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1. |
Microvascular Architecture and Exchange in Teeth |
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Microcirculation,
Volume 2,
Issue 4,
1995,
Page 305-313
B. Matthews,
D. Andrew,
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摘要:
ABSTRACTDental pulp is a low‐compliance tissue surrounded by an avascular hard tissue case. Resin casts of the microvasculature in teeth of limited growth show arterioles and venules arranged axially in the pulp with capillary loops extending out toward the dentine. The capillary density is high. There is ultrastructural evidence for lymphatics in pulp. Pulpal blood flow has been estimated in intact teeth using radiolabeled microspheres and found to be in the range 20–60 ml/min per 100 g tissue. One of the difficulties of studying this tissue is that a cavity has to be cut into the tooth with the inherent risks that this may affect the parameters under study. Measurements from exposed pulp indicate that the tissue fluid pressure is high and pulsatile. Furthermore, micropuncture studies have shown that the arteriolar pressure is lower and the venular pressure higher than in other tissues. When dentine is exposedin vivo, fluid moves out through the dentinal tubules and this appears to be formed by a process of ultrafiltration from the pulpal interstitial fluid. The flow is sufficient to retard significantly the diffusion of chemicals into dentine from the oral cav
ISSN:1073-9688
DOI:10.3109/10739689509148275
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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2. |
Early in Reperfusion Following Myocardial Ischemia, Leukocyte Activation Is Necessary for Venular Adhesion But Not Capillary Retention |
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Microcirculation,
Volume 2,
Issue 4,
1995,
Page 315-327
Leslie S. Ritter,
Donald S. Wilson,
Stuart K. Williams,
Jack G. Copeland,
Paul F. McDonagh,
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摘要:
ABSTRACTObjective: The pathobiology of leukocyte sequestration in the coronary microcircu‐lation following ischemia is unclear. We examined the location(s) and persistence of leukocyte sequestration of unactivated and preactivated blood in the coronary microcirculation early during reperfusion following ischemia.Methods: Isolated rat hearts were subjected to 30 min of 37°C, no‐flow ischemia. Hearts were initially reperfused with diluted whole blood containing fluorescent leukocytes (DWB*). At 5, 20, and 35 min of reperfusion (R), the deposition of leukocytes in the coronary capillaries and venules was observed directly using intravital fluorescence microscopy. Four groups were studied: a nonischemic control group (Gr I), and postischemic groups reperfused with DWB* treated with vehicle (Gr II) or preactivated with 10−8MN‐formylmethionyl‐leucyl‐phenylala‐nine (fMLP) (Gr III) or 10−6M fMLP (Gr IV).Results: At R5, postischemic reperfusion with unactivated blood caused a significant trapping of leukocytes in coronary capillaries (Gr I = 2.2 ± 0.4 versus Gr II = 5.6 ± 0.6 leukocytes per capillary field,P<0.05). Hearts in Gr IV exhibited significantly greater leukocyte retention in capillaries compared to all other groups at R5 (R5, Gr IV = 8.8 leukocytes per capillary field,P<0.05) and at R35. At R5, although more leukocytes were observed adhered to the venules in Gr II compared to Gr I, the difference was not statistically significant (Gr I = 1.7 ± 0.7 versus Gr II = 3.4 ± 0.5 leukocytes per 100 |μm venule, P = 0.23). DWB* preactivated with the lower concentration of fMLP (10−8M) resulted in a significant increase in venular leukocyte adhesion at R5 compared to Gr I and Gr II (Gr III 6.1 ± 0.5,P<0.05). After 35 min of reperfusion, a greater percentage of leukocytes remained in the capillaries than in the venules.Conclusions: These direct observations suggest that early in reperfusion after ischemia, both leukocyte and endothelial activation are necessary for venular adhesion, but that ischemia‐induced coronary microvascular alterations are sufficient to promote leukocyte retention in coronary capillaries. These results also indicate that during 35 min of reperfusion, the degree of leukocyte washout is greater in the venules than in the capillaries. These results suggest that the mechanisms contributing to leukocyte retention early in reperfusion following myocardial ischemia are, indeed, different in the capillaries and venules and that the mechanisms affecting retention in capillaries are more persistent
ISSN:1073-9688
DOI:10.3109/10739689509148276
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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3. |
Blood Vessel Growth in the Endometrium |
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Microcirculation,
Volume 2,
Issue 4,
1995,
Page 329-343
Anne M. Goodger,
Peter A.W. Rogers,
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摘要:
ABSTRACTAngiogenesis, or formation of new blood vessels by sprout formation from existing vessels, is generally considered to be the only mechanism by which blood vessel growth occurs. This traditional concept of angiogenesis has been derived largely from observations of experimental systems. Relatively fewer studies on angiogenesis have been carried out using normal angiogenic situations where vessel growth occurs in a controlled three‐dimensional fashion throughout the tissue. Recent advances in the treatment of infertility and outpatient gynecological procedures have led to greater accessibility to normal human endometrium, thus providing new opportunities to study the process of angiogenesis in a physiological context. However, to date, it appears that very little work had been done in relation to endometrial angiogenesis apart from the location of numerous angiogenic and other growth factors with potential to influence angiogenesis in the endometrium, and here there have been few attempts to link these observations with actual angiogenic events. The purpose of this review is to summarize the literature regarding angiogenesis in the endometrium, including work from our own laboratory, and to suggest that blood vessel growth in the endometrium may occur by a mechanism that differs from classical angiogenesi
ISSN:1073-9688
DOI:10.3109/10739689509148277
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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4. |
Plasma Skimming in Vascular Trees: Numerical Estimates of Symmetry Recovery Lengths |
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Microcirculation,
Volume 2,
Issue 4,
1995,
Page 345-353
Russell T. Carr,
Jewen Xiao,
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摘要:
ABSTRACTA new model of plasma skimming in vascular trees that includes the history of disturbances at previous bifurcations is developed. The model calculates the shift in the red blood cell concentration profile by mapping streamlines through the junction; it then computes the dissipation of that disturbance through random collisions among the cells. A numerical solution of this model is compared to experimental data on plasma skimming in serial bifurcations. Numerical values of symmetry recovery lengths downstream of the bifurcation are calculated using the model. Comparison of the computed symmetry recovery lengths with anatomical measurements in hamster cremaster muscle indicate that asymmetries in red blood cell concentration profiles are important in vessels with diameters below 55 μm
ISSN:1073-9688
DOI:10.3109/10739689509148278
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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5. |
Responses of Cremasteric Arterioles of Spontaneously Hypertensive Rats to Changes in Extracellular K+Concentration |
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Microcirculation,
Volume 2,
Issue 4,
1995,
Page 355-362
Julian H. Lombard,
William J. Stekiel,
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摘要:
ABSTRACTObjective: The goal of this study was to determine the effect of changes in extracellular K+concentration ([K+]0) on active tone in cremasteric arterioles of spontaneously hypertensive rats (SHR) and their normotensive Wistar‐Kyoto (WKY) and Wistar controls.Methods: Diameters of third‐ and fourth‐order arterioles were measured in the cremaster muscle of hypertensive and normotensive rats during abrupt changes in superfusate K+concentration from 4.7 mM to 0 mM to 15 mM K+.Results: Arterioles constricted in response to superfusion with 0 mM K+and exhibited a large, transient dilation in response to an abrupt change from 0 mM to 15 mM [K+]o. Arteriolar dilation in response to 15 mM K+was significantly larger in 12–15‐week‐old SHR than in WKY or Wistar controls. Arteriolar responses to 15 mM K+were not significantly different in 4–6‐week‐old SHR and WKY. Dilator responses to 15 mM K+were generally inhibited by 1 mM ouabain, although ouabain was less effective in inhibiting 15 mM K+‐induced dilation in arterioles of SHR and WKY than in Wistar rats.Conclusions: Dilation of cremasteric arterioles in response to 15 mM [K+]0, is mediated, at least in part, via stimulation of the electrogenic Na+/K+pump, although Na+/K+‐pump‐independent components may also contribute to the response. Arterioles of SHR with established hypertension exhibit an altered response to elevated [K+]0which is not present in SHR in the earl
ISSN:1073-9688
DOI:10.3109/10739689509148279
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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6. |
Use of Ruthenium Red Staining to Detect Mast Cell DegranulationIn Vivo |
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Microcirculation,
Volume 2,
Issue 4,
1995,
Page 363-370
Rebecca K. Shepherd,
Brian R. Duling,
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摘要:
ABSTRACTObjective: To establish a method of detecting mast cell degranulation in tissues duringin vivomicroscopy.Methods: Hamster tissues were prepared for intravital microscopy. Ruthenium red (RR) was superfused over the cheek pouch at concentrations of 0.0001–0.01% to determine the optimal concentration. Mast cells were stimulated with compound 48/80, as well as with vasoactive agents not known to be stimulatory to mast cells, following which, mast cell staining was observed. Mesenteries were stained with Toluidine Blue (TB) or RR and mast cell degranulation was assessed during treatment with compound 48/80, or control.Results: During superfusion with varying concentrations of RR, a dose dependence for background staining of unstimulated cells was observed. A RR concentration of 0.001% was optimal forin vivodetection of mast cell degranulation. Mast cells exposed to 0.001% RR were stained following stimulation with compound 48/80 but not after treatment with KC1 or acetylcholine. The latter agents are not known to stimulate mast cells. Thus, arteriolar vasomotor responses, per se, did not appear to play a role in mast cell RR uptake. Comparable results were obtained with RR versus TB in control or 48/80‐treated mesenteries.Conclusions: This RR technique facilitates rapid detection of mast cell degranulationin vivoand provides an opportunity to assess both mast cell and microvascular function simultaneou
ISSN:1073-9688
DOI:10.3109/10739689509148280
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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7. |
A Role for Dietary Copper in Nitric Oxide‐Mediated Vasodilation |
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Microcirculation,
Volume 2,
Issue 4,
1995,
Page 371-376
Dale A. Schuschke,
Jack T. Saari,
Frederick N. Miller,
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摘要:
ABSTRACTObjective: This study was designed to investigate the role of dietary copper in nitric oxide‐mediated arteriolar dilation.Methods: Male weanling Sprague—Dawley rats were fed a purified diet that was either copper‐adequate (6.0 μg Cu per g diet) or copper‐deficient (0.3 μg Cu per g diet) for a period of 4 weeks. Each rat was anesthetized with pentobarbital and its cremaster muscle was positioned in a Krebs'‐fdled bath to which graded concentrations of vasoactive agents were added. In the first series, responses to norepineph‐rine (NE 10−9‐10−6M) and acetylcholine (ACH 10−7‐10−4M) were compared in third‐order arterioles. Second, the dilator response to 10−5M ACH in the absence and presence of 240 U/ml Cu, Zn‐superoxide dismutase (SOD) was determined. Third, arteriolar dilation was determined in response to NO‐independent stimulation of soluble guanylate cyclase with hydrogen peroxide (10−7‐10−5M) and to dibutyryl cGMP (10−6‐10−4M), dibutyryl cAMP (10−6‐10−4M), and papaverine (10−4M).Results: The arteriole constrictor response to NE and the dilator response to hydrogen peroxide, dibutyryl cGMP and cAMP, and papaverine were not different between the dietary groups. Copper deficiency attenuated the ACH‐induced dilation, but the response was restored in the presence of SOD.Conclusions: The inactivation of cytosolic Cu, Zn‐SOD by restriction of dietary copper results in the depression of NO‐mediated vascular smooth‐mu
ISSN:1073-9688
DOI:10.3109/10739689509148281
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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8. |
A System for Culture of Endothelial Cells in 20–50‐μm Branching Tubes |
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Microcirculation,
Volume 2,
Issue 4,
1995,
Page 377-385
Mary D.S. Frame,
Ingrid H. Sarelius,
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摘要:
ABSTRACTObjective: To construct an in vitro endothelial cell culture system which would mimic the geometry and hemodynamic conditions of the arteriolar microcirculation.Methods: Using a photolithography technique, semicircular channels (20–50 μm in diameter) were etched in mirror‐image patterns on pairs of borosilicate microscope slide glass. One‐half of each plate pair was predrilled with perfusion port holes at funnel‐shaped fluid entrance regions. The perfusion system was constructed of micropipette glass and Teflon® tubing, and imbedded in Sylgard®. Two types of endothelial cells were grown to confluence within the half‐channels: rabbit lung microvascular endothelial cells (a gift of Dr. M.E. Gerritsen, Miles Inc.) and human umbilical vein endothelial cells. After the cells were confluent, the two mirror images were aligned and clamped together to form a complete branching system of tubes lined with endothelial cells.Results: This cell culture system can be perfused at physiological flow rates corresponding to wall shear stress values in the range 0.03–48 dyn/cm2. The fluid velocity profiles can be measured in this system by tracking the velocity and flow paths of 0.5‐μm fluorescently labeled microspheres. Endothelial cells which grow within the channel exhibit F‐actin alignment along the long axis of the channel by 3 days after seeding. Scanning electron micrographs indicate that 4 hr after seeding, endothelial cells commonly form cellular projections extending across the half‐channel; by 5 days after seeding, the projections appear to have flattened out along the bottom of the channel.Conclusions: Anin vitroendothelial cell culture system was constructed which mimics the geometry and hemodynamics conditions of resistance arterioles. This system can be used to examine endothelial cell responses to flow and flow gradients under defined and controllable conditions which mimic the arteri
ISSN:1073-9688
DOI:10.3109/10739689509148282
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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