In vitro assessment of combined Doppler ultrasound and CFD modeling in arterial blood flow quantification

The contribution of endothelial-derived miR-17∼92 to ischemia-induced arteriogenesis has not been investigated in an in vivo model. In the present study, we demonstrate a critical role for the endothelial-derived miR-17∼92 cluster in shaping physiological and ischemia-triggered arteriogenesis. Endothelial-specific deletion of miR-17∼92 results in an increase in collateral density limbs and hearts and in ischemic limbs compared with control mice, and consequently improves blood flow recovery. Individual cluster components positively or negatively regulate endothelial cell (EC) functions in vitro, and, remarkably, ECs lacking the cluster spontaneously form cords in a manner rescued by miR-17a, -18a, and -19a. Using both in vitro and in vivo analyses, we identified FZD4 and LRP6 as targets of miR-19a/b. Both of these targets were up-regulated in 17∼92 KO ECs compared with control ECs, and both were shown to be targeted by miR-19 using luciferase assays. We demonstrate that miR-19a negatively regulates FZD4, its coreceptor LRP6, and WNT signaling, and that antagonism of miR-19a/b in aged mice improves blood flow recovery after ischemia and reduces repression of these targets. Collectively, these data provide insights into miRNA regulation of arterialization and highlight the importance of vascular WNT signaling in maintaining arterial blood flow.

Download Full-text

Radial artery cannulation decreases the distal arterial blood flow measured by power Doppler ultrasound

Journal of Clinical Monitoring and Computing ◽

10.1007/s10877-014-9648-5 ◽

2014 ◽

Vol 29 (5) ◽

pp. 653-657 ◽

Cited By ~ 3

Author(s):

Atsushi Numaguchi ◽

Yushi U. Adachi ◽

Yoshitaka Aoki ◽

Yasuhiro Ishii ◽

Katsumi Suzuki ◽

...

Keyword(s):

Blood Flow ◽

Doppler Ultrasound ◽

Radial Artery ◽

Power Doppler ◽

Arterial Blood Flow ◽

Power Doppler Ultrasound ◽

Radial Artery Cannulation ◽

Artery Cannulation ◽

Arterial Blood

Download Full-text

Relationship between vascular reactivity in vitro and blood flows in rats with cirrhosis

Clinical Science ◽

10.1042/cs0970313 ◽

1999 ◽

Vol 97 (3) ◽

pp. 313-318 ◽

Cited By ~ 9

Author(s):

Dominique PATERON ◽

Frédéric OBERTI ◽

Pascale LEFILLIATRE ◽

Nary VEAL ◽

Khalid A. TAZI ◽

...

Keyword(s):

Blood Flow ◽

Vascular Reactivity ◽

Regional Blood Flow ◽

Arterial Blood Flow ◽

Blood Flows ◽

Arterial Blood ◽

Vascular Responsiveness ◽

Microsphere Method ◽

Radioactive Microsphere Method

In cirrhosis there is a hyperdynamic circulation, which occurs mainly in the systemic and splanchnic regions. Using isolated-vessel models, previous studies have shown reduced aortic reactivity to vasoconstrictors in rats with cirrhosis. The aim of the present study was to evaluate and compare the vascular responsiveness to phenylephrine in arterial rings and the blood flows from different regions in rats with cirrhosis and controls. Reactivity was studied in isolated thoracic aortic, superior mesenteric arterial and carotid arterial rings from sham-operated and bile-duct-ligated rats by measuring the cumulative concentration-dependent tension induced by phenylephrine (10-9–10-4 M). Blood flows were measured by the radioactive microsphere method. In rats with cirrhosis, a significant hyporeactivity to phenylephrine was observed in both the aorta and the superior mesenteric artery compared with the corresponding arteries of normal rats. This hyporesponsiveness was corrected by Nω-nitro-l-arginine (0.1 mM). In contrast, carotid artery reactivity and the responses to Nω-nitro-l-arginine were similar in the cirrhotic and control groups. In each case, cardiac output and mesenteric arterial blood flow were significantly higher in cirrhotic than in normal rats. Cerebral blood flows were not significantly different between the two groups. In cirrhotic rats, arterial hyporeactivity may be a consequence of increased regional blood flow and increased production of nitric oxide.

Download Full-text