美国生理学杂志-心脏和循环生理学发表关于心脏、脉管系统和淋巴系统生理学的原始调查、评论和观点。这些文章包括从完整和整合的动物和器官功能到细胞、亚细胞和分子水平的各个组织水平的心血管功能的实验和理论研究。该杂志包含了对这些功能及其控制系统的新描述，以及它们在生物化学、生物物理学、遗传学和细胞生物学中的基础。优先考虑提供重要的新机械生理学见解的研究，这些见解可以确定正常和异常心脏和循环的表现。

The American Journal of Physiology - Heart and Circulatory Physiology publishes original investigations, reviews, and perspectives on the physiology of the heart, vascular system, and lymphatic system. These articles cover experimental and theoretical studies of cardiovascular function at various levels, from whole and integrated animal and organ functions to cellular, subcellular, and molecular levels. The journal includes new descriptions of these functions and their control systems, as well as their foundations in biochemistry, biophysics, genetics, and cell biology. Research providing significant new insights into mechanical physiology that can elucidate the performance of normal and abnormal heart and circulatory functions is prioritized.

《American Journal of Physiology - Heart and Circulatory Physiology》发表关于心脏、血管系统和淋巴系统生理学的原创研究、评论和观点。这些文章涵盖了从整体和综合的动物及器官功能到细胞、亚细胞和分子水平的心血管功能的实验和理论研究。该杂志包含对这些功能及其控制系统的新描述，以及它们在生物化学、生物物理学、遗传学和细胞生物学中的基础。优先考虑提供重要的新机械生理学见解的研究，这些见解能够阐明正常和异常心脏及循环的表现。

American Journal of Physiology - Heart and Circulatory Physiology

Evaluation of the left atrioventricular coupling index (LACI) in a rest and exercise-stress cardiovascular magnetic resonance imaging protocol allows identification of patients with heart failure and preserved ejection fraction with high diagnostic accuracy. LACI holds similar diagnostic accuracy at rest compared with left atrial ejection fraction during exercise stress. This highlights the value of LACI as a widely available and cost-effective test for diastolic dysfunction, which may help to guide patient selection for referral to specialized testing/treatment.

Sören J. Backhaus

Torben Lange

Alexander Schulz

Ruben Evertz

Simon M. Frey

Gerd Hasenfuß

Andreas Schuster

AJP Heart and Circulatory Physiology

Cardiovascular magnetic resonance rest and exercise-stress left atrioventricular coupling index to detect diastolic dysfunction

心血管磁共振静息与运动应激左心房-左心室耦合指数检测舒张功能障碍

The no-reflow phenomenon refers to the observation that when an organ is made ischemic by occlusion of a large artery supplying it, restoration of patency in that artery does not restore perfusion to the microvasculature supplying the parenchyma of that organ. This has been observed after prolonged arterial occlusions in the heart (30–90 min), brain, skin, and kidney. In experimental models, zones of no reflow in the heart are characterized by ultrastructural microvascular damage, including focal endothelial swelling obstructing the lumen of small vessels. Blood elements such as neutrophil plugs, platelets, and stacking of erythrocytes have also been implicated. No reflow is associated with poor healing of the myocardial infarction. In patients, no reflow is associated with a poor clinical outcome independent of infarct size, suggesting that therapy for no reflow may be an important approach to improving outcome for ST elevation myocardial infarction. No reflow occurs after reperfusion of experimental cerebral ischemia and may be observed after only 5-min episodes of ischemia. Aggregation of blood elements may play a greater role than in cardiac no reflow. No reflow in the brain may involve cortical spreading depression with disturbed local vascular control and high, vasculotonic levels of extracellular K + concentration, postischemic swelling in endothelial cells and abutting end feet of pericytes, pericyte contraction and death, interstitial edema with collapse of cerebral capillaries, and inflammatory reaction. New guidelines suggesting that reperfusion for stroke may be considered as late as 24 h after the onset of symptoms suggest that clinicians may be seeing more no reflow in the future.

Robert A. Kloner

Kevin S. King

Michael G. Harrington

American Journal of Physiology-Heart and Circulatory Physiology

No-reflow phenomenon in the heart and brain

心脏和大脑中的无复流现象

Regional changes occur in the sympathetic innervation of the heart after myocardial infarction (MI), including loss of norepinephrine (NE) uptake and depletion of neuronal NE. This apparent denervation is accompanied by increased cardiac NE spillover. One potential explanation for these apparently contradictory findings is that the sympathetic neurons innervating the heart are exposed to environmental stimuli that alter neuronal function. To understand the changes that occur in the innervation of the heart after MI, immunohistochemical, biochemical, and molecular analyses were carried out in the heart and stellate ganglia of control and MI rats. Immunohistochemistry with panneuronal markers revealed extensive denervation in the left ventricle (LV) below the infarct, but sympathetic nerve fibers were retained in the base of the heart. Western blot analysis revealed that tyrosine hydroxylase (TH) expression (normalized to a panneuronal marker) was increased significantly in the base of the heart and in the stellate ganglia but decreased in the LV below the MI. NE transporter (NET) binding sites, normalized to total protein, were unchanged, except in the LV, where [ 3 H]nisoxetine binding was decreased. TH mRNA was increased significantly in the left and right stellate ganglia after MI, while NET mRNA was not. In the base of the heart, increased TH coupled with no change in NET may explain the increase in extracellular NE observed after MI. Coupled with substantial denervation in the LV, these changes likely contribute to the onset of cardiac arrhythmias.

Wei Li

David Knowlton

Donna M Van Winkle

Beth A Habecker

Infarction alters both the distribution and noradrenergic properties of cardiac sympathetic neurons

梗死改变心脏交感神经元的分布及去甲肾上腺素能特性

Decreased interstitial flow (IF) in secondary lymphedema is coincident with poor physiological lymphatic regeneration. However, both the existence and direction of causality between IF and lymphangiogenesis remain unclear. This is primarily because the role of IF and its importance relative to the action of the prolymphangiogenic growth factor vascular endothelial growth factor (VEGF)-C (which signals primarily through its receptor VEGFR-3) are poorly understood. To clarify this, we explored the cooperative roles of VEGFR-3 and IF in a mouse model of lymphangiogenesis in regenerating skin. Specifically, a region of lymphangiogenesis was created by substituting a portion of mouse tail skin with a collagen gel within which lymphatic capillaries completely regenerate over a period of 60 days. The relative importance of IF and VEGF-C signaling were evaluated by either inhibiting VEGFR-3 signaling with antagonistic antibodies or by reducing IF. In some cases, VEGF-C signaling was then increased with exogenous protein. To clarify the role of IF, the distribution of endogenous matrix metalloproteinases (MMPs) and VEGF-C within the regenerating region was determined. It was found that inhibition of either VEGFR-3 or IF suppressed endogenous lymphangiogenesis. Reduction of IF was found to decrease lymphatic migration and transport of endogenous MMP and VEGF-C through the regenerating region. Therapeutic VEGF-C administration restored lymphangiogenesis following inhibition of VEGFR-3 but did not increase lymphangiogenesis following inhibition of IF. These results identify IF as an important regulator of the pro-lymphangiogenic action of VEGF-C.

Jeremy Goldman

Kelly A. Conley

Alisha Raehl

Dona M. Bondy

Bronislaw Pytowski

Melody A. Swartz

Joseph M. Rutkowski

David B. Jaroch

Emily L. Ongstad

Regulation of lymphatic capillary regeneration by interstitial flow in skin

皮肤中间质流动对淋巴管再生调控的研究

The glycocalyx is crucial for normal endothelial function. It also tethers extracellular superoxide dismutase (SOD3), which protects the endothelium against oxidative damage. Proteolytic enzymes [matrix metalloproteinases (MMPs)] are capable of disrupting endothelial cell surface proteins, such as syndecans, resulting in derangements of the endothelial glycocalyx. We sought to test the role of MMPs in oxidative stress-mediated disruption of the endothelial glycocalyx and examine the effect of pharmacological inhibition of MMPs on mitigating this detrimental effect. We also examined the role of histone deacetylase (HDAC) in the oxidative stress-mediated MMP induction and glycocalyx remodeling. Oxidative stress was experimentally induced in human adipose microvascular endothelial cells using H 2 O 2 and buthionine sulfoximine in the presence and absence of potent MMP and HDAC inhibitors. H 2 O 2 and buthionine sulfoximine resulted in a notable loss of the endothelial glycocalyx; they also increased the expression and proteolytic activity of MMP-2 and MMP-9 and subsequently increased the shedding of syndecan-1 and SOD3 from the endothelial cell surface. MMP upregulation was accompanied by a decline in mRNA and protein levels of their inhibitors, tissue inhibitors of metalloproteinase (TIMPs; TIMP-1 and TIMP-3). Furthermore, oxidative stress induced HDAC activity. Inhibition of MMPs and HDAC reversed syndecan-1 and SOD3 shedding and maintained endothelial glycocalyx integrity. HDAC inhibition increased TIMP expression and reduced MMP expression and activity in endothelial cells. Our findings shed light on MMPs and HDAC as therapeutically targetable mechanisms in oxidative stress-induced glycocalyx remodeling. NEW &amp; NOTEWORTHY Oxidative stress, a hallmark of many diseases, damages the endothelial glycocalyx, resulting in vascular dysfunction. Studying the mechanistic link between oxidative stress and endothelial glycocalyx derangements might help discover new therapeutic targets to preserve vascular function. In this study, we investigated the involvement of matrix metalloproteinases and histone deacetylase in oxidative stress-induced endothelial glycocalyx degradation.

Mohamed M. Ali

Abeer M. Mahmoud

Elizabeth Le Master

Irena Levitan

Shane A. Phillips

Role of matrix metalloproteinases and histone deacetylase in oxidative stress-induced degradation of the endothelial glycocalyx

氧化应激诱导的内皮糖萼降解中基质金属蛋白酶和组蛋白去乙酰化酶的作用

The promise of injection of extracellular matrix (ECM) from animal hearts as a treatment of myocardial ischemia has been limited by immune reactions and harsh ECM-damaging extraction procedures. We developed a novel method to produce lab-grown human 3D acellular ECM particles from human mesenchymal stem cells (MSCs) to mitigate product variability, immunogenicity, and preserve ECM architecture. We hypothesized that intramyocardial injection (I/M) of this novel ECM (dia ~200 microns) would improve cardiac function in a post-myocardial infarction (MI) murine model. WT mice aged 8-10 weeks underwent ligation of the LAD artery and I/M injection of 10 uL ECM or normal saline (n=10/group). Compared to control, ECM-treated hearts showed significant reduction in infarct size (p=0.04), increased capillary density in ischemic myocardium (p=0.01), and increased fractional shortening (FS) (p>0.05) on POD 14, 21, and 28 by echocardiography. There were no significant differences in immunogenic response as determined by TNF⍺, IL6, CD86, or CD163 levels (p>0.05 for all) in the hearts. Biodistribution of fluorophore-conjugated ECM demonstrated localized epifluorescence in the heart after I/M injection, without significant peripheral end organ epifluorescence. Proteomic analysis of ischemic and perfused myocardium from control and ECM-treated hearts using LC-MS/MS (n=3/group) detected significant changes in proteins involved in cardiomyocyte contractility and fatty acid metabolism. These findings suggest that 3D ECM particles induce recovery of ischemic myocardium, by upregulating protein networks involved in cellular contractility and metabolism. Taken together, 3D ECM particles represent a promising therapy for MI, and warrant confirmatory studies in a high-fidelity large animal model.

Mark Broadwin

Katerina St. Angelo

Max Petersen

Rayane B. Teixeira

Dwight D. Harris

Christopher R. Stone

Cynthia Xu

Meghamsh Kanuparthy

Frank W. Sellke

Jeffrey Morgan

M. Ruhul Abid

Lab-grown, 3D Extracellular Matrix Particles Improve Cardiac Function and Morphology in Myocardial Ischemia

实验室培养的3D细胞外基质颗粒改善心肌缺血中的心脏功能和形态

Pediatric pulmonary hypertension is a heterogeneous disease associated with significant morbidity and mortality. MicroRNAs have been implicated as both pathologic drivers of disease and potential therapeutic targets in pediatric pulmonary hypertension. We sought to characterize the circulating microRNA profiles of a diverse array of pediatric pulmonary hypertension patients using high throughput sequencing technology. Peripheral blood samples were drawn from patients recruited at the time of a clinically indicated cardiac catheterization and microRNA sequencing followed by differential expression and target/pathway enrichment analyses were performed. Among 63 pediatric pulmonary hypertension patients, we identified specific microRNA signatures that uniquely classified patients by disease subtype, correlated with indicators of disease severity including invasive hemodynamic metrics, and changed over the course of treatment for pulmonary hypertension. These microRNA profiles include a number of specific microRNA molecules known to function in signaling pathways critical to pulmonary vascular biology and disease, including TGFβ beta, VEGF, PI3K/Akt, cGMP-PKG, and HIF-1 signaling. Circulating levels of miR-122-5p, miR-124-3p, miR-204-5p, and miR-9-5p decreased over the course of treatment in a subset of patients who had multiple samples drawn during the study period. Our findings support the further investigation of specific microRNAs as mechanistic mediators, biomarkers, and therapeutic targets in pulmonary hypertension.

Michael A. Smith

Sam Chiacchia

Jason Boehme

Sanjeev A. Datar

Emily Morell

Roberta L. Keller

Amy Romer

Elizabeth Colglazier

Claire Parker

Jasmine Becerra

Jeffrey R. Fineman

MicroRNA in pediatric pulmonary hypertension microRNA profiling to inform disease classification, severity, and treatment response in pediatric pulmonary hypertension

微小RNA在儿童肺动脉高压中的作用：通过微小RNA分析为儿童肺动脉高压的疾病分类、严重程度及治疗反应提供信息

The longitudinal motion and the intramural shear strain of the arterial wall increase dramatically in response to blood pressure, thereby impacting the vascular wall microenvironment. Exposure to a sedentary lifestyle has been identified as an independent risk factor for cardiovascular disease, but it has been shown that intermittent physical activity embedded into everyday life is enough to improve cardiovascular health. Marked changes in longitudinal motion already at low workload may explain this finding. However, to understand the mechanism linking longitudinal motion and cardiovascular health, an understanding of the physiological basis for the longitudinal motion of the arterial wall is needed. The factors underlying the longitudinal motion of the arterial wall in vivo are numerous and intertwined. As a comment and complement to the recent review by Athaide et al., we propose and discuss a comprehensive cardiovascular mechanical scenario based on current literature. In this scenario, blood pressure, typically acting in the radial direction, also acts directly in the longitudinal direction through a tapered geometry. This complements ventricular contraction, ventricular-vascular coupling, arterial diameter change, arterial stiffness in both the radial and longitudinal directions, and pre-stretch of the arterial wall. Additionally, we consider the geometry of the arterial tree and intramural friction of the arterial wall. Together, these important cardiovascular mechanical ­factors form the pattern of longitudinal motion of the arterial wall, indicating that the longitudinal motion of the arterial wall is important for cardiovascular health.

Magnus Cinthio

Artturi Petäjä

Tobias Erlöv

Åsa Rydén Ahlgren

A comment on the physiological basis for longitudinal motion of the arterial wall

关于动脉壁纵向运动的生理基础的评论

Editorial FocusCeramide toxicity in cardiomyocytes: From Farber Disease to CVDLindsey A. Fitzsimons, Harilaos Filippakis, Lindsey A. FitzsimonsCorrespondence: Lindsey A. Fitzsimons Biomedical Sciences, University of New England 11 Hills Beach Rd Pickus Center, Central Receiving Biddeford, ME 04005 lfitzsimons@une.eduPortland Laboratory for Biotechnology and Health Sciences, University of New England, Portland, ME, USACenter for Excellence in Neurosciences, University of New England, Biddeford, ME, USADepartment of Biomedical Sciences, University of New England, College of Osteopathic Medicine, Biddeford, ME, USACenter for Cell Signaling Research, University of New England, Biddeford, ME, USA and Harilaos FilippakisCenter for Excellence in Neurosciences, University of New England, Biddeford, ME, USADepartment of Biomedical Sciences, University of New England, College of Osteopathic Medicine, Biddeford, ME, USACenter for Cell Signaling Research, University of New England, Biddeford, ME, USAPublished Online:20 Dec 2024https://doi.org/10.1152/ajpheart.00843.2024MoreFiguresReferencesRelatedInformationPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookXLinkedInWeChat We recommendHigh [Na+]i in cardiomyocytes from rainbow troutRikke Birkedal, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology, 2007Silencing of MYH7 ameliorates disease phenotypes in human iPSC-cardiomyocytesAlexandra Dainis, Physiological Genomics, 2020Recovery of anoxic-reoxygenated cardiomyocytes from severe Ca2+ overloadB. Siegmund, American Journal of Physiology - Heart and Circulatory Physiology, 1992Calcium homeostasis in cardiomyocytes isolated from heat-shocked ratsR. N. Cornelussen, American Journal of Physiology - Heart and Circulatory Physiology, 1996Cardiomyocytes from postinfarction failing rat hearts have improved ischemia toleranceMohammad Nouri Sharikabad, American Journal of Physiology - Heart and Circulatory Physiology, 2009Powered by Privacy policyGoogle Analytics settings Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation More from this issue > Articles in PressPublished 20 Dec 2024 Crossmark Copyright & PermissionsCopyright © 2025 the American Physiological Societyhttps://doi.org/10.1152/ajpheart.00843.2024PubMed39705588History Received 3 December 2024 Accepted 9 December 2024 Published online 20 December 2024 KeywordsACDaseCeramideFarber Diseasecardiomyocytelysosome Metrics We recommendHigh [Na+]i in cardiomyocytes from rainbow troutRikke Birkedal, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology, 2007Silencing of MYH7 ameliorates disease phenotypes in human iPSC-cardiomyocytesAlexandra Dainis, Physiological Genomics, 2020Recovery of anoxic-reoxygenated cardiomyocytes from severe Ca2+ overloadB. Siegmund, American Journal of Physiology - Heart and Circulatory Physiology, 1992Calcium homeostasis in cardiomyocytes isolated from heat-shocked ratsR. N. Cornelussen, American Journal of Physiology - Heart and Circulatory Physiology, 1996Cardiomyocytes from postinfarction failing rat hearts have improved ischemia toleranceMohammad Nouri Sharikabad, American Journal of Physiology - Heart and Circulatory Physiology, 2009Powered by Privacy policyGoogle Analytics settings publications0supporting0mentioning0contrasting0Smart Citations0000Citing PublicationsSupportingMentioningContrastingView CitationsSee how this article has been cited at scite.aiscite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.

Lindsey A. Fitzsimons

Harilaos Filippakis

Ceramide toxicity in cardiomyocytes: From Farber Disease to CVD

ceramide在心肌细胞中的毒性：从法伯病到心血管疾病

Editorial FocusThe Six-Minute Walk Test: Improving the Prognostic PowerKaren L BallPhDKaren L Ballball@alma.eduDepartment of Integrative Physiology and Health Science, Alma College 614 W. Superior Street, Alma, Michigan 48801PhDPublished Online:20 Dec 2024https://doi.org/10.1152/ajpheart.00846.2024MoreFiguresReferencesRelatedInformationPDF (197 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookXLinkedInWeChat Abstract We recommendBrachial artery FMD with 5-minute distal cuff occlusion—a useful pathophysiological test after all!David S. Celermajer, Journal of Applied Physiology, 2005The relation of minute glucose output to minute volume of perfusion in the isolated liver of the terrapinHerbert S. Wells, American Journal of Physiology -- Legacy Content, 1923Fibroblasts and the Ground They Walk OnDaniel J. Tschumperlin, Physiology, 2013Effect of nephrectomy on the minute renal circulationMary Ellen Hartman, American Journal of Physiology -- Legacy Content, 1959The use of nitrogen for determining the circulatory minute volumeAmerican Journal of Physiology -- Legacy Content, 1928Powered by Privacy policyGoogle Analytics settings Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationSee PDF More from this issue > Articles in PressPublished 20 Dec 2024 Crossmark Copyright & PermissionsCopyright © 2025 the American Physiological Society.https://doi.org/10.1152/ajpheart.00846.2024PubMed39706581History Received 4 December 2024 Accepted 13 December 2024 Published online 20 December 2024 Metrics Downloaded 0 times We recommendBrachial artery FMD with 5-minute distal cuff occlusion—a useful pathophysiological test after all!David S. Celermajer, Journal of Applied Physiology, 2005The relation of minute glucose output to minute volume of perfusion in the isolated liver of the terrapinHerbert S. Wells, American Journal of Physiology -- Legacy Content, 1923Fibroblasts and the Ground They Walk OnDaniel J. Tschumperlin, Physiology, 2013Effect of nephrectomy on the minute renal circulationMary Ellen Hartman, American Journal of Physiology -- Legacy Content, 1959The use of nitrogen for determining the circulatory minute volumeAmerican Journal of Physiology -- Legacy Content, 1928Powered by Privacy policyGoogle Analytics settings publications0supporting0mentioning0contrasting0Smart Citations0000Citing PublicationsSupportingMentioningContrastingView CitationsSee how this article has been cited at scite.aiscite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.

Karen L Ball

The Six-Minute Walk Test: Improving the Prognostic Power

六分钟步行测试：提高预测能力

Abbreviation	Am. J. Physiol. Circ. Physiol.
Journal Impact	4.03
Quartiles(Global)	PHYSIOLOGY(Q1)

ISSN	0363-6135, 1522-1539
h-index	224

Publication Information	Publisher: American Physiological Society，Publishing cycle: Monthly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 1977，Proportion of original research papers: 83.67%，Self Citation Rate:7.30%， Gold OA Rate: 7.14%
Average review cycle	网友分享经验：较快,2-4周
Average recruitment ratio	网友分享经验：较难

American Journal of Physiology - Heart and Circulatory Physiology

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