This study aimed to clarify the effect of Type I diabetes (DIA) on transcapillary PO2 gradients, which are oxygen-driving factors between the blood and the interstitium, in the contracting muscle of rats.
Methods
Wistar male rats were divided into the diabetic (streptozocin i.p.) and sham groups. Microvascular and interstitial PO2 were measured in the extensor digitorum longus muscle during electrical stimulation-induced muscle contraction, using the phosphorescence quenching method. Transcapillary PO2 gradient, ΔPO2, was calculated as microvascular minus interstitial PO2.
Results
Resting microvascular PO2 was higher in the diabetic group than in the sham group (6.3 ± 1.7 vs. 4.7 ± 0.9 mmHg, p < 0.05) and remained for 180 s. Interstitial PO2 from rest to muscle contraction did not differ between the groups. The ΔPO2 was higher in the diabetic group than in the sham group at rest and during muscle contraction (4.03 ± 1.42 vs. 2.46 ± 0.90 mmHg at rest; 3.67 ± 1.51 vs. 2.22 ± 0.65 mmHg during muscle contraction, p < 0.05). Marked muscle atrophy was observed in the diabetic group.
Conclusion
DIA increased microvascular and transcapillary PO2 gradients in the skeletal muscle. The enhanced PO2 gradients were maintained from rest to muscle contraction in diabetic muscle.
{"title":"Transcapillary PO2 Gradients in Contracting Muscles of Type I Diabetic Rats","authors":"Ren Takamizawa, Kazuki Hotta, Yutaka Fujii, Ryo Ikegami, Naoki Hitosugi, Tatsuro Inoue, Hajime Tamiya, Atsuhiro Tsubaki","doi":"10.1111/micc.12870","DOIUrl":"10.1111/micc.12870","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study aimed to clarify the effect of Type I diabetes (DIA) on transcapillary <i>P</i>O<sub>2</sub> gradients, which are oxygen-driving factors between the blood and the interstitium, in the contracting muscle of rats.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Wistar male rats were divided into the diabetic (streptozocin i.p.) and sham groups. Microvascular and interstitial <i>P</i>O<sub>2</sub> were measured in the extensor digitorum longus muscle during electrical stimulation-induced muscle contraction, using the phosphorescence quenching method. Transcapillary <i>P</i>O<sub>2</sub> gradient, Δ<i>P</i>O<sub>2</sub>, was calculated as microvascular minus interstitial <i>P</i>O<sub>2</sub>.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Resting microvascular <i>P</i>O<sub>2</sub> was higher in the diabetic group than in the sham group (6.3 ± 1.7 vs. 4.7 ± 0.9 mmHg, <i>p</i> < 0.05) and remained for 180 s. Interstitial <i>P</i>O<sub>2</sub> from rest to muscle contraction did not differ between the groups. The Δ<i>P</i>O<sub>2</sub> was higher in the diabetic group than in the sham group at rest and during muscle contraction (4.03 ± 1.42 vs. 2.46 ± 0.90 mmHg at rest; 3.67 ± 1.51 vs. 2.22 ± 0.65 mmHg during muscle contraction, <i>p</i> < 0.05). Marked muscle atrophy was observed in the diabetic group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>DIA increased microvascular and transcapillary <i>P</i>O<sub>2</sub> gradients in the skeletal muscle. The enhanced <i>P</i>O<sub>2</sub> gradients were maintained from rest to muscle contraction in diabetic muscle.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"31 6","pages":""},"PeriodicalIF":1.9,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141162284","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}
Navid Singhrao, Victor A. Flores-Tamez, Yumna A. Moustafa, Gopireddy R. Reddy, Abby E. Burns, Kent E. Pinkerton, Chao-Yin Chen, Manuel F. Navedo, Madeline Nieves-Cintrón
Objective
This study aimed to determine nicotine's impact on receptor-mediated cyclic adenosine monophosphate (cAMP) synthesis in vascular smooth muscle (VSM). We hypothesize that nicotine impairs β adrenergic–mediated cAMP signaling in VSM, leading to altered vascular reactivity.
Methods
The effects of nicotine on cAMP signaling and vascular function were systematically tested in aortic VSM cells and acutely isolated aortas from mice expressing the cAMP sensor TEpacVV (Camper), specifically in VSM (e.g., CamperSM).
Results
Isoproterenol (ISO)-induced β-adrenergic production of cAMP in VSM was significantly reduced in cells from second-hand smoke (SHS)–exposed mice and cultured wild-type VSM treated with nicotine. The decrease in cAMP synthesis caused by nicotine was verified in freshly isolated arteries from a mouse that had cAMP sensor expression in VSM (e.g., CamperSM mouse). Functionally, the changes in cAMP signaling in response to nicotine hindered ISO-induced vasodilation, but this was reversed by immediate PDE3 inhibition.
Conclusions
These results imply that nicotine alters VSM β adrenergic–mediated cAMP signaling and vasodilation, which may contribute to the dysregulation of vascular reactivity and the development of vascular complications for nicotine-containing product users.
{"title":"Nicotine Impairs Smooth Muscle cAMP Signaling and Vascular Reactivity","authors":"Navid Singhrao, Victor A. Flores-Tamez, Yumna A. Moustafa, Gopireddy R. Reddy, Abby E. Burns, Kent E. Pinkerton, Chao-Yin Chen, Manuel F. Navedo, Madeline Nieves-Cintrón","doi":"10.1111/micc.12871","DOIUrl":"10.1111/micc.12871","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study aimed to determine nicotine's impact on receptor-mediated cyclic adenosine monophosphate (cAMP) synthesis in vascular smooth muscle (VSM). We hypothesize that nicotine impairs β adrenergic–mediated cAMP signaling in VSM, leading to altered vascular reactivity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The effects of nicotine on cAMP signaling and vascular function were systematically tested in aortic VSM cells and acutely isolated aortas from mice expressing the cAMP sensor <sup>T</sup>Epac<sup>VV</sup> (Camper), specifically in VSM (e.g., Camper<sub>SM</sub>).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Isoproterenol (ISO)-induced β-adrenergic production of cAMP in VSM was significantly reduced in cells from second-hand smoke (SHS)–exposed mice and cultured wild-type VSM treated with nicotine. The decrease in cAMP synthesis caused by nicotine was verified in freshly isolated arteries from a mouse that had cAMP sensor expression in VSM (e.g., Camper<sub>SM</sub> mouse). Functionally, the changes in cAMP signaling in response to nicotine hindered ISO-induced vasodilation, but this was reversed by immediate PDE3 inhibition.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These results imply that nicotine alters VSM β adrenergic–mediated cAMP signaling and vasodilation, which may contribute to the dysregulation of vascular reactivity and the development of vascular complications for nicotine-containing product users.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"31 6","pages":""},"PeriodicalIF":1.9,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141162281","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}
We attempted to record the regional cerebral blood flow (CBF) simultaneously at various regions of the cerebral cortex and the striatum during middle cerebral artery (MCA) occlusion and to evaluate neurological deficits and infarct formation.
Methods
In male C57BL/6J mice, CBF was recorded in three regions including the ipsilateral cerebral cortex and the striatum with laser Doppler flowmeters, and the origin of MCA was occluded with a monofilament suture for 15–90 min. After 48 h, neurological deficits were evaluated, and infarct was examined by triphenyltetrazolium chloride (TTC) staining.
Results
CBF decrease in the striatum was approximately two-thirds of the MCA-dominant region of the cortex during MCA occlusion. The characteristic CBF fluctuation because of spontaneously occurred spreading depolarization observed throughout the cortex was not found in the striatum. Ischemic foci with slight lower staining to TTC were found in the ipsilateral striatum in MCA-occluded mice for longer than 30 min (n = 54). Twenty-nine among 64 MCA-occluded mice exhibited neurological deficits even in the absence of apparent infarct with minimum staining to TTC in the cortex, and the severity of neurological deficits was not correlated with the size of the cortical infarct.
Conclusion
Neurological deficits might be associated with the ischemic striatum rather than with cortical infarction.
{"title":"Striatal Blood Flow Changes by Middle Cerebral Artery Occlusion and Its Effect on Neurological Deficits in Mice","authors":"Miyuki Unekawa, Naoki Tsukada, Tsubasa Takizawa, Yutaka Tomita, Jin Nakahara, Yoshikane Izawa","doi":"10.1111/micc.12861","DOIUrl":"10.1111/micc.12861","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>We attempted to record the regional cerebral blood flow (CBF) simultaneously at various regions of the cerebral cortex and the striatum during middle cerebral artery (MCA) occlusion and to evaluate neurological deficits and infarct formation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In male C57BL/6J mice, CBF was recorded in three regions including the ipsilateral cerebral cortex and the striatum with laser Doppler flowmeters, and the origin of MCA was occluded with a monofilament suture for 15–90 min. After 48 h, neurological deficits were evaluated, and infarct was examined by triphenyltetrazolium chloride (TTC) staining.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>CBF decrease in the striatum was approximately two-thirds of the MCA-dominant region of the cortex during MCA occlusion. The characteristic CBF fluctuation because of spontaneously occurred spreading depolarization observed throughout the cortex was not found in the striatum. Ischemic foci with slight lower staining to TTC were found in the ipsilateral striatum in MCA-occluded mice for longer than 30 min (<i>n</i> = 54). Twenty-nine among 64 MCA-occluded mice exhibited neurological deficits even in the absence of apparent infarct with minimum staining to TTC in the cortex, and the severity of neurological deficits was not correlated with the size of the cortical infarct.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Neurological deficits might be associated with the ischemic striatum rather than with cortical infarction.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"31 6","pages":""},"PeriodicalIF":1.9,"publicationDate":"2024-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.12861","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141065951","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}
Qing Pan, Huanghui Shen, Peilun Li, Biyun Lai, Akang Jiang, Wenjie Huang, Fei Lu, Hong Peng, Luping Fang, Wolfgang M. Kuebler, Axel R. Pries, Gangmin Ning
Objective
Designing physiologically adequate microvascular trees is of crucial relevance for bioengineering functional tissues and organs. Yet, currently available methods are poorly suited to replicate the morphological and topological heterogeneity of real microvascular trees because the parameters used to control tree generation are too simplistic to mimic results of the complex angiogenetic and structural adaptation processes in vivo.
Methods
We propose a method to overcome this limitation by integrating a conditional deep convolutional generative adversarial network (cDCGAN) with a local fractal dimension-oriented constrained constructive optimization (LFDO-CCO) strategy. The cDCGAN learns the patterns of real microvascular bifurcations allowing for their artificial replication. The LFDO-CCO strategy connects the generated bifurcations hierarchically to form microvascular trees with a vessel density corresponding to that observed in healthy tissues.
Results
The generated artificial microvascular trees are consistent with real microvascular trees regarding characteristics such as fractal dimension, vascular density, and coefficient of variation of diameter, length, and tortuosity.
Conclusions
These results support the adoption of the proposed strategy for the generation of artificial microvascular trees in tissue engineering as well as for computational modeling and simulations of microcirculatory physiology.
{"title":"In Silico Design of Heterogeneous Microvascular Trees Using Generative Adversarial Networks and Constrained Constructive Optimization","authors":"Qing Pan, Huanghui Shen, Peilun Li, Biyun Lai, Akang Jiang, Wenjie Huang, Fei Lu, Hong Peng, Luping Fang, Wolfgang M. Kuebler, Axel R. Pries, Gangmin Ning","doi":"10.1111/micc.12854","DOIUrl":"10.1111/micc.12854","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Designing physiologically adequate microvascular trees is of crucial relevance for bioengineering functional tissues and organs. Yet, currently available methods are poorly suited to replicate the morphological and topological heterogeneity of real microvascular trees because the parameters used to control tree generation are too simplistic to mimic results of the complex angiogenetic and structural adaptation processes in vivo.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We propose a method to overcome this limitation by integrating a conditional deep convolutional generative adversarial network (cDCGAN) with a local fractal dimension-oriented constrained constructive optimization (LFDO-CCO) strategy. The cDCGAN learns the patterns of real microvascular bifurcations allowing for their artificial replication. The LFDO-CCO strategy connects the generated bifurcations hierarchically to form microvascular trees with a vessel density corresponding to that observed in healthy tissues.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The generated artificial microvascular trees are consistent with real microvascular trees regarding characteristics such as fractal dimension, vascular density, and coefficient of variation of diameter, length, and tortuosity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These results support the adoption of the proposed strategy for the generation of artificial microvascular trees in tissue engineering as well as for computational modeling and simulations of microcirculatory physiology.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"31 5","pages":""},"PeriodicalIF":1.9,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140827969","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}
Both low serum albumin (SA) concentration and coronary microvascular dysfunction (CMD) are risk factors for the development of heart failure (HF). We hypothesized that SA concentration is associated with myocardial flow reserve (MFR) and implicated in pathophysiological mechanism of HF.
Methods
We retrospectively studied 454 patients undergoing dynamic cardiac cadmium-zinc-telluride myocardial perfusion imaging from April 2018 to February 2020. The population was categorized into three groups according to SA level (g/dL): Group 1: >4, Group 2: 3.5–4, and Group 3: <3.5. Myocardial blood flow (MBF) and myocardial flow reserve (MFR, defined as stress/rest MBF ratio) were compared.
Results
The mean age of the whole cohort was 66.2 years, and 65.2% were men. As SA decreased, stress MBF (mL min−1 g−1) and MFR decreased (MBF: 3.29 ± 1.03, MFR: 3.46 ± 1.33 in Group 1, MBF: 2.95 ± 1.13, MFR: 2.51 ± 0.93 in Group 2, and MBF: 2.64 ± 1.16, MFR: 1.90 ± 0.50 in Group 3), whereas rest MBF (mL min−1 g−1) increased (MBF: 1.05 ± 0.42 in Group 1, 1.27 ± 0.56 in Group 2, and 1.41 ± 0.61 in Group 3). After adjusting for covariates, compared with Group 1, the odds ratios for impaired MFR (defined as MFR < 2.5) were 3.57 (95% CI: 2.32–5.48) for Group 2 and 34.9 (95% CI: 13.23–92.14) for Group 3. The results would be similar if only regional MFR were assessed. The risk prediction for CMD using SA was acceptable, with an AUC of 0.76.
Conclusion
Low SA concentration was associated with the severity of CMD in both global and regional MFR as well as MBF.
{"title":"Significant Association of Serum Albumin With the Severity of Coronary Microvascular Dysfunction Using Dynamic CZT-SPECT","authors":"Shih-Chieh Chien, Shan-Ying Wang, Cheng-Ting Tsai, Yu-Chien Shiau, Yen-Wen Wu","doi":"10.1111/micc.12853","DOIUrl":"10.1111/micc.12853","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Both low serum albumin (SA) concentration and coronary microvascular dysfunction (CMD) are risk factors for the development of heart failure (HF). We hypothesized that SA concentration is associated with myocardial flow reserve (MFR) and implicated in pathophysiological mechanism of HF.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We retrospectively studied 454 patients undergoing dynamic cardiac cadmium-zinc-telluride myocardial perfusion imaging from April 2018 to February 2020. The population was categorized into three groups according to SA level (g/dL): Group 1: >4, Group 2: 3.5–4, and Group 3: <3.5. Myocardial blood flow (MBF) and myocardial flow reserve (MFR, defined as stress/rest MBF ratio) were compared.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The mean age of the whole cohort was 66.2 years, and 65.2% were men. As SA decreased, stress MBF (mL min<sup>−1</sup> g<sup>−1</sup>) and MFR decreased (MBF: 3.29 ± 1.03, MFR: 3.46 ± 1.33 in Group 1, MBF: 2.95 ± 1.13, MFR: 2.51 ± 0.93 in Group 2, and MBF: 2.64 ± 1.16, MFR: 1.90 ± 0.50 in Group 3), whereas rest MBF (mL min<sup>−1</sup> g<sup>−1</sup>) increased (MBF: 1.05 ± 0.42 in Group 1, 1.27 ± 0.56 in Group 2, and 1.41 ± 0.61 in Group 3). After adjusting for covariates, compared with Group 1, the odds ratios for impaired MFR (defined as MFR < 2.5) were 3.57 (95% CI: 2.32–5.48) for Group 2 and 34.9 (95% CI: 13.23–92.14) for Group 3. The results would be similar if only regional MFR were assessed. The risk prediction for CMD using SA was acceptable, with an AUC of 0.76.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Low SA concentration was associated with the severity of CMD in both global and regional MFR as well as MBF.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"31 5","pages":""},"PeriodicalIF":1.9,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140827847","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}
Vacuolar H+-ATPase (V-ATPase) is a multisubunit protein complex which, along with its accessory proteins, resides in almost every eukaryotic cell. It acts as a proton pump and as such is responsible for regulating pH in lysosomes, endosomes, and the extracellular space. Moreover, V-ATPase has been implicated in receptor-mediated signaling. Although numerous studies have explored the role of V-ATPase in cancer, osteoporosis, and neurodegenerative diseases, research on its involvement in vascular disease remains limited. Vascular diseases pose significant challenges to human health. This review aimed to shed light on the role of V-ATPase in hypertension and atherosclerosis. Furthermore, given that vascular complications are major complications of diabetes, this review also discusses the pathways through which V-ATPase may contribute to such complications. Beginning with an overview of the structure and function of V-ATPase in hypertension, atherosclerosis, and diabetes, this review ends by exploring the pharmacological potential of targeting V-ATPase.
{"title":"Vacuolar H+-ATPase in Diabetes, Hypertension, and Atherosclerosis","authors":"Na Wang, Liwei Ren, A. H. Jan Danser","doi":"10.1111/micc.12855","DOIUrl":"10.1111/micc.12855","url":null,"abstract":"<p>Vacuolar H<sup>+</sup>-ATPase (V-ATPase) is a multisubunit protein complex which, along with its accessory proteins, resides in almost every eukaryotic cell. It acts as a proton pump and as such is responsible for regulating pH in lysosomes, endosomes, and the extracellular space. Moreover, V-ATPase has been implicated in receptor-mediated signaling. Although numerous studies have explored the role of V-ATPase in cancer, osteoporosis, and neurodegenerative diseases, research on its involvement in vascular disease remains limited. Vascular diseases pose significant challenges to human health. This review aimed to shed light on the role of V-ATPase in hypertension and atherosclerosis. Furthermore, given that vascular complications are major complications of diabetes, this review also discusses the pathways through which V-ATPase may contribute to such complications. Beginning with an overview of the structure and function of V-ATPase in hypertension, atherosclerosis, and diabetes, this review ends by exploring the pharmacological potential of targeting V-ATPase.</p>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"31 5","pages":""},"PeriodicalIF":1.9,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.12855","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140827965","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}
The microvasculature is integral to nearly every tissue in the body, providing not only perfusion to and from the tissue, but also homing sites for immune cells, cellular niches for tissue dynamics, and cooperative interactions with other tissue elements. As a microtissue itself, the microvasculature is a composite of multiple cell types exquisitely organized into structures (individual vessel segments and extensive vessel networks) capable of considerable dynamics and plasticity. Consequently, it has been challenging to include a functional microvasculature in assembled or fabricated tissues. Isolated fragments of intact microvessels, which retain the cellular composition and structures of native microvessels, are proving effective in a variety of vascularization applications including tissue in vitro disease modeling, vascular biology, mechanistic discovery, and tissue prevascularization in regenerative therapeutics and grafting. In this review, we will discuss the importance of recapitulating native tissue biology and the successful vascularization applications of isolated microvessels.
{"title":"Isolated Fragments of Intact Microvessels: Tissue Vascularization, Modeling, and Therapeutics","authors":"Hannah A. Strobel, Sarah M. Moss, James B. Hoying","doi":"10.1111/micc.12852","DOIUrl":"10.1111/micc.12852","url":null,"abstract":"<div>\u0000 \u0000 <p>The microvasculature is integral to nearly every tissue in the body, providing not only perfusion to and from the tissue, but also homing sites for immune cells, cellular niches for tissue dynamics, and cooperative interactions with other tissue elements. As a microtissue itself, the microvasculature is a composite of multiple cell types exquisitely organized into structures (individual vessel segments and extensive vessel networks) capable of considerable dynamics and plasticity. Consequently, it has been challenging to include a functional microvasculature in assembled or fabricated tissues. Isolated fragments of intact microvessels, which retain the cellular composition and structures of native microvessels, are proving effective in a variety of vascularization applications including tissue in vitro disease modeling, vascular biology, mechanistic discovery, and tissue prevascularization in regenerative therapeutics and grafting. In this review, we will discuss the importance of recapitulating native tissue biology and the successful vascularization applications of isolated microvessels.</p>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"31 4","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140595034","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}
Chest pain is a relatively long-term symptom that commonly occurs in patients who have contracted COVID-19. The reasons for these symptoms remain unclear, with coronary microvascular dysfunction (CMD) emerging as a potential factor. This study aimed to assess the presence of CMD in these patients by measuring the angio-derived index of microcirculatory resistance (AMR).
Methods
In this cross-sectional case–control study, patients who had chest pain and a history of COVID-19 infection within the preceding 30 to 60 days were included. The control subjects were patients without COVID-19. Demographic, clinical, and echocardiographic data were recorded. Angiographic images were collected for AMR analysis through an angioplus quantitative flow ratio measurement system. Propensity score matching (PSM) was performed to match the two groups. Multivariate logistic regression was used to examine the association between COVID-19 incidence and the increase in AMR (AMR > 285 mmHg*s/m) after correction for other confounders.
Results
After PSM, there were 58 patients in each group (the mean age was 66.3 ± 9.04 years, and 55.2% were men). The average time between the onset of COVID-19 infection and patient presentation at the hospital for coronary angiography was 41 ± 9.5 days. Moreover, there was no significant difference in the quantitative flow ratio between the two groups. Patients with COVID-19 had a greater mean AMR (295 vs. 266, p = 0.002). Multivariate logistic regression analysis revealed that COVID-19 (OR = 3.32, 95% CI = 1.50–7.60, p = 0.004) was significantly associated with an increase in AMR.
Conclusions
Long-term COVID-19 patients who experience chest pain without evidence of myocardial ischemia exhibit an increase in AMR, and CMD may be one of the reasons for this increase. COVID-19 is an independent risk factor for an increase in AMR.
背景和目的：胸痛是一种相对长期的症状，常见于感染 COVID-19 的患者。出现这些症状的原因尚不清楚，冠状动脉微血管功能障碍（CMD）是一个潜在因素。本研究旨在通过测量血管衍生的微循环阻力指数（AMR）来评估这些患者是否存在CMD：在这项横断面病例对照研究中，纳入了在之前 30 到 60 天内有胸痛和 COVID-19 感染史的患者。对照组为未感染 COVID-19 的患者。研究人员记录了人口统计学、临床和超声心动图数据。收集血管造影图像，通过血管造影定量流量比测量系统进行 AMR 分析。进行倾向得分匹配（PSM）以匹配两组患者。在校正其他混杂因素后，采用多变量逻辑回归法检测 COVID-19 发病率与 AMR（AMR > 285 mmHg*s/m）增加之间的关联：PSM 后，每组有 58 名患者（平均年龄为 66.3 ± 9.04 岁，55.2% 为男性）。从感染 COVID-19 到患者到医院接受冠状动脉造影术的平均时间为 41 ± 9.5 天。此外，两组患者的定量血流比率没有明显差异。COVID-19 患者的平均 AMR 更大（295 对 266，P = 0.002）。多变量逻辑回归分析显示，COVID-19（OR = 3.32，95% CI = 1.50-7.60，p = 0.004）与 AMR 的增加显著相关：结论：长期患有 COVID-19 的胸痛但无心肌缺血证据的患者会出现 AMR 增高，而 CMD 可能是导致 AMR 增高的原因之一。COVID-19是导致AMR增加的一个独立风险因素。
{"title":"Increased Angio-Derived Index of Microcirculatory Resistance Within a Timeframe of 30–60 days After COVID-19 Infection","authors":"Lei Dong, Ritai Na, Lang Peng, Xinye Xu","doi":"10.1111/micc.12851","DOIUrl":"10.1111/micc.12851","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Objectives</h3>\u0000 \u0000 <p>Chest pain is a relatively long-term symptom that commonly occurs in patients who have contracted COVID-19. The reasons for these symptoms remain unclear, with coronary microvascular dysfunction (CMD) emerging as a potential factor. This study aimed to assess the presence of CMD in these patients by measuring the angio-derived index of microcirculatory resistance (AMR).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this cross-sectional case–control study, patients who had chest pain and a history of COVID-19 infection within the preceding 30 to 60 days were included. The control subjects were patients without COVID-19. Demographic, clinical, and echocardiographic data were recorded. Angiographic images were collected for AMR analysis through an angioplus quantitative flow ratio measurement system. Propensity score matching (PSM) was performed to match the two groups. Multivariate logistic regression was used to examine the association between COVID-19 incidence and the increase in AMR (AMR > 285 mmHg*s/m) after correction for other confounders.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>After PSM, there were 58 patients in each group (the mean age was 66.3 ± 9.04 years, and 55.2% were men). The average time between the onset of COVID-19 infection and patient presentation at the hospital for coronary angiography was 41 ± 9.5 days. Moreover, there was no significant difference in the quantitative flow ratio between the two groups. Patients with COVID-19 had a greater mean AMR (295 vs. 266, <i>p</i> = 0.002). Multivariate logistic regression analysis revealed that COVID-19 (OR = 3.32, 95% CI = 1.50–7.60, <i>p</i> = 0.004) was significantly associated with an increase in AMR.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Long-term COVID-19 patients who experience chest pain without evidence of myocardial ischemia exhibit an increase in AMR, and CMD may be one of the reasons for this increase. COVID-19 is an independent risk factor for an increase in AMR.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"31 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140143763","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}
Erin Zhao, Jared Barber, Shomita S. Mathew-Steiner, Savita Khanna, Chandan K. Sen, Julia Arciero
Objective
An improved understanding of the role of the leptomeningeal collateral circulation in blood flow compensation following middle cerebral artery (MCA) occlusion can contribute to more effective treatment development for ischemic stroke. The present study introduces a model of the cerebral circulation to predict cerebral blood flow and tissue oxygenation following MCA occlusion.
Methods
The model incorporates flow regulation mechanisms based on changes in pressure, shear stress, and metabolic demand. Oxygen saturation in cerebral vessels and tissue is calculated using a Krogh cylinder model. The model is used to assess the effects of changes in oxygen demand and arterial pressure on cerebral blood flow and oxygenation after MCA occlusion.
Results
An increase from five to 11 leptomeningeal collateral vessels was shown to increase the oxygen saturation in the region distal to the occlusion by nearly 100%. Post-occlusion, the model also predicted a loss of autoregulation and a decrease in flow to the ischemic territory as oxygen demand was increased; these results were consistent with data from experiments that induced cerebral ischemia.
Conclusions
This study highlights the importance of leptomeningeal collaterals following MCA occlusion and reinforces the idea that lower oxygen demand and higher arterial pressure improve conditions of flow and oxygenation.
{"title":"Modeling cerebrovascular responses to assess the impact of the collateral circulation following middle cerebral artery occlusion","authors":"Erin Zhao, Jared Barber, Shomita S. Mathew-Steiner, Savita Khanna, Chandan K. Sen, Julia Arciero","doi":"10.1111/micc.12849","DOIUrl":"10.1111/micc.12849","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>An improved understanding of the role of the leptomeningeal collateral circulation in blood flow compensation following middle cerebral artery (MCA) occlusion can contribute to more effective treatment development for ischemic stroke. The present study introduces a model of the cerebral circulation to predict cerebral blood flow and tissue oxygenation following MCA occlusion.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The model incorporates flow regulation mechanisms based on changes in pressure, shear stress, and metabolic demand. Oxygen saturation in cerebral vessels and tissue is calculated using a Krogh cylinder model. The model is used to assess the effects of changes in oxygen demand and arterial pressure on cerebral blood flow and oxygenation after MCA occlusion.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>An increase from five to 11 leptomeningeal collateral vessels was shown to increase the oxygen saturation in the region distal to the occlusion by nearly 100%. Post-occlusion, the model also predicted a loss of autoregulation and a decrease in flow to the ischemic territory as oxygen demand was increased; these results were consistent with data from experiments that induced cerebral ischemia.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study highlights the importance of leptomeningeal collaterals following MCA occlusion and reinforces the idea that lower oxygen demand and higher arterial pressure improve conditions of flow and oxygenation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"31 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.12849","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139729967","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}
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