by 13.6 ± 13.3% after infusion of moxaverine, but this effect was not significant compared with placebo (p = 0.25). In the optic nerve head moxaverine also tended to increase blood flow (11.8 ± 12.7%), but, again, this effect was not significant versus placebo (p = 0.12). Neither moxaverine nor placebo had an effect on retinal arterial diameters. In retinal veins moxaverine tended to induce vasodilation (2.6 ± 2.8%) and to increase blood flow (19.6 ± 16.5%), but these effects were not significant (both p = 0.12). Conclusions:, The present study indicates an increase in choroidal blood flow after systemic infusion of a single dose of moxaverine in healthy subjects. Further studies are warranted to investigate whether these effects are also seen after longterm treatment in patients with ocular vascular disease. [source] Cerebral Thrombosis And Microcirculation Of The Rat During The Oestrous Cycle And After OvariectomyCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2002H Ono SUMMARY 1. The effects of oestrogen on thrombogenesis and the cerebral microcirculation of the female rat were studied during the oestrous cycle and after ovariectomy. 2. Serum levels of oestradiol (E2) and plasma concentrations of nitric oxide (NO) metabolites were significantly greater at pro-oestrus than at dioestrus. Blood vessel diameter, mean red cell velocity, wall shear rate and blood flow at pro-oestrus were significantly higher than at dioestrus. Thrombotic tendency, assessed using a He,Ne laser-induced thrombosis model, was significantly decreased at pro-oestrus compared with dioestrus. 3. The long-term deprivation of oestrogen by ovariectomy significantly depressed serum levels of E2 and plasma concentrations of NO metabolites. Thrombotic tendency was significantly increased 4 weeks after ovariectomy. Vessel diameter, mean red cell velocity, wall shear rate and blood flow in pial arterioles were significantly reduced after ovariectomy. 4. Exogenous administration of oestrogen (17,-oestradiol) after surgery reversed the increased thrombotic tendency mediated by ovariectomy. 5. These results strongly indicate that oestrogen mediates beneficial effects on the cerebral microcirculation and moderates cerebral thrombotic mechanisms in the female rat. [source] | ||||||||||