Microcirculation最新文献

{"title":"Numerical Investigation of Hemodynamic Factors in Cellular Blood Flow: Insights From Curved Microvessels","authors":"Mojtaba Amir Aslan Pour,&nbsp;Wenbin Mao","doi":"10.1111/micc.70013","DOIUrl":"https://doi.org/10.1111/micc.70013","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study investigates the effects of hemodynamic factors on blood cell suspension flows and their properties in curved microvessels. A parametric study is employed to compare these properties between curved and straight vessels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A 3D fluid solver coupled with a cell membrane modeling framework via the immersed boundary method was used to simulate cell-resolved blood flow in straight and curved vessels featuring a 90° bend with moderate curvature.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Blood flow in curved vessels shows lower and higher shear rates in the inner and outer bulk regions, respectively, compared to straight vessels. Asymmetry in hematocrit profiles is linked to less dense suspensions, smaller diameters, and higher Capillary numbers, while the maximum velocity location remains consistent with straight vessels. At physiological shear rates, moderate curvatures, and large diameters, curvature has minimal impact on apparent viscosity. However, diffusivity is elevated at the center of curved vessels compared to straight ones.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study reveals new insights into blood suspension flows in curved microvessels with a 90° bend, highlighting key differences from straight vessels under certain hemodynamic conditions. These findings lay the groundwork for future research on realistic microvessel geometries and their implications.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144135534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eugene M Renkin. His Many Contributions to Microvascular Research With Examples of How They Inform Current Investigations of Microvascular Dysfunction","authors":"FitzRoy E. Curry,&nbsp;C. Charles Michel","doi":"10.1111/micc.70010","DOIUrl":"https://doi.org/10.1111/micc.70010","url":null,"abstract":"<p>Eugene Renkin used simplified uniform models of microvascular exchange units to describe the fundamental functions of the microcirculation: a cylindrical pore to characterize the barriers to exchange of water and solutes; a uniformly perfused capillary to distinguish flow-limited exchange from diffusion-limited exchange; and a membrane with large and small pores to describe macromolecule exchange between blood and lymph. A key idea linking these concepts to microvascular dysfunction is that local blood flows, microvascular pressures, and the permeability of the vascular wall are not uniformly distributed within microvascular beds. Renkin's concept of microvascular clearance of small solute was extended to show how heterogeneity in blood transit times compromised exchange. It was also extended to evaluate the relative contribution of diffusion, convection, and vesicle exchange to microvascular exchange of macromolecules when there is heterogeneity in macromolecule permeability, measured by the presence of large pores. An extension of his analysis to smaller proteins (14–20 KDa) showed that convective transport may limit the diffusion of inflammatory peptides, therapeutic agents, and toxins from the tissue into circulating blood. We include recent examples of the growing understanding of microvascular dysfunction in chronic disease and approaches to modeling heterogeneity in normal and diseased states.</p>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144118023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Relevance of Animal Models of Lymphatic Dysfunction and Lymphedema","authors":"Pritam Saha Podder,&nbsp;Debasree Bhadra,&nbsp;Soumiya Pal,&nbsp;V. Suzanne Klimberg,&nbsp;Amanda J. Stolarz","doi":"10.1111/micc.70009","DOIUrl":"https://doi.org/10.1111/micc.70009","url":null,"abstract":"<p>Lymphedema is a chronic progressive condition, and treatment options are limited to physical therapy or surgical intervention, underscoring the need to develop preventative strategies. To do so, we must first understand the underlying mechanisms that contribute to the development of clinical lymphedema, which can be caused by a myriad of factors, including genetic mutations, infectious agents, and cancer treatments. Animal models are essential to study the pathogenesis of clinical lymphedema and to develop therapeutic interventions. Many animal models mimic the various aspects of lymphatic dysfunction and lymphedema seen in humans, and some species better represent different aspects or causes of lymphedema. However, no single model perfectly recapitulates human disease in a cost- and time-efficient manner; therefore, findings should be verified in multiple models and multiple species. In doing so, researchers will increase the likelihood of collecting rigorous, reliable data that could be effectively and efficiently translated into the clinic. This review explores genetic, infectious, and surgical animal models of lymphatic dysfunction and lymphedema and describes how these models can be used to understand clinical forms of lymphedema. Collectively, this information can provide valuable insight for the translational study of lymphatic diseases.</p>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidized Cell-Free Hemoglobin Induces Mitochondrial Dysfunction by Activation of the Mitochondrial Permeability Transition Pore in the Pulmonary Microvasculature","authors":"Kyle J. Riedmann,&nbsp;Jamie E. Meegan,&nbsp;Aqeela Afzal,&nbsp;Yatzil Cervantes-Cruz,&nbsp;Sarah Obeidalla,&nbsp;Avery M. Bogart,&nbsp;Lorraine B. Ware,&nbsp;Ciara M. Shaver,&nbsp;Julie A. Bastarache","doi":"10.1111/micc.70012","DOIUrl":"https://doi.org/10.1111/micc.70012","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Cell-free hemoglobin (CFH) is released into the circulation during sepsis where it can redox cycle from the ferrous 2+ to ferric 3+ and disrupt endothelial function, but the mechanisms of CF-mediated endothelial dysfunction are unknown. We hypothesized that oxidized CFH induces mitochondrial dysfunction via the mitochondrial permeability transition pore (mPTP) in pulmonary endothelial cells, leading to the release of mitochondrial DNA (mtDNA).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Human lung microvascular endothelial cells were treated with CFH2+/CFH3+. We measured mitochondrial mPTP activation (flow cytometry), network and mass (immunostaining), structure (electron microscopy), mtDNA release (PCR), and oxygen consumption rate (OCR; Seahorse). Plasma from critically ill patients and conditioned cell media were quantified for mtDNA and CFH.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>CFH3+ disrupted the mitochondrial network, activated the mPTP (1434 (874–1642) vs. 2302 (1729–2654) mean fluorescent intensity, <i>p</i> = 0.02), increased the spare respiratory capacity (30.61 (29.36–37.78) vs. 7.83 (3.715–10.63) OCR, <i>p</i> = 0.004), and caused the release of mtDNA. CFH was associated with circulating mtDNA (<i>R</i>² = 0.1912, <i>p</i> = 0.0077) in plasma from critically ill patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>CFH3+, not CFH2+, is the primary driver of CFH-induced lung microvascular mitochondrial dysfunction. Activation of the mPTP and the release of mtDNA are a feature of CFH3+ mediated injury.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144100609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding Vascular Reactivity","authors":"Manuel F. Navedo,&nbsp;Scott Earley,&nbsp;Brant E. Isakson","doi":"10.1111/micc.70008","DOIUrl":"https://doi.org/10.1111/micc.70008","url":null,"abstract":"&lt;p&gt;Blood vessels form an intricate network of dynamic conduits responsible for delivering blood throughout the body. Consequently, the structural and functional integrity of blood vessels is critical for optimal circulation and tissue function. Vascular reactivity is an essential physiological process by which blood vessels dynamically adjust their diameter in response to various stimuli. This adaptive process ensures that blood flow meets tissue-specific metabolic demands. Vascular reactivity is also essential for controlling blood pressure, as changes in the radius of resistance vessels dramatically affect peripheral vascular resistance.&lt;/p&gt;&lt;p&gt;Vascular reactivity is governed by sophisticated signaling cascades within and between various cell types constituting the vascular wall (smooth muscle cells, pericytes, and endothelial cells), perivascular adipose tissue that surrounds most blood vessels, and many types of additional extravascular cells. These diverse signaling cascades give rise to regional heterogeneity in vascular responses, leading to distinctive reactivity patterns tailored to the physiological role of individual vessel segments. An array of different hormones and circulating factors can also influence vascular reactivity, and considering sex as a biological variable has provided valuable insights into the mechanisms underlying vascular function.&lt;/p&gt;&lt;p&gt;The importance of vascular reactivity extends beyond basic vessel physiology, as its altered function underpins physiological vascular adaptation during pregnancy and numerous pathological conditions such as hypertension, heart failure, and stroke. Thus, elucidating the intricate mechanisms, functional implications, and adaptive responses, as well as developing new tools and approaches to better study vascular reactivity, is paramount for advancing cardiovascular research and the development of new treatment strategies.&lt;/p&gt;&lt;p&gt;In this Special Topics Issue (STI), we present a curated collection of reviews and original studies that expand our current knowledge of mechanisms and functional implications of vascular reactivity in health, physiological adaptation, and disease states. The reader will also find studies introducing innovative methodological approaches and analytical techniques for examining vascular reactivity, creating opportunities to advance future research endeavors in vascular biology.&lt;/p&gt;&lt;p&gt;This STI begins with a review by Li and colleagues [&lt;span&gt;1&lt;/span&gt;] dissecting the role of ion channels in vascular cells and their contributions to vascular hyporesponsiveness during shock. The authors examine how structural and functional alterations in various ion channels (e.g., K&lt;sup&gt;+&lt;/sup&gt;, Ca&lt;sup&gt;2+&lt;/sup&gt;, and Na&lt;sup&gt;+&lt;/sup&gt; channels) contribute to altered vascular reactivity during shock and how this new mechanistic insight could be exploited for the development of new therapies to treat shock-induced vascular complications.&lt;/p&gt;&lt;p&gt;Following the ion channel theme, Mbiakop and J","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 3","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143880042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Convection Effect of Plasma Flow on Oxygen Transport in Capillaries: An In-Depth Numerical Investigation","authors":"Junfeng Zhang","doi":"10.1111/micc.70011","DOIUrl":"https://doi.org/10.1111/micc.70011","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The convection effect of plasma flow on gas transport in the microcirculation has been a controversial topic in the literature. We aim to clarify this concern via thorough and rigorous analysis of the oxygen release process from red blood cells (RBCs) to the surrounding tissue.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We develop a comprehensive model that considers the plasma flow, RBC deformation, oxygen transport and oxygen-hemoglobin reaction kinetics. The boundary integral and lattice Boltzmann methods are employed in the numerical solutions. In particular, the oxygen fluxes due to plasma convection and mass diffusion are separately calculated along the capillary wall for further comparison.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Our results show that the most significant diffusive flux occurs in the narrow gap between the RBC side surface and the capillary wall and the diffusive flux is primarily directed outward, which favors oxygen release into the surrounding tissue. Furthermore, although the axial convective flux is the most profound in magnitude, it contributes little to the overall blood-to-tissue oxygen transport in the radial direction. The radial convective flux also has a larger magnitude compared to the diffusive oxygen flux, but is limited to two small areas and to opposite directions. This results in a negligible net effect of the plasma convection compared to the diffusive flux on the overall oxygen transport. This observation is further confirmed by comparing the oxygen distributions and diffusive fluxes from simulations with and without considering the plasma convection flow relative to RBCs. Moreover, we revisit the Peclet number definition and propose that different characteristic length scales should be adopted for oxygen diffusion and convection in capillaries. The revised Peclet number has a value three orders of magnitude lower than that from the classical Peclet number definition.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our simulation results show that the influence of plasma convection on the overall oxygen transport can be neglected in typical microcirculation situations. This is consistent with the revised Peclet number value, suggesting that the revised Peclet number can better reflect the relative importance of convection and diffusion mechanisms in microvascular gas transport.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 3","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143850976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physiologically—Modeled Dynamic Stimulation and Growth Factors Induce Differentiation of Mesenchymal Stem Cells to a Vascular Endothelial Cell Phenotype","authors":"Mediha Gurel,&nbsp;Helena Zomer,&nbsp;Calum McFetridge,&nbsp;Walter L. Murfee,&nbsp;Peter S. McFetridge","doi":"10.1111/micc.70007","DOIUrl":"https://doi.org/10.1111/micc.70007","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Mesenchymal stem cells (MSCs) represent an attractive option as an endothelial cell (EC) source for regenerative medicine therapies. However, the differentiation of MSCs toward an ECs phenotype can be regulated by a complex and dynamic microenvironment, including specific growth factors as well as local mechanical cues. The objective of this work was to evaluate whether Physiologically-modeled dynamic stimulation (PMDS) characterized by continuous variability in pulse frequencies mimicking the dynamic temporal range of cardiac function would enhance MSC differentiation toward ECs compared to a constant frequency stimulation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Mesenchymal stem cells were grown in a complex growth factor cocktail versus standard culture media to initiate the endothelial differentiation process, then subsequently exposed to PMDS that vary in duration and constant flow (CF) at a fixed 10 dynes/cm² shear stress and 1.3 Hz frequency.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Both PMDS and media type strongly influence cell differentiation and function. Cells were shown to significantly upregulate eNOS activity and displayed lower TNF-a induced leukocyte adhesion compared to cells cultured under CF, consistent with a more quiescent ECs phenotype that regulates anti-inflammatory and anti-thrombotic states.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings suggest that the dynamic microenvironment created by perfusion, in contrast to constant frequency, combined with growth factors, enhances MSCs differentiation toward a vascular endothelial-like phenotype.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 3","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143689463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of BzATP-Induced Blood–Brain Barrier Endothelial Cell Hyperpermeability by NLRP3 Inflammasome Inhibition","authors":"Aliyah Anderson,&nbsp;O'lisa Yaa Waithe,&nbsp;Gabriela Seplovich,&nbsp;Oluwatoyin Olagunju,&nbsp;Christlyn Greene,&nbsp;Amrendra Singh,&nbsp;Saravanakumar Muthusamy,&nbsp;Binu Tharakan","doi":"10.1111/micc.70006","DOIUrl":"https://doi.org/10.1111/micc.70006","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The blood–brain barrier (BBB) is a semi-permeable microvascular barrier, composed of endothelial cells conjoined by tight junction proteins. Following pathological conditions, i.e., traumatic brain injury (TBI), BBB dysfunction occurs, leading to microvascular hyperpermeability, resulting in cerebral edema formation and elevated intracranial pressure. Recent evidence suggests that the activation of pro-inflammatory signaling pathways is critical to BBB dysfunction. The NLRP3 inflammasome has been implicated as a key component of pro-inflammatory signaling. The aim of this study was to determine the upstream regulators of NLRP3 inflammasome activation that cause subsequent BBB aberration and microvascular hyperpermeability.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Brain microvascular endothelial cells were exposed to benzoyl ATP (BzATP) with or without MCC950. We employed immunocytochemical localization of tight junction proteins, fluorometric enzymatic assays, total gene expression analyses of ZO-1, and monolayer permeability studies to assess the effect of BzATP-induced injury on NLRP3 inflammasome activation/inhibition.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>BzATP treatment induced monolayer hyperpermeability and increased caspase-1 and MMP-9 activities. NLRP3 inhibition decreased caspase-1 and MMP-9 activities and rescued BzATP-induced monolayer permeability significantly.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>NLRP3 inflammasome signaling is critical to BBB endothelial cell dysfunction. Extracellular ATP is an upstream promoter of BBB hyperpermeability. NLRP3 inflammasome activation leads to subsequent caspase-1 and MMP-9-mediated tight junction protein disarray.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 3","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143571407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperspectral Imaging in the Healing Prognosis of Diabetes Related Foot Ulcers. A Systematic Review and Meta-Analysis","authors":"Patricia M. González-Villacorta,&nbsp;Mateo López-Moral,&nbsp;Marta García-Madrid,&nbsp;Esther García-Morales,&nbsp;Aroa Tardáguila-García,&nbsp;José Luis Lázaro-Martínez","doi":"10.1111/micc.70005","DOIUrl":"https://doi.org/10.1111/micc.70005","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The diagnostic capability of hyperspectral (HSI) imaging has been focused on the prognosis of wound healing in patients with peripheral artery disease and diabetic foot ulcers (DFUs). The aim of this study was to evaluate the performance characteristics of HSI to determine the pretest probability for the prognosis of DFU healing.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A systematic search was performed on the PubMed, Medline, and Cochrane databases to identify studies evaluating HSI in predicting the prognosis of DFUs. This study was registered with PROSPERO (CRD42023495391). All selected studies were evaluated using the STROBE guidelines to assess the reporting quality for observational studies. Meta-DiSc software was used to analyze the collected data.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Nine publications (142 participants) were evaluated for systematic review. The meta-analysis included four publications examining the prospective diagnostic capability of HSI. Concerning the prognostic accuracy of HSI, it had a pooled sensitivity of 0.84 (0.75–0.9) and a specificity of 0.79 (0.66–0.88) for predicting DFU healing, as well as an odds ratio of 20.4, resulting in a positive likelihood ratio of 4.1 and a negative likelihood ratio of 0.2 (heterogeneity <i>I</i>² = 0).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The meta-analysis revealed promising prognostic capability of HSI for the healing of DFU. More randomized clinical trials need to be published as our results are based on only prospective and comparative studies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 3","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143554408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Small Arteries From Old Spontaneously Hypertensive Rats Exhibit Enhanced Endothelium-Independent Vasodilatory Capacity and Reduced Stiffness","authors":"Francisco I. Ramirez-Perez,&nbsp;Thomas J. Jurrissen,&nbsp;Marc A. Augenreich,&nbsp;Jorge A. Castorena-Gonzalez,&nbsp;Mariana Morales-Quinones,&nbsp;Christopher A. Foote,&nbsp;Zahra Nourian,&nbsp;Olubodun M. Lateef,&nbsp;Natnicha Imkaew,&nbsp;Zhe Sun,&nbsp;Michael A. Hill,&nbsp;Gerald A. Meininger,&nbsp;Jaume Padilla,&nbsp;Luis A. Martinez-Lemus","doi":"10.1111/micc.70004","DOIUrl":"https://doi.org/10.1111/micc.70004","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>In conduit arteries, aging and hypertension are associated with stiffening characterized by increased cytoskeletal F-actin and endothelial dysfunction. Herein, we determined if this also happens at the level of the resistance vasculature.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We retrospectively compared the mechanical and structural characteristics of small arteries isolated from older hypertensive and younger normotensive (64.7 ± 2.8 vs. 32.1 ± 1.9 years old) human subjects. The intersection of aging and hypertension was studied in small mesenteric arteries from old (88 weeks of age) spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) normotensive rats.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Arteries from older hypertensive subjects were stiffer and had more F-actin, relative to those from younger normotensives. Comparatively, arteries from old SHRs showed reduced stiffness and increased vasodilation to sodium nitroprusside without changes in F-actin. Matrix metalloproteinase-2 (MMP-2) and -9 (MMP-9) were increased in the SHR arteries and exposure of naive arteries to exogenous MMP-2 and MMP-9 augmented responsiveness to sodium nitroprusside and adenosine.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>In conclusion, resistance arteries from old SHRs are softer and vasodilate more to exogenous nitric oxide than those of WKY rats. This improved endothelial-independent vasodilation is associated with an increased vascular expression of MMP-2 and MMP-9. We further conclude that aging and hypertension effects on the microcirculation may vary between species and vascular beds.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 2","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143431137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}