Influence of thigh blood flow upon the arterial pressure gradient over the collateral arteries in patients with occlusion of the superficial femoral artery

1982 ◽  
Vol 16 (6) ◽  
pp. 304-307 ◽  
Author(s):  
K AGERSKOV
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pressure Gradient ◽  
Femoral Artery ◽  
Superficial Femoral Artery ◽  
Collateral Arteries

Microvascular pressure in venules of skeletal muscle during arterial pressure reduction

1986 ◽  
Vol 250 (5) ◽  
pp. H838-H845 ◽  
Author(s):  
S. D. House ◽  
P. C. Johnson
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Pressure Gradient ◽  
Pressure Difference ◽  
Reactive Hyperemia ◽  
Sartorius Muscle ◽  
Pressure Reduction ◽  
Large Vein ◽  
The Difference

It has been suggested from whole organ studies that the viscosity of blood in skeletal muscle venules varies inversely with flow over physiological flow ranges. If this is the case, the hydrostatic pressure gradient in venules should change less than flow as flow is altered. To test this hypothesis, pressure in venules of cat sartorius muscle was measured during stepwise arterial pressure reduction to 20 mmHg. Large vein pressure remained constant at about 5 mmHg. Average pressures in the large venules (40–185 microns) ranged from 13.6 to 10.0 mmHg. The difference between pressure in these venules and large vein pressure fell in proportion to the reduction in blood pressure and blood flow. Pressures in the smallest venules studied (25 microns) averaged 19.7 +/- 6.2 (SD) mmHg. The pressure difference between the smallest venules and the large vein fell less than the arteriovenous pressure difference or blood flow when arterial pressure was reduced. During reactive hyperemia the pressure gradient between the smallest venules and the large vein rose proportionately less than blood flow. The stability of pressure in the smallest venules is consistent with the hypothesis that blood viscosity varies inversely with flow rate.

Blood flow in the lower limb after balloon angioplasty of the superficial femoral artery

1996 ◽  
Vol 83 (6) ◽  
pp. 791-795 ◽  
Author(s):  
S. T. Hussain ◽  
R. E. Smith ◽  
A. L. Clark ◽  
R. F. M. Wood
Keyword(s):  
Blood Flow ◽  
Femoral Artery ◽  
Balloon Angioplasty ◽  
Superficial Femoral Artery ◽  
Lower Limb

scholarly journals Requirement of β1 integrin for endothelium-dependent vasodilation and collateral formation in hindlimb ischemia

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Carina Henning ◽  
Anna Branopolski ◽  
Dominik Schuler ◽  
Dimitrios Dimitroulis ◽  
Patrik Huelsemann ◽  
...  
Keyword(s):  
Blood Flow ◽  
Endothelial Cell ◽  
Femoral Artery ◽  
Β1 Integrin ◽  
Hindlimb Ischemia ◽  
High Frequency Ultrasound ◽  
Blocking Antibody ◽  
Arterial Lumen ◽  
Collateral Arteries ◽  
Acute Increase

AbstractAn acute increase in blood flow triggers flow-mediated dilation (FMD), which is mainly mediated by endothelial nitric oxide synthase (eNOS). A long-term increase in blood flow chronically enlarges the arterial lumen, a process called arteriogenesis. In several common human diseases, these processes are disrupted for as yet unknown reasons. Here, we asked whether β1 integrin, a mechanosensory protein in endothelial cells, is required for FMD and arteriogenesis in the ischemic hindlimb. Permanent ligation of the femoral artery in C57BL/6 J mice enlarged pre-existing collateral arteries and increased numbers of arterioles in the thigh. In the lower leg, the numbers of capillaries increased. Notably, injection of β1 integrin-blocking antibody or tamoxifen-induced endothelial cell-specific deletion of the gene for β1 integrin (Itgb1) inhibited both arteriogenesis and angiogenesis. Using high frequency ultrasound, we demonstrated that β1 integrin-blocking antibody or endothelial cell-specific depletion of β1 integrin attenuated FMD of the femoral artery, and blocking of β1 integrin function did not further decrease FMD in eNOS-deficient mice. Our data suggest that endothelial β1 integrin is required for both acute and chronic widening of the arterial lumen in response to hindlimb ischemia, potentially via functional interaction with eNOS.

Tortuosity of the superficial femoral artery and its influence on blood flow patterns and risk of atherosclerosis

2019 ◽  
Vol 18 (4) ◽  
pp. 883-896 ◽  
Author(s):  
Xuanyu Li ◽  
Xiaosheng Liu ◽  
Xiao Li ◽  
Lijian Xu ◽  
Xin Chen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Femoral Artery ◽  
Superficial Femoral Artery ◽  
Flow Patterns ◽  
Blood Flow Patterns

Impaired superficial femoral artery vasodilation and leg blood flow in young obese women following an oral glucose tolerance test

2012 ◽  
Vol 37 (1) ◽  
pp. 176-183 ◽  
Author(s):  
T.D. Olver ◽  
T.J. Hazell ◽  
C.D. Hamilton ◽  
J.K. Shoemaker ◽  
P.W.R. Lemon
Keyword(s):  
Blood Flow ◽  
Glucose Tolerance ◽  
Young Women ◽  
Femoral Artery ◽  
Superficial Femoral Artery ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Obese Women ◽  
Leg Blood Flow ◽  
Glucose Ingestion

This study was designed to test the hypothesis that glucose ingestion following an overnight fast increases leg vascular conductance (LVCd) and superficial femoral artery (SFA) vasodilation in lean but not obese young women. Obese (23.5 ± 4.0 years, 84.7 ± 14.7 kg, 37.2% ± 6.4% fat; mean ± SD, n = 8) and lean (23.8 ± 2.4 years, 60.6 ± 4.0 kg, 22.3% ± 2.8% fat; n = 8) women arrived in the laboratory at 0830 h after a 12-h overnight fast for body composition (densitometry) assessment. Then, capillary blood glucose (BGlu), plasma insulin, heart rate, cardiac output, mean arterial pressure, leg blood flow (Doppler ultrasound), and LVCd were measured (after 15 min in the supine position), and at 30-min intervals for 2 h following glucose ingestion (75 g glucose load, 12.5% solution). Fasting BGlu concentration was not different between groups (obese = 5.1 ± 0.47 vs. lean = 4.9 ± 0.37 mmol·L–1, p = 0.71) but 60, 90, and 120 min postingestion BGlu was elevated (p ≤ 0.03) in the obese women. Insulin differences were not significant. Fasting LVCd was not different between groups (lean = 0.72 ± 0.49 vs. obese = 0.70 ± 0.19 mL·min–1·mm Hg–1; p = 0.48); however, LVCd, as well as Δ in SFA diameter were significantly elevated (p ≤ 0.04) in the lean compared with the obese group at 60, 90, and 120 min postglucose ingestion (LVCd, peak lean = 1.4 ± 0.5 vs. peak obese = 0.8 ± 0.1 mL·min–1·mm Hg–1; Δ in SFA, peak lean = 0.51 ± 0.30 vs. peak obese = 0.09 ± 0.45 mm). The reduced LVCd following glucose ingestion could contribute to impaired glucose tolerance. Further, the lack of SFA dilation may be evidence of impaired vascular insulin responsiveness in these obese young women.

Resistive exercise versus resistive vibration exercise to counteract vascular adaptations to bed rest

2010 ◽  
Vol 108 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Noortje T. L. van Duijnhoven ◽  
Dick H. J. Thijssen ◽  
Daniel J. Green ◽  
Dieter Felsenberg ◽  
Daniel L. Belavý ◽  
...  
Keyword(s):  
Blood Flow ◽  
Femoral Artery ◽  
Superficial Femoral Artery ◽  
Vascular Function ◽  
Bed Rest ◽  
Flow Mediated Dilation ◽  
Resistive Exercise ◽  
Vibration Exercise ◽  
Echo Doppler Ultrasound ◽  
The Impact

Bed rest results in marked vascular adaptations, and resistive vibration exercise (RVE) has been shown to be an effective countermeasure. As vibration exercise has practical and logistical limitations, the use of resistive exercise (RES) alone has the preference under specific circumstances. However, it is unknown if RES is sufficient to prevent vascular adaptations to bed rest. Therefore, the purpose of the present study was to examine the impact of RES and RVE on the vascular function and structure of the superficial femoral artery in young men exposed to 60 days of bed rest. Eighteen healthy men (age: 31 ± 8 yr) were assigned to bed rest and randomly allocated to control, RES, or RVE groups. Exercise was applied 3 times/wk for 5–7 min/session. Resting diameter, blood flow, flow-mediated dilation (FMD), and dilator capacity of the superficial femoral artery were measured using echo-Doppler ultrasound. Bed rest decreased superficial femoral artery diameter and dilator capacity ( P < 0.001), which were significantly attenuated in the RVE group ( P < 0.01 and P < 0.05, respectively) but not in the RES group ( P = 0.202 and P = 0.696, respectively). Bed rest significantly increased FMD ( P < 0.001), an effect that was abolished by RVE ( P < 0.005) but not RES ( P = 0.078). Resting and hyperemic blood flow did not change in any of the groups. Thus, RVE abolished the marked increase in FMD and decrease in baseline diameter and dilator capacity normally associated with prolonged bed rest. However, the stimulus provided by RES alone was insufficient to counteract the vascular adaptations to bed rest.

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