Regulation of the microvascular circulation in the leg muscles, pancreas and small intestine in rats

Maeda, Hisashi; Kurose, Tomoyuki; Kawamata, Seiichi

doi:10.1186/s40064-015-1102-8

Cited by 4 publications

(4 citation statements)

References 33 publications

(62 reference statements)

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“…RBC flux is present in most capillaries at rest and increases with exercise to meet the muscle demand [41]. In agreement with this, Maeda et al [42] reported that the number of capillaries exchanging oxygen was 93.0 + 5.5% of all blood-perfused capillaries in rat soleus muscle. A higher difference in these numbers was found by Fraser et al [43] in rat extensor digitorum longus muscle (EDL), i.e.…”

Section: Assessment Of Microvascular Oxygen Exchange Capabilitysupporting

confidence: 69%

Image-based modelling of skeletal muscle oxygenation

Zeller‐Plumhoff

Roose

Clough

et al. 2017

J. R. Soc. Interface.

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The supply of oxygen in sufficient quantity is vital for the correct functioning of all organs in the human body, in particular for skeletal muscle during exercise. Disease is often associated with both an inhibition of the microvascular supply capability and is thought to relate to changes in the structure of blood vessel networks. Different methods exist to investigate the influence of the microvascular structure on tissue oxygenation, varying over a range of application areas, i.e. biological in vivo and in vitro experiments, imaging and mathematical modelling. Ideally, all of these methods should be combined within the same framework in order to fully understand the processes involved. This review discusses the mathematical models of skeletal muscle oxygenation currently available that are based upon images taken of the muscle microvasculature in vivo and ex vivo. Imaging systems suitable for capturing the blood vessel networks are discussed and respective contrasting methods presented. The review further informs the association between anatomical characteristics in health and disease. With this review we give the reader a tool to understand and establish the workflow of developing an image-based model of skeletal muscle oxygenation. Finally, we give an outlook for improvements needed for measurements and imaging techniques to adequately investigate the microvascular capability for oxygen exchange.

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Section: Assessment Of Microvascular Oxygen Exchange Capabilitysupporting

confidence: 69%

Image-based modelling of skeletal muscle oxygenation

Zeller‐Plumhoff

Roose

Clough

et al. 2017

J. R. Soc. Interface.

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“…However, after imaging, most of the blood vessels observed were microvessels, and almost no large vessels were found in the data blocks included in the analysis. This limitation might be related to the staining characteristics of lycopersicon esculentum lectin, which primarily labels the endothelium of small vessels in microvascular beds ( Porter et al, 1990 ), and marks only a few larger vessels ( Robertson et al, 2015 ), thus is often used for microvessel staining to observe and evaluate the microvascular system ( Xu et al, 2004 ; Benton et al, 2008 ; Maeda et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Dl-3-N-Butylphthalide Promotes Angiogenesis in an Optimized Model of Transient Ischemic Attack in C57BL/6 Mice

Wang

et al. 2021

Front. Pharmacol.

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Transient ischemic attack (TIA) has been widely regarded as a clinical entity. Even though magnetic resonance imaging (MRI) results of TIA patients are negative, potential neurovascular damage might be present, and may account for long-term cognitive impairment. Animal models that simulate human diseases are essential tools for in-depth study of TIA. Previous studies have clarified that Dl-3-N-butylphthalide (NBP) promotes angiogenesis after stroke. However, the effects of NBP on TIA remain unknown. This study aims to develop an optimized TIA model in C57BL/6 mice to explore the microscopic evidence of ischemic injury after TIA, and investigate the therapeutic effects of NBP on TIA. C57BL/6 mice underwent varying durations (7, 8, 9 or 10 min) of middle cerebral artery occlusion (MCAO). Cerebral artery occlusion and reperfusion were assessed by laser speckle contrast imaging. TIA and ischemic stroke were distinguished by neurological testing and MRI examination at 24 h post-operation. Neuronal apoptosis was examined by TUNEL staining. Images of submicron cerebrovascular networks were obtained via micro-optical sectioning tomography. Subsequently, the mice were randomly assigned to a sham-operated group, a vehicle-treated TIA group or an NBP-treated TIA group. Vascular density was determined by immunofluorescent staining and fluorescein isothiocyanate method, and the expression of angiogenic growth factors were detected by western blot analysis. We found that an 8-min or shorter period of ischemia induced neither permanent neurological deficits nor MRI detectable brain lesions in C57BL/6 mice, but histologically caused neuronal apoptosis and cerebral vasculature abnormalities. NBP treatment increased the number of CD31+ microvessels and perfused microvessels after TIA. NBP also up-regulated the expression of VEGF, Ang-1 and Ang-2 and improved the cerebrovascular network. In conclusion, 8 min or shorter cerebral ischemia induced by the suture MCAO method is an appropriate TIA model in C57BL/6 mice, which conforms to the definition of human TIA, but causes microscopic neurovascular impairment. NBP treatment increased the expression of angiogenic growth factors, promoted angiogenesis and improved cerebral microvessels after TIA. Our study provides new insights on the pathogenesis and potential treatments of TIA.

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“…The sections were incubated with the streptavidin‐biotin complex (dilution 1:50; Elite ABC; Vector). Immunoreactivity was detected by ImmPACT DAB (SK‐4105; Vector) (Maeda et al ., 2014; Maeda et al ., 2015). The sections were observed, and images were obtained using NanoZoomer S60 (Hamamatsu Photonics, Hamamatsu, Japan).…”

Section: Methodsmentioning

confidence: 99%

Increased contribution of KCa channels to muscle contraction induced vascular and blood flow responses in sedentary and exercise trained ZFDM rats

Sonobe

Tsuchimochi

Maeda

et al. 2022

The Journal of Physiology

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In resistance arteries, endothelium‐dependent hyperpolarization (EDH)‐mediated vasodilatation is depressed in diabetes. We hypothesized that downregulation of KCa channel derived EDH reduces exercise‐induced vasodilatation and blood flow redistribution in diabetes. To test this hypothesis, we evaluated vascular function in response to hindlimb muscle contraction, and the contribution of KCa channels in anaesthetised ZFDM, metabolic disease rats with type 2 diabetes. We also tested whether exercise training ameliorated the vascular response. Using in vivo microangiography, the hindlimb vasculature was visualized before and after rhythmic muscle contraction (0.5 s tetanus every 3 s, 20 times) evoked by sciatic nerve stimulation (40 Hz). Femoral blood flow of the contracting hindlimb was simultaneously measured by an ultrasonic flowmeter. The contribution of KCa channels was investigated in the presence and absence of apamin and charybdotoxin. We found that vascular and blood flow responses to muscle contraction were significantly impaired at the level of small artery segments in ZFDM fa/fa rats compared to its lean control fa/+ rats. The contribution of KCa channels was also smaller in fa/fa than in fa/+ rats. Low‐intensity exercise training for 12 weeks in fa/fa rats demonstrated minor changes in the vascular and blood flow response to muscle contraction. However, the KCa‐derived component in the response to muscle contraction was much greater in exercise trained than in sedentary fa/fa rats. These data suggest that exercise training increases the contribution of KCa channels among endothelium‐dependent vasodilatory mechanisms to maintain vascular and blood flow responses to muscle contraction in this metabolic disease rat model. Key points Microvascular dysfunction in type 2 diabetes impairs blood flow redistribution during exercise and limits the performance of skeletal muscle and may cause early fatigability. Endothelium‐dependent hyperpolarization (EDH), which mediates vasodilatation in resistance arteries, is known to be depressed in animals with diabetes. Here, we report that low‐intensity exercise training in ZFDM rats increased the KCa channel‐derived component in the vasodilator responses to muscle contraction compared to that in sedentary rats, partly as a result of the increase in KCNN3 expression. These results suggest that low‐intensity exercise training improves blood flow redistribution in contracting skeletal muscle in metabolic disease with diabetes via upregulation of EDH.

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Regulation of the microvascular circulation in the leg muscles, pancreas and small intestine in rats

Cited by 4 publications

References 33 publications

Image-based modelling of skeletal muscle oxygenation

Image-based modelling of skeletal muscle oxygenation

Dl-3-N-Butylphthalide Promotes Angiogenesis in an Optimized Model of Transient Ischemic Attack in C57BL/6 Mice

Increased contribution of KCa channels to muscle contraction induced vascular and blood flow responses in sedentary and exercise trained ZFDM rats

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