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1. |
Influence of Microvascular Architecture on Oxygen Exchange in Skeletal Muscle |
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Microcirculation,
Volume 2,
Issue 1,
1995,
Page 1-18
Roland N. Pittman,
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摘要:
ABSTRACTThe normal function of skeletal muscle requires that a continuous supply of oxygen be provided by the cardiovascular system. This article reviews the development of our understanding of the role of microvascular architecture on the oxygen transport system, with emphasis on direct microcirculatory observations and mathematical modeling dating from the work of August Krogh to present studies. The contributions of the various elements of the vascular network (i.e., arterioles, capillaries, and venules) and microvascular hemodynamics to oxygen exchange are discussed. Oxygen moves through the microvascular network by convection, almost all of it being reversibly bound to the hemoglobin within red blood cells. Thus, the flow properties and distribution of the red cells within the network can play a significant role in oxygen transport. Because the walls of all the vessels in the microcirculation appear to be permeable to oxygen, it continuously diffuses between the blood and the interstitium, the direction depending on the oxygen partial pressure difference. Because of the high permeability of the vascular wall to oxygen, the complex spatial relationships among the various microvessels lead to correspondingly complex diffusive interactions among them. The proximity of capillaries, arterioles, and venules, along with the anastomotic connections and tortuosity of capillaries, provides the “complex spatial relationships” that lead to diffusive interactions between neighboring capillaries, between capillaries and nearby arterioles and venules, and between paired arterioles and venules. Although there are a number of outstanding problems regarding our understanding of oxygen transport at the microcirculatory level, the most interesting and significant of these has to do with the adjustments that are made in the transition from the resting state to that of sustained aerobic exerc
ISSN:1073-9688
DOI:10.3109/10739689509146755
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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2. |
The Influence of Flow and Hematocrit on the Laser Doppler Flux Signal from the Surface of the Perfused Pig Liver |
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Microcirculation,
Volume 2,
Issue 1,
1995,
Page 19-25
ANTHONY M. WHEATLEY,
ROSEMARY HICKMAN,
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摘要:
ABSTRACTObjective:We tested the hypothesis that the measurement volume of the laser Doppler flowmeter (LDF) is too small to provide reliable quantitative estimates of total liver blood flow of large mammals, such as the pig.Methods:In a perfused pig liver, the influence of changing (i) hepatic arterial (HA) and portal venous flows individually (n= 9), (ii) HA flow at fixed portal venous flow (50%, 70%, and 100% expected total liver blood flow), and (iii) hematocrit (0–30%) at fixed total liver blood flow on LDF flux was tested (n= 8).Results:Linearity of LDF with hepatic arterial flow and portal venous flow was confirmed; however, the slope of the regression lines was higher for hepatic artery [1.92 ± 0.60 (SD)] than portal vein perfused livers (0.66 ± 0.34;P30%. At constant total liver blood flow (100 ml/min per 100 g), LDF response decreased linearly by a factor of about 2 on changing the hematocrit from 30% to 5% and markedly fell as the hematocrit was further decreased to zero.Conclusions:These results suggest that (i) the LDF flux signal from the liver surface provides a poor measure of hepatic microcirculatory blood flow during changes in total liver blood flow as the LDF responds with about three times greater sensitivity to changes in hepatic arterial than in portal venous flow, and (ii) when hematocrit is falling, LDF may underestimate hepatic perfusion to a significant extent. In addition, due to high measurement variability, the LDF flux signal cannot be quantified in absolute perfusion un
ISSN:1073-9688
DOI:10.3109/10739689509146756
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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3. |
Estimation ofIn VivoPulmonary Microvascular and Interstitial Geometry Using Digital Image Analysis |
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Microcirculation,
Volume 2,
Issue 1,
1995,
Page 27-40
DANIELE VENTUROLI,
BEATRICE CRISAFULLI,
MASSIMO FABBRO,
DANIELA NEGRINI,
GIUSEPPE MISEROCCHI,
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摘要:
ABSTRACTObjective:To determine microvascular diameter and perivascular interstitium thickness at the lung surface in thein situ, in vivolung.Methods:Microscopic images of the lung surface collected through a “pleural window” by a videocamera were digitized with a monochrome frame grabber (512 × 512 pixels, 8 bits per pixels) to be computer analyzed by image processing techniques.Results:We found that the maxima in the distribution of the standard deviations of gray levels in adjacent neighbors 7 × 7 pixels wide identify the edges between the microvessel lumen and the surrounding perivascular interstitium. Furthermore, the maxima in the distribution of the standard deviation of the standard deviations of gray levels identify the edges between the perivascular interstitium and the lung tissue.Conclusions:This technique can be applied to microvessels ranging in diameter from 30 μm to 200 μm and perivascular interstitial thickness of the order of 10–150 μm. Our approach allows for the definition of microvascular geometry even for noisy images and represents an improvement compared to other edge detection methods. The proposed analytical procedure may provide a useful tool to study lung fluid balance and microvascular reactivity in thein situlung in the normal state and in response to a variety of functional
ISSN:1073-9688
DOI:10.3109/10739689509146757
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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4. |
A Circumferential Stress‐Growth Rule Predicts Arcade Arteriole Formation in a Network Model |
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Microcirculation,
Volume 2,
Issue 1,
1995,
Page 41-51
RICHARD J. PRICE,
THOMAS C. SKALAK,
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摘要:
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 σθijwere then recomputed. The diameters of transverse arteriolar segments with σθijgreater than a σθthreshold were increased by an amount that was dependent on the original diameter and the difference between σθand the σθthreshold. 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 τijwere also performed for comparison.Results:Arterialization patterns from simulations of σθijstimulated arteriolar remodeling were representative of those seenin vivowith arterialization of back‐connection capillaries leading to arcade arteriole formation. Simulations based on similar rules for τijyielded arterio‐venous shunts, which are rarely seenin 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
ISSN:1073-9688
DOI:10.3109/10739689509146758
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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5. |
Nitric Oxide Mediates C5a‐Induced Vasodilation in the Small Intestine |
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Microcirculation,
Volume 2,
Issue 1,
1995,
Page 53-61
HONG Y. LUO,
WILLIAM B. WEAD,
SAI YANG,
MARK A. WILSON,
Patrick D. Harris,
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摘要:
ABSTRACTObjective:This study was designed to investigate the microvascular responses of the small intestine to complement C5a and to define the role of nitric oxide in the C5a‐induced response.Methods:Male Sprague–Dawley rats were anesthetized with pentobarbital, and a loop of small intestine was exteriorized and suffused with Krebs solution. The diameters of large and small arterioles of the small intestinal wall were measured within vivovideomicroscopy following the application of experimental mediators. Four 1‐hr C5a dose‐response trials were performed (10−14M, 10−12M, 10−10M, and 10−8M). Then, we completed acetylcholine dose‐response curves with and withoutNω‐nitro‐L‐arginine (N‐Arg) to document the adequacy of nitric oxide synthase inhibition. The microvascular response to the topical application of C5a (10−12M) was recorded in the presence of 2 × 10−4M N‐Arg. Additionally, experiments of C5a‐induced response with N‐Arg were repeated in the presence of L‐arginine (L‐Arg; the precursor of nitric oxide synthesis) or with systemic administration of superoxide dismutase (SOD).Results:(1) C5a induces a dose‐dependent vasodilation in the small intestine, and the maximal vasodilation occurs in A3 arterioles at C5a concentration of 10−12M; (2) N‐Arg inhibits the Ach‐induced vasodilation in the rat small intestine; and (3) L‐Arg or SOD partially reverses the inhibitory effect of N‐Arg.Conclusions:Nitric oxide mediates the C5a‐induced vasodilation in small intestinal microvessels. Superoxide is, at least partially, responsible for the v
ISSN:1073-9688
DOI:10.3109/10739689509146759
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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6. |
Abstracts from 42nd Annual Conference Microcirculatory Society 8–9 April 1995: Listed in Numerical Order of Appearance in Session Program |
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Microcirculation,
Volume 2,
Issue 1,
1995,
Page 63-113
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ISSN:1073-9688
DOI:10.3109/10739689509146760
出版商:Blackwell Publishing Ltd
年代:1995
数据来源: WILEY
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