Microcirculation最新文献

{"title":"COVID-19 Patients Have Peripheral Microvascular Dysfunction and Tissue Hypoxia in Spite of Successful Treatment of Lung Failure: A Proof of Concept Study","authors":"Knut Kvernebo,&nbsp;L. Liv Kristin Wikslund,&nbsp;Kamila Drezek,&nbsp;Andrea Jaramillo,&nbsp;Luigino Capone,&nbsp;Maged Helmy,&nbsp;Yunong Zhao,&nbsp;Aaron Aguirre,&nbsp;David D'Alessandro","doi":"10.1111/micc.70014","DOIUrl":"https://doi.org/10.1111/micc.70014","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Availability of oxygen (O₂) is essential for life and function of all cells of the human body (<i>n</i> ≈ 10¹³–10¹⁴ cells). COVID-19 patients often have impaired lung function with compromised oxygen uptake, but little is known about microvascular oxygen delivery and tissue oxygenation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Use the Oxygen Delivery Index (ODIN) concept to assess peripheral microvascular regulation and oxygen extraction in COVID-19 patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The ODIN concept includes two technologies (diffuse reflectance spectroscopy—DRS and computer assisted microscopy—CAM) for data acquisition from subepidermal nutritive capillaries. Output parameters are microvascular oxygen saturation (SmvO₂) and functional capillary density (FCD).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Forty patients hospitalized for COVID-19 grouped into early discharge (&lt; 7 days, <i>n</i> = 11), severe (beyond 7 days, <i>n</i> = 24) and non-survivors (<i>n</i> = 5), and healthy controls (<i>n</i> = 23) were examined.</p>\u0000 \u0000 <p>Microvascular oxygen saturation (SmvO₂) and the corresponding O₂ extraction (SaO₂—SmvO₂) was 56% ± 4%/42% ± 9% (mean ± SD) in healthy controls (<i>n</i> = 11), 61 ± 10/37 ± 10 for historic controls (<i>n</i> = 12), significantly different (<i>p</i> &lt; 0.01) as compared with all COVID-19 groups (early discharge: 40% ± 13%/54% ± 13%, severe: 34% ± 15%/60% ± 15%, non-survivors 22% ± 15%/73% ± 16%). FCD expressed as the relative number of red pixels (belonging to a capillary erythrocyte) in a CAM frame were reduced in alle patient groups as compared to historic controls (<i>p</i> &lt; 0⋅05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Results show skin microvascular dysregulation and tissue hypoxia in patients, indicative of hypoxia also in other tissues. We hypothesize that tissue hypoxia is a cause of reversible and non-reversible long COVID-19 symptoms and of mortality.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 5","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144525030","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":"Regulatory T Cells Control Vascular Adhesion Molecule Expression in Skin Under Inflammatory and Homeostatic Conditions","authors":"M. Ursula Norman,&nbsp;Brandon Lim,&nbsp;Lucinda Jenkins,&nbsp;Pam Hall,&nbsp;Sarah L. Snelgrove,&nbsp;Michael J. Hickey","doi":"10.1111/micc.70017","DOIUrl":"https://doi.org/10.1111/micc.70017","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>During skin inflammation, inhibition of adhesion of regulatory T cells (Tregs) to the dermal microvascular endothelium leads to exacerbation of inflammation, evidence that the dermal endothelium is a key target of the anti-inflammatory actions of Tregs. The aim of this study was to investigate the capacity of Tregs to control the expression of endothelial adhesion molecules in inflamed and resting skin.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Treg function was assessed in a two-challenge contact hypersensitivity (CHS) model, measuring dermal adhesion molecule expression via imaging of cleared skin. Treg depletion was achieved using <i>Foxp3</i>^<i>DTR</i> mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>CHS induced upregulation of E-selectin and ICAM-1 but not P-selectin and VCAM-1. Elimination of Tregs following CHS challenge resulted in exacerbated skin inflammation and enhanced expression of E-selectin, P-selectin and ICAM-1 in the dermal microvasculature. Multiphoton imaging revealed that at this phase of the response, Tregs were enriched near blood vessels and underwent dynamic migration adjacent to the microvasculature. Additionally, in skin that was not undergoing hapten challenge, absence of Tregs also resulted in upregulation of E-selectin and ICAM-1 in skin vessels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These observations demonstrate that the microvascular endothelium is a target of the anti-inflammatory actions of Tregs in the skin, both during CHS and in steady-state skin.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 5","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144514649","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":"Modulatory Role of Nitric Oxide on the Vasomotor Actions of NPY in Porcine Cerebral Arteries","authors":"Gabriela Delgado,&nbsp;Cameron J. Morse,&nbsp;Breanna Barlage,&nbsp;M. Harold Laughlin,&nbsp;Craig A. Emter,&nbsp;Erika M. Boerman,&nbsp;Jaume Padilla,&nbsp;Corey R. Tomczak,&nbsp;T. Dylan Olver","doi":"10.1111/micc.70016","DOIUrl":"https://doi.org/10.1111/micc.70016","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <p>Neuropeptide Y (NPY) is a sympathetic co-transmitter that mediates vasoconstriction. However, there is evidence that it may also mediate dilation through a nitric oxide (NO)-dependent mechanism.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>We used a swine model to examine how NPY influences cerebral vascular regulation and hypothesized that NPY would elicit both vasoconstrictor and vasodilatory effects, and that such effects would be modulated partially by NO signaling.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Briefly, cerebral perfusion and blood pressure were monitored during intracarotid saline or NPY infusion (0.1 μg/kg) in the presence and absence of NO synthase (NOS) inhibition (<i>N</i>^G-nitro-l-arginine methyl ester; 0.35 mg/kg/min). Separately, Y1 receptor distribution (immunohistochemistry) and vasomotor responses to intra- and extraluminal NPY under control and NOS inhibition conditions were examined in isolated arteries.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Intracarotid NPY infusions elicited transient dilation that was blocked by NOS inhibition. In isolated pial arteries, distinct populations of NPY-Y1 receptors were observed on both the vascular smooth muscle (VSM) and endothelium. Extraluminal application of NPY elicited vasoconstriction, while intraluminal delivery elicited vasodilation. NOS inhibition enhanced the magnitude of vasoconstriction in isolated pial arteries. Endothelial denudation, Y1 receptor antagonism, and NOS inhibition each blunted NPY-induced vasodilation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These data suggest both vasoconstrictor and vasodilatory effects of NPY are modulated partially by NO signaling.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 5","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144503276","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":"The Effect of Renal Denervation on Capillary Density in Patients With Uncontrolled Hypertension","authors":"Lefki Nikolopoulou,&nbsp;Kyriakos Dimitriadis,&nbsp;Nikolaos Pyrpyris,&nbsp;Fotios Tatakis,&nbsp;Panagiotis Iliakis,&nbsp;Costas Thomopoulos,&nbsp;Dimitrios Konstantinidis,&nbsp;Loukianos Rallidis,&nbsp;Dimitrios Tousoulis,&nbsp;Konstantinos Tsioufis","doi":"10.1111/micc.70015","DOIUrl":"https://doi.org/10.1111/micc.70015","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Hypertension is related to the pathogenesis of microvascular dysfunction. Renal denervation is a guideline-endorsed intervention for the management of uncontrolled hypertension. However, the effect of renal denervation on skin capillary density, as assessed by nailfold capillaroscopy, is unknown.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Individuals with stage I/II uncontrolled hypertensions were enrolled and allocated to either undergo renal denervation or serve as controls. Nailfold capillaroscopy was performed at baseline and at 12 months. Furthermore, the albumin to creatinine ratio (ACR) and office/ambulatory blood pressure (BP) levels were monitored throughout the study.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 45 individuals (28 renal denervation, 17 control) were enrolled in our study. No difference was found in baseline capillary density. At 12 months, all patients had controlled BP, while the denervation arm had a significantly greater number of capillaries, compared with control (90.9 ± 14.0 vs. 82.5 ± 10.6 capillaries/mm²; <i>p</i> = 0.036). However, the change from baseline capillary density was not significantly different between groups (4.6 ± 6.1 vs. 1.39 ± 8.8 capillaries/mm²; <i>p</i> = 0.150). Moreover, the change of ACR was not different between groups (−2.7 ± 13.8 vs. 0.46 ± 5.2; <i>p</i> = 0.365).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In patients with uncontrolled stage I/II hypertension, renal denervation may have a beneficial effect on skin capillary density.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 5","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144339192","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":"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":"<p>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.</p><p>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.</p><p>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.</p><p>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.</p><p>This STI begins with a review by Li and colleagues [<span>1</span>] 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⁺, Ca²⁺, and Na⁺ 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.</p><p>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}