Subcutaneous and transcutaneous monitoring of murine hindlimb ischemia byin vivoRaman spectroscopy

The Analyst ◽  
2019 ◽  
Vol 144 (15) ◽  
pp. 4677-4686
Author(s):  
Rida Al-Rifai ◽  
Claire Tournois ◽  
Samar Kheirallah ◽  
Nicole Bouland ◽  
Gaël Poitevin ◽  
...  

We have investigated the development of murine hindlimb ischemia from day 1 to day 55 after femoral artery ligation (FAL) using blood flow analysis, functional tests, histopathological staining, andin vivoRaman spectroscopy.

Author(s):  
Hiroko Kadowaki ◽  
Takuya Kishimoto ◽  
Takeshi Tokunaga ◽  
Koji Mori ◽  
Takashi Saito

Abstract Although blood viscosity has attracted much attention for its effect on hemodynamic parameters related to atherosclerosis, quantitative method for evaluating blood viscosity in vivo is not currently established. The purpose of this study was to verify the feasibility of blood viscosity estimation by a two-dimensional ultrasonic-measurement-integrated (2D-UMI) analysis system that computes an intravascular blood flow field by feeding back an ultrasonic measurement data to a numerical simulation. A method to estimate blood viscosity was proposed by reproducing the flow field of an analysis object in the feedback domain of ultrasonic Doppler velocity in a 2D-UMI blood flow analysis system, and evaluating the variation of the Doppler velocity caused by the analysis viscosity in the nonfeedback domain at the downstream side. In a numerical experiment, a viscosity estimation was performed for numerical solutions of sinusoidal oscillating flows analyzed as a blood flow model in a human common carotid artery at four different types of blood viscosities. The estimation viscosities were made to correspond to those of all analysis objects by giving proper conditions on the feedback gain and feedback domain to optimize the accuracy of the 2D-UMI blood flow analysis. In conclusion, the feasibility of blood viscosity estimation by 2D-UMI analysis was established. Simultaneous measurement of the in vivo blood viscosity and flow field can be easily performed in many clinical cases by its widespread use at clinical sites, thereby clarifying the relationship between hemodynamics and vascular pathology for various blood flow fields.


2016 ◽  
Vol 121 (4) ◽  
pp. 849-857 ◽  
Author(s):  
Crystal L. Coolbaugh ◽  
Emily C. Bush ◽  
Charles F. Caskey ◽  
Bruce M. Damon ◽  
Theodore F. Towse

Automated software improves the accuracy and reliability of blood velocity, vessel diameter, blood flow, and shear rate ultrasound measurements, but existing software offers limited flexibility to customize and validate analyses. We developed FloWave.US —open-source software to automate ultrasound blood flow analysis—and demonstrated the validity of its blood velocity (aggregate relative error, 4.32%) and vessel diameter (0.31%) measures with a skeletal muscle ultrasound flow phantom. Compared with a commercial, manual analysis software program, FloWave.US produced equivalent in vivo cardiac cycle time-averaged mean (TAMean) velocities at rest and following a 10-s muscle contraction (mean bias <1 pixel for both conditions). Automated analysis of ultrasound blood flow data was 9.8 times faster than the manual method. Finally, a case study of a lower extremity muscle contraction experiment highlighted the ability of FloWave.US to measure small fluctuations in TAMean velocity, vessel diameter, and mean blood flow at specific time points in the cardiac cycle. In summary, the collective features of our newly designed software—accuracy, reliability, reduced processing time, cost-effectiveness, and flexibility—offer advantages over existing proprietary options. Further, public distribution of FloWave.US allows researchers to easily access and customize code to adapt ultrasound blood flow analysis to a variety of vascular physiology applications.


Author(s):  
Jos� G. Lobo Filho ◽  
Maria C. A. Leit�o ◽  
Heraldo G. Lobo Filho ◽  
Andr� A. Silva ◽  
Jo�o J. A. Machado ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Sachiko Nishimoto ◽  
Daiju Fukuda ◽  
Yasutomi Higashikuni ◽  
Kimie Tanaka ◽  
Yoichiro Hirata ◽  
...  

Background: Peripheral artery disease causes significant functional disability and results in impaired quality of life. Toll-like receptor (TLR)-2, 3 and 4 are suggested to participate in blood flow recovery in ischemic limb by modulating inflammation and angiogenesis, however, the role of TLR9 remains unknown. TLR9 recognizes bacterial unmethylated DNA and plays a role in innate defense, although it can also provoke inflammation in response to fragmented DNA released from regenerated mammalian cells. This study tested the hypothesis that genetic deletion of TLR9 accelerates blood flow recovery after femoral artery ligation by inhibiting inflammation and improving endothelial cell function. Methods and Results: Unilateral femoral artery ligation was performed in TLR9-deficient (TLR9KO) mice and wild type (WT) mice. Femoral artery ligation significantly increased RNA expression of TLR9 (20-times) in WT mice and plasma levels of single-stranded DNA and double-stranded DNA, endogenous ligands for TLR9, in both strains of mice compared with each sham-operated group (P<0.05). Laser Doppler perfusion imaging demonstrated that TLR9KO mice significantly improved the ratio of the blood flow in the ischemic to non-ischemic limb compared with WT mice at 2 weeks after ligation (P<0.05). TLR9KO mice showed less accumulation of macrophages and less expression of inflammatory molecules (e.g., TNF-α, MCP-1 and IL-1β in ischemic muscle compared with WT mice (P<0.05, respectively). In vitro experiments using thioglycolate-stimulated peritoneal macrophages demonstrated that CpG ODN, agonistic oligonucleotide for TLR9, promoted the expression of pro-inflammatory molecules (e.g., MCP-1 and TNF-α) in WT macrophages (P<0.05, respectively) but not in TLR9 KO macrophages. Furthermore, activation of TLR9 by CpG ODN inhibited migration and proliferation of endothelial cells as determined by scratch-wound assay and MTS assay, respectively (P<0.05). Conclusion: Our results suggested that TLR9 enhances inflammation and affects migration and proliferation of endothelial cells, leading to impaired blood flow recovery in ischemic limb. TLR9 may serve as a potential therapeutic target for ischemic limb disease.


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