Modeling of the blood flow in the lower extremities for dynamic diffuse optical tomography of Peripheral Artery Disease

Author(s):  
A. Marone ◽  
J.W. Hoi ◽  
M.A. Khalil ◽  
H.K. Kim ◽  
G. Shrikhande ◽  
...  
2018 ◽  
Vol 315 (1) ◽  
pp. H101-H108 ◽  
Author(s):  
Nicholas T. Kruse ◽  
Kenichi Ueda ◽  
William E. Hughes ◽  
Darren P. Casey

Peripheral artery disease (PAD) is characterized by a reduced blood flow (BF) and an elevated blood pressure (pressor) response during lower extremity exercise. Although PAD is evident in the upper extremities, no studies have determined BF and pressor responses during upper extremity exercise in PAD. Emerging evidence suggests that inorganic nitrate supplementation may serve as an alternative dietary strategy to boost nitric oxide bioavailability, improving exercising BF and pressor responses during exercise. The present study investigated 1) BF and pressor responses to forearm exercise in patients with PAD ( n = 21) relative to healthy age-matched control subjects ( n = 16) and 2) whether 8 wk of NaNO3 supplementation influenced BF and pressor responses to forearm exercise in patients with PAD. Patients with moderate to severe PAD were randomly assigned to a NaNO3 (1 g/day, n = 13)-treated group or a placebo (microcrystalline cellulose, n = 8)-treated group. Brachial artery forearm BF (FBF; via Doppler) and blood pressure (via finger plethysmography) were measured during mild-intensity (~3.5-kg) and moderate-intensity (~7-kg) handgrip exercise. The absolute change (from baseline) in FBF was reduced (except in the 3.5-kg condition) and BP responses were increased in patients with PAD compared with healthy control subjects in 3.5- and 7-kg conditions (all P < 0.05). Plasma nitrate and nitrite were elevated, exercising (7-kg) ΔFBF was improved (from 141 ± 17 to 172 ± 20 ml/min), and mean arterial pressure response was reduced (from 13 ± 1 to 9 ± 1 mmHg, P < 0.05) in patients with PAD that received NaNO3 supplementation for 8 wk relative to those that received placebo. These results suggest that the BF limitation and exaggerated pressor response to moderate-intensity forearm exercise in patients with PAD are improved with 8 wk of NaNO3 supplementation. NEW & NOTEWORTHY Peripheral artery disease (PAD) results in an exaggerated pressor response and reduced blood flow during lower limb exercise; however, the effect of PAD in the upper limbs has remained unknown. These results suggest that 8 wk of inorganic nitrate supplementation improves the blood flow limitation and exaggerated pressor response to moderate-intensity forearm exercise in PAD.


2020 ◽  
Vol 318 (4) ◽  
pp. H916-H924 ◽  
Author(s):  
Danielle Jin-Kwang Kim ◽  
Marcos Kuroki ◽  
Jian Cui ◽  
Zhaohui Gao ◽  
J. Carter Luck ◽  
...  

Patients with peripheral artery disease (PAD) have an accentuated exercise pressor reflex (EPR) during exercise of the affected limb. The underlying hemodynamic changes responsible for this, and its effect on blood flow to the exercising extremity, are unclear. We tested the hypothesis that the exaggerated EPR in PAD is mediated by an increase in total peripheral resistance (TPR), which augments redistribution of blood flow to the exercising limb. Twelve patients with PAD and 12 age- and sex-matched subjects without PAD performed dynamic plantar flexion (PF) using the most symptomatic leg at progressive workloads of 2–12 kg (increased by 1 kg/min until onset of fatigue). We measured heart rate, beat-by-beat blood pressure, femoral blood flow velocity (FBV), and muscle oxygen saturation ([Formula: see text]) continuously during the exercise. Femoral blood flow (FBF) was calculated from FBV and baseline femoral artery diameter. Stroke volume (SV), cardiac output (CO), and TPR were derived from the blood pressure tracings. Mean arterial blood pressure and TPR were significantly augmented in PAD compared with control during PF. FBF increased during exercise to an equal extent in both groups. However, [Formula: see text] of the exercising limb remained significantly lower in PAD compared with control. We conclude that the exaggerated pressor response in PAD is mediated by an abnormal TPR response, which augments redistribution of blood flow to the exercising extremity, leading to an equal rise in FBF compared with controls. However, this increase in FBF is not sufficient to normalize the SmO2 response during exercise in patients with PAD. NEW & NOTEWORTHY In this study, peripheral artery disease (PAD) patients and healthy control subjects performed graded, dynamic plantar flexion exercise. Data from this study suggest that previously reported exaggerated exercise pressor reflex in patients with PAD is driven by greater vasoconstriction in nonexercising vascular territories which also results in a redistribution of blood flow to the exercising extremity. However, this rise in femoral blood flow does not fully correct the oxygen deficit due to changes in other mechanisms that require further investigation.


2016 ◽  
Vol 21 (3) ◽  
pp. 281-286 ◽  
Author(s):  
Mehdi H Shishehbor ◽  
Herbert D Aronow ◽  
John R Bartholomew ◽  
Joshua A Beckman ◽  
James B Froehlich ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Zhaohui Gao ◽  
Matthew D Muller ◽  
Cheryl Blaha ◽  
Aimee Cauffman ◽  
Kristen Brandt ◽  
...  

Exercise is associated with a rise in heart rate, blood pressure (BP) and blood flow to active skeletal muscle that is mediated by the exercise pressor reflex and modified by regional release of vasodilator factors. In peripheral artery disease (PAD) the exercise pressor reflex is enhanced and the ability to raise blood flow to the affected limb is impaired. To assess the functional impact of the enhanced exercise pressor reflex on regional blood flow in limbs affected by PAD, we determined beat-by-beat BP and mean blood velocity (MBV, Doppler) in the popliteal artery, and calculated vascular conductance index (VC, MBV/mean BP) in the exercising (ipsilateral) or contralateral resting leg during graded rhythmic plantar flexion exercise in 7 patients with symptomatic PAD (age 67±2 yrs, body-mass-index 27.9±1.1) and in 5 healthy age-matched controls (2 exercise trials with each leg). At peak exercise (2.0 kg, 1 contraction/sec), the pressor effect was greatest in PAD when exercise was performed with the “ischemic” leg (ankle-brachial index 0.58±0.05; mean ΔBP +9.1±2.0 mmHg), lower with the less affected leg (ankle brachial index 0.76±0.07; mean ΔBP +6.9±1.6 mmHg) and lowest in the controls (ankle brachial index 1.11±0.04; mean ΔBP +3.9±1.8 mmHg). In controls, VC increased in the exercising leg ( P <0.05) but did not change in the inactive contralateral leg ( P =NS). Similarly, in PAD, VC increased in the exercising “ischemic” leg ( P <0.05) but did not change in the inactive contralateral leg ( P =NS). In sharp contrast, while VC increased in the less affected exercising leg ( P <0.05), in the contralateral resting “ischemic” leg VC decreased by 24±10% ( P <0.05). Similarly, when static handgrip at 30% maximum voluntary contraction to fatigue served as the exercise stimulus, vasoconstriction was noted in the “ischemic” leg (n=5; P <0.05). Thus, unlike in the exercising leg, in the resting “ischemic” leg activation of the exercise pressor reflex resulted in substantial vasoconstriction. This suggests that despite activation of peripheral vasodilator mechanisms downstream to the arterial obstruction, the vasculature of the “ischemic” leg is exquisitely sensitive to reflex vasoconstriction.


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