Increased vascular resistance during complement-activated plasma infusion in swine

1987 ◽  
Vol 253 (1) ◽  
pp. H58-H65
Author(s):  
L. J. Swenson ◽  
G. A. Pantely ◽  
C. G. Anselone ◽  
J. D. Bristow
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Femoral Artery ◽  
Femoral Vein ◽  
Adrenergic Blockade ◽  
Plasma Infusion ◽  
Artery Pressure ◽  
Femoral Artery Blood Flow ◽  
Acute Increase ◽  
Control Infusion

To investigate the acute effects of complement activation on blood flow, we infused complement-activated plasma into the femoral artery of the isolated hindlimb of 19 anesthetized swine. Femoral artery blood flow decreased abruptly, was lowest at 1 min of the infusion, and thereafter slowly increased despite continued infusion. There was no significant change in femoral artery pressure or femoral vein pressure, confirming an acute increase in vascular resistance. Control infusion of heat-decomplemented-activated plasma caused no change in pressure or flow. Slope of the femoral artery pressure-flow relationship during maximal vasodilation with adenosine was significantly lower after infusion of complement-activated plasma, confirming a persistent increase in vascular resistance. Neither the acute nor the persistent increase in vascular resistance was prevented by alpha-adrenergic blockade with phentolamine or granulocytopenia produced by cyclophosphamide. We conclude that complement-activated plasma infusion in the femoral circulation causes an abrupt increase in vascular resistance that persists during pharmacologically maximal vasodilation, is not due to alpha-mediated vasoconstriction, and is not altered by severe granulocytopenia.

Systemic α-adrenergic and nitric oxide inhibition on basal limb blood flow: effects of endurance training in middle-aged and older adults

2007 ◽  
Vol 293 (3) ◽  
pp. H1466-H1472 ◽  
Author(s):  
Jun Sugawara ◽  
Hidehiko Komine ◽  
Koichiro Hayashi ◽  
Mutsuko Yoshizawa ◽  
Takeshi Otsuki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Older Adults ◽  
Blood Flow ◽  
Exercise Training ◽  
Femoral Artery ◽  
Exercise Intervention ◽  
Adrenergic Blockade ◽  
Artery Blood Flow ◽  
Middle Aged ◽  
Femoral Artery Blood Flow

Endurance training improves endothelium-dependent vasodilation, yet it does not increase basal blood flow in the legs. We determined the effects of a 3-mo aerobic exercise intervention on basal leg blood flow and α-adrenergic vasoconstriction and nitric oxide (NO) release in seven apparently healthy middle-aged and older adults (60 ± 3 yr). Basal femoral artery blood flow (via Doppler ultrasound) (pretraining: 354 ± 29; posttraining: 335 ± 34 ml/min) and vascular conductance did not change significantly with the exercise training. Before the exercise intervention, femoral artery blood flow increased 32 ± 16% with systemic α-adrenergic blockade (with phentolamine) ( P < 0.05), and the addition of nitric oxide synthase (NOS) inhibition using NG-monomethyl-l-arginine (l-NMMA) did not affect femoral artery blood flow. After training was completed, femoral artery blood flow increased 47 ± 7% with α-adrenergic blockade ( P < 0.01) and then decreased 18 ± 7% with the subsequent administration of l-NMMA ( P < 0.05). Leg vascular conductance showed a greater α-adrenergic blockade-induced vasodilation (+1.7 ± 0.5 to +3.0 ± 0.5 units, P < 0.05) as well as NOS inhibition-induced vasoconstriction (−0.8 ± 0.4 to −2.7 ± 0.7 units, P < 0.05) after the exercise intervention. Resting plasma norepinephrine concentration significantly increased after the training. These results suggest that regular aerobic exercise training enhances NO bioavailability in middle-aged and older adults and that basal limb blood flow does not change with exercise training because of the contrasting influences of sympathetic nervous system activity and endothelium-derived vasodilation on the vasculature.

Kinetics of V̇o2 and femoral artery blood flow during heavy-intensity, knee-extension exercise

2005 ◽  
Vol 99 (2) ◽  
pp. 683-690 ◽  
Author(s):  
Nicole D. Paterson ◽  
John M. Kowalchuk ◽  
Donald H. Paterson
Keyword(s):  
Blood Flow ◽  
Femoral Artery ◽  
Time Course ◽  
Slow Component ◽  
Knee Extension ◽  
Artery Blood Flow ◽  
Phase 2 ◽  
Femoral Artery Blood Flow ◽  
Knee Extension Exercise ◽  
Kinetics Of

It has been suggested that, during heavy-intensity exercise, O2 delivery may limit oxygen uptake (V̇o2) kinetics; however, there are limited data regarding the relationship of blood flow and V̇o2 kinetics for heavy-intensity exercise. The purpose was to determine the exercise on-transient time course of femoral artery blood flow (Q̇leg) in relation to V̇o2 during heavy-intensity, single-leg, knee-extension exercise. Five young subjects performed five to eight repeats of heavy-intensity exercise with measures of breath-by-breath pulmonary V̇o2 and Doppler ultrasound femoral artery mean blood velocity and vessel diameter. The phase 2 time frame for V̇o2 and Q̇leg was isolated and fit with a monoexponent to characterize the amplitude and time course of the responses. Amplitude of the phase 3 response was also determined. The phase 2 time constant for V̇o2 of 29.0 s and time constant for Q̇leg of 24.5 s were not different. The change (Δ) in V̇o2 response to the end of phase 2 of 0.317 l/min was accompanied by a ΔQ̇leg of 2.35 l/min, giving a ΔQ̇leg-to-ΔV̇o2 ratio of 7.4. A slow-component V̇o2 of 0.098 l/min was accompanied by a further Q̇leg increase of 0.72 l/min (ΔQ̇leg-to-ΔV̇o2 ratio = 7.3). Thus the time course of Q̇leg was similar to that of muscle V̇o2 (as measured by the phase 2 V̇o2 kinetics), and throughout the on-transient the amplitude of the Q̇leg increase achieved (or exceeded) the Q̇leg-to-V̇o2 ratio steady-state relationship (ratio ∼4.9). Additionally, the V̇o2 slow component was accompanied by a relatively large rise in Q̇leg, with the increased O2 delivery meeting the increased V̇o2. Thus, in heavy-intensity, single-leg, knee-extension exercise, the amplitude and kinetics of blood flow to the exercising limb appear to be closely linked to the V̇o2 kinetics.

Effects of arginine vasopressin on cerebral microvascular pressure

1988 ◽  
Vol 255 (1) ◽  
pp. H70-H76 ◽  
Author(s):  
F. M. Faraci ◽  
W. G. Mayhan ◽  
P. G. Schmid ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Arginine Vasopressin ◽  
Cerebral Arteries ◽  
Aortic Pressure ◽  
Artery Pressure ◽  
Large Arteries ◽  
Pial Artery ◽  
Vessel Resistance

The goal of this study was to examine effects of arginine vasopressin and angiotensin on cerebral microvascular pressure and segmental vascular resistance. We measured pressure (servo-null) in pial arteries that were approximately 200 micron in diameter and cerebral blood flow (microspheres) in anesthetized cats, and we calculated resistance of large and small cerebral vessels. Resistance of large arteries (greater than 200 micron diam) was approximately 45% of total cerebral vascular resistance under control conditions. Vasopressin (40 mU/kg iv) decreased resistance of large arteries by 22 +/- 7%, increased pial artery pressure by 10 +/- 2 mmHg when aortic pressure was maintained at control levels, and increased small vessel resistance by 27 +/- 11%. This increase in small vessel resistance apparently was an autoregulatory response to the increase in pial pressure. Cerebral blood flow was not changed (38 +/- 4 vs. 37 +/- 3 ml.min-1.100 g-1). Intravenous infusion of angiotensin (2 micrograms.kg-1.min-1) increased large artery resistance by 32 +/- 6%, decreased pial artery pressure 6 +/- 3 mmHg with aortic pressure maintained constant, and decreased cerebral blood flow by 12 +/- 1%. Thus circulating vasopressin, at concentrations similar to those observed during hemorrhage, selectively dilates large cerebral arteries and increases microvascular pressure without changes in cerebral blood flow. In contrast to vasopressin, angiotensin selectively increases resistance of large cerebral arteries and decreases cerebral microvascular pressure. Thus vasopressin and angiotensin, at doses that have minimal effects on cerebral blood flow, may play an important role in regulation of cerebral microvascular pressure.

Ultrasound Doppler estimates of femoral artery blood flow during dynamic knee extensor exercise in humans

1997 ◽  
Vol 83 (4) ◽  
pp. 1383-1388 ◽  
Author(s):  
G. Rådegran
Keyword(s):  
Blood Flow ◽  
Femoral Artery ◽  
Coefficient Of Variation ◽  
Knee Extensor ◽  
Dynamic Exercise ◽  
Artery Blood Flow ◽  
Ultrasound Doppler ◽  
Femoral Artery Blood Flow ◽  
Human Limb ◽  
Exercise In Humans

Rådegran, G. Ultrasound Doppler estimates of femoral artery blood flow during dynamic knee extensor exercise in humans. J. Appl. Physiol.83(4): 1383–1388, 1997.—Ultrasound Doppler has been used to measure arterial inflow to a human limb during intermittent static contractions. The technique, however, has neither been thoroughly validated nor used during dynamic exercise. In this study, the inherent problems of the technique have been addressed, and the accuracy was improved by storing the velocity tracings continuously and calculating the flow in relation to the muscle contraction-relaxation phases. The femoral arterial diameter measurements were reproducible with a mean coefficient of variation within the subjects of 1.2 ± 0.2%. The diameter was the same whether the probe was fixed or repositioned at rest (10.8 ± 0.2 mm) or measured during dynamic exercise. The blood velocity was sampled over the width of the diameter and the parabolic velocity profile, since sampling in the center resulted in an overestimation by 22.6 ± 9.1% ( P< 0.02). The femoral arterial Doppler blood flow increased linearly ( r = 0.997, P < 0.001) with increasing load [Doppler blood flow = 0.080 ⋅ load (W) + 1.446 l/min] and was correlated positively with simultaneous thermodilution venous outflow measurements ( r = 0.996, P < 0.001). The two techniques were linearly related (Doppler = thermodilution ⋅ 0.985 + 0.071 l/min; r = 0.996, P < 0.001), with a coefficient of variation of ∼6% for both methods.

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.

Muscle Capillary and Femoral Artery Blood Flow Kinetics following the Onset of Exercise

2006 ◽  
Vol 38 (Supplement) ◽  
pp. S196-S197
Author(s):  
Allison J. Harper ◽  
Leonardo F. Ferreira ◽  
Barbara J. Lutjemeier ◽  
Dana K. Townsend ◽  
Thomas J. Barstow
Keyword(s):  
Blood Flow ◽  
Femoral Artery ◽  
Artery Blood Flow ◽  
Femoral Artery Blood Flow
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