Background The potential for microbial modulation to serve as both a therapeutic and prophylactic strategy against type 2 diabetes mellitus (T2DM)-induced microvasculopathy remains underexplored. We therefore compared the efficacy of the gut-centric herbal formulation Intestinal Flora Balance (IFB, BNFF™), when used for therapeutic reversal, synergistic rescue, or prophylactic protection. Methods A murine T2DM model was used to compare three arms, IFB monotherapy, IFB-metformin combination therapy, and IFB pretreatment administered prior to disease induction. Pancreatic and intestinal microcirculation was quantified using in vivo laser Doppler and fiber optic probes. Fecal microbiota composition was analyzed via 16S rRNA gene sequencing. Results As a therapeutic agent, IFB monotherapy effectively lowered blood glucose and restored microvascular function by reversing diabetic gut dysbiosis. Combination with metformin, while not further improving glycemia, acted synergistically to provide superior rescue of pancreatic microcirculation, indicating complementary modes of action. Prophylactic administration of IFB conferred protection, preserving microbial homeostasis and significantly attenuating the onset of both hyperglycemia and microvascular damage. IFB enhanced the richness and diversity of the intestinal microbiome in T2DM mice and restored the Bacteroidetes/Firmicutes ratio. Conclusions By demonstrating that IFB ecologically restores the microbiome, in contrast to metformin's pharmacological modulation, our study provides a new framework for its use as a prophylactic, a restorative monotherapy, or a synergistic partner to build microcirculatory resilience.

AIMS:Renal microvascular dysfunction is a central driver of diabetic kidney disease, yet the potential for rapid therapeutic reversal remains obscure. We investigated the effect of short-term liraglutide on early changes in the renal microcirculation post-induction of diabetes. MATERIALS AND METHODS:Type 2 diabetes mellitus (T2DM) was induced in BALB/c mice via high-fat diet and streptozotocin. Following induction, mice received insulin or liraglutide treatments for 1 or 2 weeks. Renal microhemodynamics was analysed using laser Doppler flowmetry and wavelet analysis. Histopathological evaluations via Masson trichrome and haematoxylin-eosin staining assessed fibrosis and microvascular integrity. Primary renal microvascular endothelial cells (RMECs) were isolated to evaluate angiogenic and migratory behaviours. Metabolomics analyses were performed to link metabolic changes with microcirculatory alterations. RESULTS:T2DM induced significant impairments in renal microcirculation, characterised by dysregulated microhemodynamics, disturbed oxygen saturation, altered haemoglobin distribution and compromised blood perfusion. These functional defects were accompanied by elevated creatinine, reduced cystatin C and impaired angiogenic and migratory capacity of RMECs under glucotoxicity. Both insulin and liraglutide treatments ameliorated renal microcirculatory oxygen profiles and improved renal function biomarkers. Histological data revealed decreased fibrosis and enhanced microvascular architecture post-treatment. Metabolomic profiling revealed that liraglutide preferentially restored depleted amino acid levels associated with microvascular function, a change associated with the normalisation of metabolic profiles potentially involving peptide transport pathways. CONCLUSIONS:Our findings demonstrate that short-term liraglutide restores renal microcirculatory homeostasis in the post-induction phase, mitigating microvascular dysfunction and preserving kidney structure, highlighting the potential therapeutic value in preventing the progression of diabetic renal injury.

The microcirculation is a determinant of organ function, translating systemic signals into local physiological responses. However, whether the regulation of microhemodynamics is sexually dimorphic within the pancreas has remained unknown. Here, using a multi-scale approach in healthy mice, we report a sexual dimorphism in pancreatic microhemodynamics that is anatomically restricted to the exocrine compartment, defined by divergent expression of the endothelial marker CD31 and estrogen receptor ERβ, whereas the endocrine islet microvasculature remains conserved between sexes. We demonstrate that microhemodynamic dimorphism is functionally coupled to divergent systemic steroid hormone profiles, a male signature characterized by elevated androgens and steroidogenic precursors, and a female signature dominated by glucocorticoids and estrogen metabolites. The distinction manifests as fundamentally different regulatory principles for vascular control, where pancreatic blood flow in males is directly coupled to systemic blood pressure, whereas in females, the relationship is defined by correlations between blood pressure and the oscillatory components of microhemodynamics. Collectively, our data identify the pancreatic microcirculation as a primary site of physiological sexual dimorphism and establish its role as a fundamental conduit for translating the systemic hormonal milieu into sex-specific organ homeostasis.

BACKGROUND The integrity and functionality of the hepatic microcirculation are essential for maintaining liver health, which is influenced by sex and genetic background. Understanding these variations is crucial for addressing disparities in liver disease outcomes. AIM To investigate the sexual dimorphism and genetic heterogeneity of liver microcirculatory function in mice. METHODS We assessed hepatic microhemodynamics in BALB/c, C57BL/6J, and KM mouse strains using laser Doppler flowmetry and wavelet analysis. We analyzed the serum levels of alanine transaminase, glutamic acid aminotransferase, total bile acid, total protein, alkaline phosphatase, and glucose. Histological and immunohistochemical staining were employed to quantify microvascular density and the expression levels of cluster of differentiation (CD) 31, and estrogen receptor alpha, and beta. Statistical analyses, including the Mantel test and Pearson correlation, were conducted to determine the relationships among hepatic function, microcirculation, and marcocirculation between different sexes and across genetic backgrounds. RESULTS We identified sex-based disparities in hepatic microhemodynamics across all strains, with males exhibiting higher microvascular perfusion and erythrocyte concentration, but lower blood velocity. Strain-specific differences were evident, particularly in the endothelial oscillatory characteristics of the erythrocyte concentration. No sex-dependent differences in estrogen receptor expression were observed, while significant variations in CD31 expression and microvascular density were observed. The correlations highlighted relationships between hepatic microhemodynamics and liver function indicators. CONCLUSION Our findings indicate the influence of genetic and sex differences on hepatic microcirculation and liver function, highlighting the necessity of incorporating both genetic background and sex into hepatic physiology studies and potential liver disease management strategies.

BACKGROUND The prevalence of diabetes and its association with microcirculatory dysfunction presents a significant challenge in contemporary global health. Addressing this nexus is crucial for developing targeted therapeutic interventions. AIM To trace the progression and delineate the current state of interdisciplinary research concerning diabetes and microcirculation. METHODS Employing a bibliometric approach, this study scrutinizes 12886 peer-reviewed publications retrieved from the PubMed and Web of Science databases. The focus is on elucidating the research trajectory and thematic concentrations at the confluence of diabetes and microcirculation. RESULTS Research outputs have surged since 2011, with the United States, China, and the United Kingdom leading in the quantity and quality of publications. This analysis revealed that journals such as Diabetes Care and The New England Journal of Medicine, along with top research institutions, have significantly contributed to advancing the understanding of microvascular processes affected by diabetes. The central themes identified include inflammation, oxidative stress, and endothelial dysfunction, which are critical in mediating the microvascular complications of diabetes. CONCLUSION This bibliometric evaluation reveals an evolving landscape focusing on diabetes and microcirculatory dysfunction. The complexity of diabetic microvascular issues encouraged multidisciplinary research strategies that are imperative for global health outcomes.

BACKGROUND: Diabetes and prediabetes significantly increase the risk of atherosclerotic cardiovascular disease (ASCVD), posing a major global health challenge. Although traditional ASCVD risk factors have been extensively studied, there is limited research on applying machine learning. METHODS: This study used data from the NHANES survey spanning 2007 to 2018, including 4,211 participants diagnosed with diabetes or prediabetes. Key variables were identified through univariate and multivariate logistic regression analyses. The dataset was randomly split into training and validation sets at a 7:3 ratio. Nine machine learning models (including CART, SVM, and GBM) were developed and evaluated using AUC, Brier scores, calibration curves, and decision curve analysis. Additionally, an online risk prediction platform was created to provide real-time ASCVD risk assessments, helping clinicians with early screening and intervention. RESULTS: Eight variables significantly associated with ASCVD risk were identified through univariate and multivariate logistic regression analyses, including age, waist circumference, poverty–income ratio, blood urea nitrogen, total cholesterol, systolic blood pressure, hypertension, and smoking status. Based on these predictors, the SVM model achieved AUC values of 0.831 in the training set and 0.859 in the validation set, demonstrating excellent discriminative ability. Calibration curves indicated good agreement between predicted and observed risks across different risk levels, while Brier scores further supported the overall predictive accuracy of the model. Decision curve analysis showed that the model provided substantial net clinical benefit. Collectively, these evaluation metrics highlight the strong predictive performance and practical utility of the SVM model. CONCLUSION: The SVM model effectively predicts ASCVD risk in individuals with diabetes or prediabetes, emphasizing the importance of managing modifiable risk factors such as dyslipidemia, hypertension, smoking, and abdominal obesity. This model offers an effective tool for individualized risk assessment and early prevention, and the online platform further supports clinical application by enabling early identification and intervention for high-risk populations.

Addressing the existing gaps in our understanding of sex- and strain-dependent disparities in renal microhemodynamics, this study conducted an investigation into the variations in renal function and related biological oscillators. Using the genetically diverse mouse models BALB/c, C57BL/6, and Kunming, which serve as established proxies for the study of renal pathophysiology, we implemented laser Doppler flowmetry conjoined with wavelet transform analyses to interrogate dynamic renal microcirculation. Creatinine, urea, uric acid, glucose, and cystatin C levels were quantified to investigate potential divergences attributable to sex and genetic lineage. Our findings reveal marked sexual dimorphism in metabolite concentrations, as well as strain-specific variances, particularly in creatinine and cystatin C levels. Through the combination of Mantel tests and Pearson correlation coefficients, we delineated the associations between renal functional metrics and microhemodynamics, uncovering interactions in female BALB/c mice for creatinine and uric acid, and in male C57BL/6 mice for cystatin C. Histopathologic examination confirmed an augmented microvascular density in female mice and elucidating variations in the expression of estrogen receptor β among the strains. These data collectively highlight the influence of both sex and genetic constitution on renal microcirculation, providing an understanding that may inform the etiologic exploration of renal ailments.

Background Intestinal microcirculation is a critical interface for nutrient exchange and energy transfer, and is essential for maintaining physiological integrity. Our study aimed to elucidate the relationships among intestinal microhemodynamics, genetic background, sex, and microbial composition.Methods To dissect the microhemodynamic landscape of the BALB/c, C57BL/6J, and KM mouse strains, laser Doppler flowmetry paired with wavelet transform analysis was utilized to determine the amplitude of characteristic oscillatory patterns. Microbial consortia were profiled using 16S rRNA gene sequencing. To augment our investigation, a broad-spectrum antibiotic regimen was administered to these strains to evaluate the impact of gut microbiota depletion on intestinal microhemodynamics. Immunohistochemical analyses were used to quantify platelet endothelial cell adhesion molecule-1 (PECAM-1), estrogen receptor alpha (ESR1), and estrogen receptor beta (ESR2) expression.Results Our findings revealed strain-dependent and sex-related disparities in microhemodynamic profiles and characteristic oscillatory behaviors. Significant differences in the gut microbiota contingent upon sex and genetic lineage were observed, with correlational analyses indicating an influence of the microbiota on microhemodynamic parameters. Following antibiotic treatment, distinct changes in blood perfusion levels and velocities were observed, including a reduction in female C57BL/6J mice and a general decrease in perfusion velocity. Enhanced erythrocyte aggregation and modulated endothelial function post-antibiotic treatment indicated that a systemic response to microbiota depletion impacted cardiac amplitude. Immunohistochemical data revealed strain-specific and sex-specific PECAM-1 and ESR1 expression patterns that aligned with observed intestinal microhemodynamic changes.Conclusions This study highlights the influence of both genetic and sex-specific factors on intestinal microhemodynamics and the gut microbiota in mice. These findings also emphasize a substantial correlation between intestinal microhemodynamics and the compositional dynamics of the gut bacterial community.

Coronary microvascular dysfunction (CMD) refers to structural and functional abnormalities of the microcirculation that impair myocardial perfusion. CMD plays a pivotal role in numerous cardiovascular diseases, including myocardial ischemia with non-obstructive coronary arteries, heart failure, and acute coronary syndromes. This review summarizes recent advances in CMD pathophysiology, assessment, and treatment strategies, as well as ongoing challenges and future research directions. Signaling pathways implicated in CMD pathogenesis include adenosine monophosphate-activated protein kinase/Krüppel-like factor 2/endothelial nitric oxide synthase (AMPK/KLF2/eNOS), nuclear factor erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE), Angiotensin II (Ang II), endothelin-1 (ET-1), RhoA/Rho kinase, and insulin signaling. Dysregulation of these pathways leads to endothelial dysfunction, the hallmark of CMD. Treatment strategies aim to reduce myocardial oxygen demand, improve microcirculatory function, and restore endothelial homeostasis through mechanisms including vasodilation, anti-inflammation, and antioxidant effects. Traditional Chinese medicine (TCM) compounds exhibit therapeutic potential through multi-targeted actions. Small molecules and regenerative approaches offer precision therapies. However, challenges remain in translating findings to clinical practice and developing effective pharmacotherapies. Integration of engineering with medicine through microfabrication, tissue engineering and AI presents opportunities to advance the diagnosis, prediction, and treatment of CMD.

Type 1 diabetes mellitus (T1DM) is predominantly managed using insulin replacement therapy, however, pancreatic microcirculatory disturbances play a critical role in T1DM pathogenesis, necessitating alternative therapies. This study aimed to investigate the protective effects of glycine supplementation on pancreatic microcirculation in T1DM. Streptozotocin-induced T1DM and glycine-supplemented mice (n = 6 per group) were used alongside control mice. Pancreatic microcirculatory profiles were determined using a laser Doppler blood perfusion monitoring system and wavelet transform spectral analysis. The T1DM group exhibited disorganized pancreatic microcirculatory oscillation. Glycine supplementation significantly restored regular biorhythmic contraction and relaxation, improving blood distribution patterns. Further-more, glycine reversed the lower amplitudes of endothelial oscillators in T1DM mice. Ultrastructural deterioration of islet microvascular endothelial cells (IMECs) and islet microvascular pericytes, including membrane and organelle damage, collagenous fiber proliferation, and reduced edema, was substantially reversed by glycine supplementation. Additionally, glycine supplementation inhibited the production of IL-6, TNF-α, IFN-γ, pro-MMP-9, and VEGF-A in T1DM, with no significant changes in energetic metabolism observed in glycine-supplemented IMECs. A statistically significant decrease in MDA levels accompanied by an increase in SOD levels was also observed with glycine supplementation. Notably, negative correlations emerged between inflammatory cytokines and microhemodynamic profiles. These findings suggest that glycine supplementation may offer a promising therapeutic approach for protecting against pancreatic microcirculatory dysfunction in T1DM.

BACKGROUND The intestinal microcirculation functions in food absorption and metabolic substance exchanges. Accumulating evidence indicates that intestinal microcirculatory dysfunction is a significant source of multiple gastrointestinal diseases. To date, there has not been a scientometric analysis of intestinal microcirculatory research. AIM To investigate the current status, development trends, and frontiers of intestinal microcirculatory research based on bibliometric analysis. METHODS VOSviewer and CiteSpace 6.1.R2 were used to identify the overall characteristics and knowledge map of intestinal microcirculatory research based on the core literature published from 2000 to 2021 in the Web of Science database. The characteristics of each article, country of origin, institution, journal, cocitations, and other information were analyzed and visualized. RESULTS There were 1364 publications enrolled in the bibliometric analysis, exhibiting an upward trend from 2000 to 2021 with increased participation worldwide. The United States and Dalhousie University took the lead among countries and institutions, respectively. Shock was the most prolific journal, and Nature Reviews Microbiology Clinical had the most citations. The topical hotspots and frontiers in intestinal microcirculatory research were centered on the pathological processes of functional impairment of intestinal microvessels, diverse intestinal illnesses, and clinical treatment. CONCLUSION Our study highlights insights into trends of the published research on the intestinal microcirculation and offers serviceable guidance to researchers by summarizing the prolific areas in intestinal disease research to date.

Background: Coronary microcirculation has a fundamental role in the regulation of coronary blood flow in response to cardiac requirements, which has aroused wide concerns in basic science and clinical cardiovascular research. We aimed to analyze coronary microcirculation-associated literatures over 30 years and provide insightful information on the evolutionary path, frontier research hotspots, and future developmental trends. Methods: Publications were retrieved from the Web of Science Core Collection (WoSCC). VOSviewer was used to perform co-occurrence analyses for countries, institutions, authors, and keywords and to generate visualized collaboration maps. CiteSpace was used to visualize the knowledge map derived from reference co-citation analysis, burst references, and keywords detection. Results: This analysis was performed based on 11,702 publications including 9981 articles and 1721 reviews. The United States and Harvard University ranked at the top among all the countries and institutions. The majority of articles were published in Circulation, and it also was the most co-cited journal. Thematic hotspots and frontiers were focused on coronary microvascular dysfunction, magnetic resonance imaging, fractional flow reserve, STEMI, and heart failure. Additionally, keywords burst and co-occurrence cluster analysis showed that management, microvascular dysfunction, microvascular obstruction, prognostic value, outcomes, and guidelines were current knowledge gaps and future directions. Conclusions: Coronary microcirculation presented a research hotspot relevant wide spectrum of cardiovascular diseases. Definite diagnostics and prognostics are particularly valued. The protection of cardiovascular events that influence clinical outcomes should be an insightful concern in the future. Multidisciplinary collaborations will provide significant advances for the development of coronary microcirculation.

The contractile behavior of collecting lymphatic vessels occurs in essential hypertension in response to homeostasis, suggesting a possible role for microcirculation. We aimed to clarify the nature of the lymphatic microcirculation profile in spontaneously hypertensive rats (SHRs) and normotensive controls. The vasomotion of collecting lymphatic vessels in eight- and thirteen-week-old SHRs and age-matched Wistar-Kyoto rats (WKYs, n  = 4 per group) was visualized by intravital video and VasTrack. The lymphatic vasomotion profile (frequency and amplitude) and contractile parameters (contraction fraction and total contractility activity index) were compared. Plasma nitrite/nitrate levels were assessed by the Griess reaction, and plasma endothelin-1 was measured by enzyme-linked immunosorbent assay. WKYs and SHRs differed in the vasomotion of collecting lymphatic vessels. Both eight- and thirteen-week-old WKYs revealed a high-amplitude pumping pattern, whereas a low-amplitude pattern was observed in SHRs. Moreover, compared with age-matched WKYs, SHRs exhibited deteriorated output and reflux capability and lost the ability to regulate collecting lymphatic vasomotion. Additionally, the chemistry complements the microcirculatory lymphatic profile as demonstrated by an increase in plasma nitrite, nitrate, and endothelin-1 in SHRs. ET-1 inhibitor meliorated the lymphatic contractile capability in SHRs partially through regulating frequency of lymphatic vasomotion. We used an intravital lymphatic imaging system to observe that SHRs exhibit an impaired collecting lymphatic vasomotion profile and deteriorated contractility and reflux.

Atherosclerosis is the leading cause of coronary heart disease. In recent years, circ_0029589 (circCHFR) has been found to be associated with atherosclerosis development. However, the molecular mechanism of circCHFR action in atherosclerosis development is unknown. This study was aimed to investigate the function and action mechanism of circCHFR in atherosclerosis development. An atherosclerosis cell model was created by exposing human vascular endothelial cells (HUVECs) to oxidized low-density lipoprotein. The expression of circCHFR, microRNA(miR)-15b-5p, growth arrest and DNA damage inducible gamma (GADD45G), and their associated proteins was evaluated using quantitative reverse transcription-polymerase chain reaction and Western blotting. Additionally, cell viability, apoptosis, and cytokine levels were determined using Cell Counting Kit-8 (CCK8) assay, flow cytometry, and enzyme-linked immunosorbent assay, respectively. circCHFR expression was upregulated in patients with atherosclerosis and oxidized low-density lipoprotein (ox-LDL)-exposed HUVECs, whereas miR-15b-5p expression was downregulated. circCHFR silencing significantly improved viability and reduced apoptosis of HUVECs. In addition, the pro-apoptotic protein Bax and atherosclerosis-associated cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-α) were significantly downregulated, whereas the anti-apoptotic protein Bcl-2 was upregulated. Further, we discovered that circCHFR serves as a molecular sponge of miR-15b-5p. GADD45G was found to be an important target of miR-15b-5p; miR-15b-5p mimic inhibited GADD45G expression, reduced apoptosis and proinflammatory cytokine secretion, and improved cell survival. However, these effects of miR-15b-5p on (ox-LDL) induced HUVECs were reversed with GADD45G plasmid co-transfection. In conclusion, circCHFR promotes atherosclerosis progression via the miR-15b-5p/GADD45G axis and may be an important target for atherosclerosis treatment.

BACKGROUND:The pancreatic islet microcirculation adapts its metabolism to cope with limited oxygen availability and nutrient delivery. In diabetes, the balance between oxygen delivery and consumption is impaired. Insulin has been proven to exert complex actions promoting the maintenance of homeostasis of the pancreas under glucotoxicity.AIM:To test the hypothesis that insulin administration can improve the integrated pancreatic microcirculatory oxygen profile and bioenergetics.METHODS:The pancreatic microcirculatory partial oxygen pressure (PO2), relative hemoglobin (rHb) and hemoglobin oxygen saturation (SO2) were evaluated in nondiabetic, type 1 diabetes mellitus (T1DM), and insulin-treated mice. A three-dimensional framework was generated to visualize the microcirculatory oxygen profile. Ultrastructural changes in the microvasculature were examined using transmission electron microscopy. An Extracellular Flux Analyzer was used to detect the real-time changes in bioenergetics by measuring the oxygen consumption rate and extracellular acidification rate in islet microvascular endothelial cells (IMECs).RESULTS:Significantly lower PO2, rHb, and SO2 values were observed in T1DM mice than in nondiabetic controls. Insulin administration ameliorated the streptozotocin-induced decreases in these microcirculatory oxygen parameters and improved the mitochondrial ultrastructural abnormalities in IMECs. Bioenergetic profiling revealed that the IMECs did not have spare respiratory capacity. Insulin-treated IMECs exhibited significantly greater basal respiration than glucotoxicity-exposed IMECs (P < 0.05). An energy map revealed increased energetic metabolism in insulin-treated IMECs, with significantly increased ATP production, non-mitochondrial respiration, and oxidative metabolism (all P < 0.05). Significant negative correlations were revealed between microcirculatory SO2 and bioenergetic parameters.CONCLUSION:Glucotoxicity deteriorates the integrated pancreatic microcirculatory oxygen profile and bioenergetics, but this deterioration can be reversed by insulin administration.

Background: Asthma is a chronic airway disorder associated with aberrant inflammatory, remodeling and angiogenesis, indicating that the altered pulmonary microcirculatory may exist in the local and contribute to the pathogenesis. There are rare studies in vivo, which could directly prove the disorders of microcirculation in asthmatic lungs. This study aimed to establish Micro-in-One platform and set up the first profile of the integrated asthmatic pulmonary microcirculation. Methods: Using murine models of asthma induced by ovalbumin (OVA) and house dust mite (HDM), the raw data set of pulmonary microcirculation was collected and visualized by multimodal device and computer algorithm-based Micro-in-One platform. A three-dimensional framework was constructed, and changes of pulmonary microcirculatory oxygen, microhemodynamics were compared. The contributions of biological oscillators were revealed by wavelet transform analysis. Additionally, levels of microcirculation-associated proteins in serum were measured by antibody-pair-based assay. Results: Microcirculatory profile of the lungs in both OVA-induced and HDM-induced asthma groups exhibited a loss of microhemodynamic coherence compare to the control mice, including the decreased microvascular blood perfusion, decreased PO , and significantly increased index of pulmonary microcirculatory resistance (IMRp). In addition, amplitude regimens separated by (NO-dependent and NO-independent) endothelial components were related to the changes in pulmonary microcirculation in asthmatic models. Meanwhile, matrix-based hierarchical clustering analysis showed that IMRp positively correlated to amplitude in both asthmatic groups. Conclusions: Micro-in-One is a validated and reliable method to measure and visualize the integrated pulmonary microcirculation. Data suggest that there is the dysfunctional status of pulmonary microcirculation in asthma.

Wide variation in magnitudes, units, and ranges of the microcirculatory variables brings hindrance in describing and evaluating the integrated microcirculatory function of tissues. We designed to establish common microcirculatory framework that contains microhemodynamic and microcirculatory oxygen parameters. To integrate microcirculatory information, demo microcirculatory permutations were generated by a computer algorithm based on microcirculatory characteristics. Four dimensionless methods (Z-score, Min-max, L2, and median scaling) were applied to transform microcirculatory data set into the dimensionless form. Three-dimensional (3-D) common microcirculatory framework was constructed and visualized by using Python and Apache ECharts. The performance of the four dimensionless methods in the pre-processing of multiple microcirculatory variables and the establishment of the common microcirculatory framework were compared. Microhemodynamic and microcirculatory oxygen parameters were embedded in the common microcirculatory framework. After processing by Min-max normalization, the transformed multiple microcirculatory values remained positive with fixed range mapping within [0, 1] and maintained the identity property of microcirculation both of microhemodynamic and microcirculatory oxygen variables in the common microcirculatory framework. Conclusively, Min-max normalization displays preferable integration efficiency, compatibility, and adaptability in the establishment of the 3-D visualized multiparametric common microcirculatory framework.