scholarly journals Performance assessment and optimization of Pulse Wave Imaging (PWI) in ex vivo canine aortas and in vivo normal human arteries

2012 ◽  
Author(s):  
R. X. Li ◽  
W. W. Qaqish ◽  
D. Shahmirzadi ◽  
E. E. Konofagou
Keyword(s):  
Performance Assessment ◽  
Pulse Wave ◽  
Ex Vivo ◽  
Wave Imaging ◽  
Normal Human ◽  
Human Arteries

A Novel Noninvasive Technique for Pulse-Wave Imaging and Characterization of Clinically-Significant Vascular Mechanical Properties In Vivo

2007 ◽  
Vol 29 (3) ◽  
pp. 137-154 ◽  
Author(s):  
Kana Fujikura ◽  
Jianwen Luo ◽  
Viktor Gamarnik ◽  
Mathieu Pernot ◽  
Royd Fukumoto ◽  
...  
Keyword(s):  
Aortic Wall ◽  
Pulse Wave ◽  
Distal Region ◽  
Noninvasive Technique ◽  
Abdominal Aortic ◽  
Wave Imaging ◽  
Risk Patients ◽  
Noninvasive Mapping ◽  
Clinically Significant

The pulse-wave velocity (PWV) has been used as an indicator of vascular stiffness, which can be an early predictor of cardiovascular mortality. A noninvasive, easily applicable method for detecting the regional pulse wave (PW) may contribute as a future modality for risk assessment. The purpose of this study was to demonstrate the feasibility and reproducibility of PW imaging (PWI) during propagation along the abdominal aortic wall by acquiring electrocardiography-gated (ECG-gated) radiofrequency (rf) signals noninvasively. An abdominal aortic aneurysm (AAA) was induced using a CaCl2 model in order to investigate the utility of this novel method for detecting disease. The abdominal aortas of twelve normal and five CaCl2, mice were scanned at 30 MHz and electrocardiography (ECG) was acquired simultaneously. The radial wall velocities were mapped with 8000 frames/s. Propagation of the PW was demonstrated in a color-coded ciné-loop format in all cases. In the normal mice, the wave propagated in linear fashion from a proximal to a distal region. However, in CaCl2 mice, multiple waves were initiated from several regions (i.e., most likely initiated from various calcified regions within the aortic wall). The regional PWV in normal aortas was 2.70 ± 0.54 m/s ( r2 = 0.85 ± 0.06, n = 12), which was in agreement with previous reports using conventional techniques. Although there was no statistical difference in the regional PWV between the normal and CaCl2-treated aortas (2.95 ± 0.90 m/s ( r2 = 0.51 ± 0.22, n = 5)), the correlation coefficient was found to be significantly lower in the CaCl2-treated aortas ( p<0.01). This state-of-the-art technique allows noninvasive mapping of vascular disease in vivo. In future clinical applications, it may contribute to the detection of early stages of cardiovascular disease, which may decrease mortality among high-risk patients.

scholarly journals Feasibility and Validation of 4-D Pulse Wave Imaging in Phantoms and In Vivo

2017 ◽  
Vol 64 (9) ◽  
pp. 1305-1317 ◽  
Author(s):  
Iason-Zacharias Apostolakis ◽  
Pierre Nauleau ◽  
Clement Papadacci ◽  
Matthew D. McGarry ◽  
Elisa E. Konofagou
Keyword(s):  
Pulse Wave ◽  
Wave Imaging

scholarly journals An Ex Vivo Vessel Injury Model to Study Remodeling

2018 ◽  
Vol 27 (9) ◽  
pp. 1375-1389 ◽  
Author(s):  
Mehmet H. Kural ◽  
Guohao Dai ◽  
Laura E. Niklason ◽  
Liqiong Gui
Keyword(s):  
Shear Stress ◽  
Animal Models ◽  
Intimal Hyperplasia ◽  
Vascular Remodeling ◽  
Ex Vivo ◽  
Vessel Injury ◽  
Injury Model ◽  
Human Arteries

Objective: Invasive coronary interventions can fail due to intimal hyperplasia and restenosis. Endothelial cell (EC) seeding to the vessel lumen, accelerating re-endothelialization, or local release of mTOR pathway inhibitors have helped reduce intimal hyperplasia after vessel injury. While animal models are powerful tools, they are complex and expensive, and not always reflective of human physiology. Therefore, we developed an in vitro 3D vascular model validating previous in vivo animal models and utilizing isolated human arteries to study vascular remodeling after injury. Approach: We utilized a bioreactor that enables the control of intramural pressure and shear stress in vessel conduits to investigate the vascular response in both rat and human arteries to intraluminal injury. Results: Culturing rat aorta segments in vitro, we show that vigorous removal of luminal ECs results in vessel injury, causing medial proliferation by Day-4 and neointima formation, with the observation of SCA1+ cells (stem cell antigen-1) in the intima by Day-7, in the absence of flow. Conversely, when endothelial-denuded rat aortae and human umbilical arteries were subjected to arterial shear stress, pre-seeding with human umbilical ECs decreased the number and proliferation of smooth muscle cell (SMC) significantly in the media of both rat and human vessels. Conclusion: Our bioreactor system provides a novel platform for correlating ex vivo findings with vascular outcomes in vivo. The present in vitro human arterial injury model can be helpful in the study of EC-SMC interactions and vascular remodeling, by allowing for the separation of mechanical, cellular, and soluble factors.

scholarly journals Impact of chronic hypoxia on proximal pulmonary artery wave propagation and mechanical properties in rats

2018 ◽  
Vol 314 (6) ◽  
pp. H1264-H1278 ◽  
Author(s):  
Junjing Su ◽  
Charmilie C. Logan ◽  
Alun D. Hughes ◽  
Kim H. Parker ◽  
Niti M. Dhutia ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Tensile Strength ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Wave Reflection ◽  
Chronic Hypoxia ◽  
Pulse Wave ◽  
Ex Vivo ◽  
Pulmonary Arteries

Arterial stiffness and wave reflection are important components of the ventricular afterload. Therefore, we aimed to assess the arterial wave characteristics and mechanical properties of the proximal pulmonary arteries (PAs) in the hypoxic pulmonary hypertensive rat model. After 21 days in normoxic or hypoxic chambers (24 animals/group), animals underwent transthoracic echocardiography and PA catheterization with a dual-tipped pressure and Doppler flow sensor wire. Wave intensity analysis was performed. Artery rings obtained from the pulmonary trunk, right and left PAs, and aorta were subjected to a tensile test to rupture. Collagen and elastin content were determined. In hypoxic rats, proximal PA wall thickness, collagen content, tensile strength per unit collagen, maximal elastic modulus, and wall viscosity increased, whereas the elastin-to-collagen ratio and arterial distensibility decreased. Arterial pulse wave velocity was also increased, and the increase was more prominent in vivo than ex vivo. Wave intensity was similar in hypoxic and normoxic animals with negligible wave reflection. In contrast, the aortic maximal elastic modulus remained unchanged, whereas wall viscosity decreased. In conclusion, there was no evidence of altered arterial wave propagation in proximal PAs of hypoxic rats while the extracellular matrix protein composition was altered and collagen tensile strength increased. This was accompanied by altered mechanical properties in vivo and ex vivo. NEW & NOTEWORTHY In rats exposed to chronic hypoxia, we have shown that pulse wave velocity in the proximal pulmonary arteries increased and pressure dependence of the pulse wave velocity was steeper in vivo than ex vivo leading to a more prominent increase in vivo.

scholarly journals Sodium Stibogluconate (Pentostam) Potentiates Oxidant Production in Murine Visceral Leishmaniasis and in Human Blood

2000 ◽  
Vol 44 (9) ◽  
pp. 2406-2410 ◽  
Author(s):  
Samira Rais ◽  
Axel Perianin ◽  
Monique Lenoir ◽  
Abderrahim Sadak ◽  
Daniele Rivollet ◽  
...  
Keyword(s):  
Human Blood ◽  
Ex Vivo ◽  
Platelet Activating Factor ◽  
Sodium Stibogluconate ◽  
Potentiation Effect ◽  
Normal Human ◽  
Ros Formation ◽  
Oxidant Production

ABSTRACT Sodium stibogluconate (Sbb), a leishmanicidal drug, was studied for its in vivo effect on the formation of reactive oxygen species (ROS), assessed by chemiluminescence (CL) in the whole blood of mice infected with Leishmania infantum. Stimulation of ROS formation induced ex vivo by zymosan particles or the protein kinase C activator phorbol myristate acetate (PMA) was reduced by approximately 25% (P < 0.05) after infection of mice. Treatment of infected mice with Sbb (50 to 400 mg/kg of body weight) enhanced the blood CL induced by zymosan and PMA (47 to 96%, P < 0.01). The drug potentiation effect also occurred in uninfected mice. In vitro treatment of normal human blood with Sbb (1, 10, or 100 μg/ml) for 1 h primed the CL response to PMA (29 to 54%). The priming effect of Sbb was also observed on the production of superoxide by isolated polymorphonuclear leukocytes stimulated either by PMA and zymosan or by the chemoattractants N-formyl-Met-Leu-Phe and platelet-activating factor. These data provide the first evidence of priming of the phagocyte respiratory burst by Sbb. This novel property of Sbb may contribute to the drug's leishmanicidal effect.

Abstract 543: Increased Aortic Pulse Wave Velocity in Type 2 Diabetic db/db Mice is Dependent on Blood Pressure

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Mircea Anghelescu ◽  
Keith J Gooch ◽  
Aaron J Trask
Keyword(s):  
Blood Pressure ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Aortic Stiffness ◽  
Pulse Wave ◽  
Ex Vivo ◽  
Aortic Pulse Wave Velocity ◽  
Type 2 Diabetic

Pulse wave velocity (PWV) is the gold standard for in vivo aortic stiffness measurements but can be dependent upon blood pressure and/or heart rate. Previous studies from our and other labs have shown increased aortic PWV in type 2 diabetic db/db mice. Moreover, preliminary ex vivo pressure myography data from our lab has also shown a lack of increase in passive aortic stiffness, suggesting that increased PWV in vivo , and therefore, increased stiffness in db/db mice may be dependent upon other mechanisms. In this study, we tested the hypothesis that increased aortic pulse wave velocity measured in db/db mice in vivo is blood pressure dependent under anesthesia. 16-wk old normal Db/db (n=9) and type 2 diabetic db/db (n=5) mice were anesthetized with 2% isoflurane and instrumented with two 1.2F pressure-tip catheters: one inserted in the left carotid artery and advanced to the thoracic aorta, the other inserted into the left femoral artery and advanced into the abdominal aorta. Blood pressure was continuously recorded and PWV was calculated using the foot-to-foot method. A microcannula was inserted into the right jugular vein for the administration of drugs. After a stabilization period of 25-30 mins, baseline BPs and PWVs were measured, after which mice were infused with increasing doses of phenylephrine (Phe, 100-500 nmol/kg/min) and sodium nitroprusside (SNP, 100-500 nmol/kg/min) to increase and decrease blood pressure, respectively. At baseline (prior to the infusion of any drugs), mean arterial pressure and aortic PWV were significantly elevated in db/db mice under anesthesia (MAP; Db/db: 77±5 vs. db/db: 100±4 mmHg, p <0.05; PWV; Db/db: 0.31±0.01 vs. db/db: 0.35±0.01 cm/ms, p <0.05). The increase in aortic PWV in db/db mice at baseline was completely abrogated when measured at equivalent MAPs ranging from 40-120 mmHg during the Phe and SNP infusions ( p >0.05). In both Db/db and db/db mice, aortic PWV was significantly correlated with MAP (Db/db: r=0.94, p <0.001; db/db: r=0.97, p <0.0001). These data show that increased aortic PWV, and therefore increased aortic stiffness in db/db mice in vivo is dependent upon blood pressure.

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