scholarly journals The Effect of Lower Limb Revascularization on Flow, Perfusion, and Systemic Endothelial Function: A Systematic Review

Angiology ◽  
2020 ◽  
pp. 000331972096954
Author(s):  
Pasha Normahani ◽  
Sodabeh Khosravi ◽  
Viknesh Sounderajah ◽  
Mohamed Aslam ◽  
Nigel J. Standfield ◽  
...  

Peripheral arterial disease (PAD) is associated with reduced lower limb blood flow and tissue perfusion. The consequent reduction in vessel wall shear stress as well as ischemia–reperfusion injury has also been associated with systemic endothelial dysfunction and inflammation. We aimed to explore the impact of lower limb revascularization on (1) lower limb blood flow, (2) tissue perfusion, and (3) systemic endothelial function. We performed a systematic literature search using the MEDLINE, Embase, and Web of Science databases. Eligible studies measured changes in lower limb blood flow, perfusion, or systemic endothelial function following revascularization for the treatment of symptomatic PAD. We found 19 eligible studies, which were limited by considerable heterogeneity. Current evidence suggests that revascularization has a positive effect on flow, perfusion, and systemic endothelial dysfunction. Any changes may take a number of weeks to become apparent. There is a need for well-designed studies to explore the association between flow, perfusion, and endothelial dysfunction.

Author(s):  
Ellen C. McGarity-Shipley ◽  
Sarah M. Schmitter ◽  
Jennifer S. Williams ◽  
Trevor J. King ◽  
Iain A. C. McPhee ◽  
...  

2007 ◽  
Vol 32 (5) ◽  
pp. 936-941 ◽  
Author(s):  
Mette Paulli Sonne ◽  
Celena Scheede-Bergdahl ◽  
David Benee Olsen ◽  
Lise Højbjerre ◽  
Amra Alibegovic ◽  
...  

The term “endothelial dysfunction” refers to the inability or attenuated effect of the endothelial cells in participating in the relaxation of the adjacent smooth muscle, thus causing less vasodilation. Although endothelial dysfunction is often seen in patients with type 2 diabetes, it does not necessarily follow that insulin resistance and (or) hyperglycemia is causing the inability to respond properly to vasodilatory stimuli. Rather, this could be related to the impact of concomitant cardiovascular risk factors that are almost invariably present in patients with type 2 diabetes. The impact of physical training — or the opposite, inactivity — on endothelial function is not fully elucidated. Some studies have shown positive effects of physical training, whereas others have not. In general, physical training can improve endothelial function when this is impaired. However, physical training does not seem to have any effect on endothelial function when this is normal.


2018 ◽  
Vol 315 (4) ◽  
pp. R820-R824 ◽  
Author(s):  
Lauro C. Vianna ◽  
Igor A. Fernandes ◽  
Thales C. Barbosa ◽  
Tatiana G. Amaral ◽  
Natalia G. Rocha ◽  
...  

Endothelial dysfunction is observed in the peripheral vasculature of hypertensive patients, but it is unclear how the cerebral circulation is affected. More specifically, little is known about the impact of human hypertension on vertebral artery (VA) endothelial function. This study evaluated whether the endothelial function of the VA is impaired in hypertensive men. For 13 male hypertensive subjects (46 ± 3 yr) and eight age-matched male controls (46 ± 4 yr), blood pressure (BP; photoplethysmography), VA, and common carotid (CC) blood flow (duplex ultrasound) were determined at rest and during 30 min of intravenous l-arginine (30 g; a precursor of nitric oxide) or isotonic saline infusion. Controls and hypertensive subjects demonstrated a similar resting CC (601 ± 30 vs. controls 570 ± 43 ml/min; P = 0.529) and VA blood flow (119 ± 11 vs. controls 112 ± 9 ml/min; P = 0.878). During administration of l-arginine, CC blood flow increased similarly between groups (hypertensive 12 ± 3%, controls 13 ± 2%; P = 0.920). In contrast, the increase in VA blood flow was nonexistent in the hypertensive subjects (0.8 ± 3% vs. controls: 16 ± 4%; P = 0.015) with no significant change in BP. Both CC and VA flow returned to near-resting values within 30 min after the infusion, and for four hypertensive subjects and three controls, time-control experiments using 0.9% saline did not affect VA or CC blood flow significantly. The results demonstrate endothelial dysfunction in the posterior cerebral circulation of middle-aged hypertensive men.


PEDIATRICS ◽  
1985 ◽  
Vol 76 (6) ◽  
pp. 918-921
Author(s):  
Frans J. Walther ◽  
Paul Y. K. Wu ◽  
Bijan Siassi

Phototherapy is known to increase peripheral blood flow in neonates, but information on the associated cardiovascular effects is not available. Using pulsed Doppler echocardiography we evaluated cardiac output and stroke volume in 12 preterm and 13 term neonates during and after phototherapy. We concomitantly measured arterial limb blood flow by strain gauge plethysmography and skin blood flow by photoplethysmography. Cardiac output decreased by 6% due to reduced stroke volume during phototherapy, whereas total limb blood flow and skin blood flow increased by 38% and 41%, respectively. Peripheral blood flow increments tended to be higher in the preterm than in the term infants. The reduced stroke volume during phototherapy may be an expression of reduced activity of the newborn during phototherapy. For healthy neonates the reduction in cardiac output is minimal, but for sick infants with reduced cardiac output, this reduction may further aggravate the decrease in tissue perfusion.


2018 ◽  
Vol 119 (2) ◽  
pp. 377-387 ◽  
Author(s):  
Matthew A. Kilgas ◽  
John McDaniel ◽  
Jon Stavres ◽  
Brandon S. Pollock ◽  
Tyler J. Singer ◽  
...  

2012 ◽  
Vol 302 (5) ◽  
pp. E481-E495 ◽  
Author(s):  
Rinrada Kietadisorn ◽  
Rio P. Juni ◽  
An L. Moens

Endothelial nitric oxide synthase (eNOS) serves as a critical enzyme in maintaining vascular pressure by producing nitric oxide (NO); hence, it has a crucial role in the regulation of endothelial function. The bioavailability of eNOS-derived NO is crucial for this function and might be affected at multiple levels. Uncoupling of eNOS, with subsequently less NO and more superoxide generation, is one of the major underlying causes of endothelial dysfunction found in atherosclerosis, diabetes, hypertension, cigarette smoking, hyperhomocysteinemia, and ischemia/reperfusion injury. Therefore, modulating eNOS uncoupling by stabilizing eNOS activity, enhancing its substrate, cofactors, and transcription, and reversing uncoupled eNOS are attractive therapeutic approaches to improve endothelial function. This review provides an extensive overview of the important role of eNOS uncoupling in the pathogenesis of endothelial dysfunction and the potential therapeutic interventions to modulate eNOS for tackling endothelial dysfunction.


2001 ◽  
Vol 33 (5) ◽  
pp. S209 ◽  
Author(s):  
T T. Garrison ◽  
H A. Kluess ◽  
M A. Welsch ◽  
R H. Wood

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