Acute increase in femoral artery resistance in response to direct physical stimuli in the human fetus

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.

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Mechanical and Physical Regulation of Fibroblast–Myofibroblast Transition: From Cellular Mechanoresponse to Tissue Pathology

Frontiers in Bioengineering and Biotechnology ◽

10.3389/fbioe.2020.609653 ◽

2020 ◽

Vol 8 ◽

Author(s):

Mirko D'Urso ◽

Nicholas A. Kurniawan

Keyword(s):

Cardiac Fibrosis ◽

Morphological Properties ◽

Pathological State ◽

Cell Behaviors ◽

Protein Deposition ◽

Cell Substrate ◽

Physical Stimuli ◽

A Cell ◽

Acute Increase ◽

Phenotype Transition

Fibroblasts are cells present throughout the human body that are primarily responsible for the production and maintenance of the extracellular matrix (ECM) within the tissues. They have the capability to modify the mechanical properties of the ECM within the tissue and transition into myofibroblasts, a cell type that is associated with the development of fibrotic tissue through an acute increase of cell density and protein deposition. This transition from fibroblast to myofibroblast—a well-known cellular hallmark of the pathological state of tissues—and the environmental stimuli that can induce this transition have received a lot of attention, for example in the contexts of asthma and cardiac fibrosis. Recent efforts in understanding how cells sense their physical environment at the micro- and nano-scales have ushered in a new appreciation that the substrates on which the cells adhere provide not only passive influence, but also active stimulus that can affect fibroblast activation. These studies suggest that mechanical interactions at the cell–substrate interface play a key role in regulating this phenotype transition by changing the mechanical and morphological properties of the cells. Here, we briefly summarize the reported chemical and physical cues regulating fibroblast phenotype. We then argue that a better understanding of how cells mechanically interact with the substrate (mechanosensing) and how this influences cell behaviors (mechanotransduction) using well-defined platforms that decouple the physical stimuli from the chemical ones can provide a powerful tool to control the balance between physiological tissue regeneration and pathological fibrotic response.

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Increased vascular resistance during complement-activated plasma infusion in swine

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.253.1.h58 ◽

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.

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Proximal deep venous thrombosis following PTA of the superficial femoral artery – an obligation to disclose a complication that is rarely taken into account

VASA ◽

10.1024/0301-1526.35.1.41 ◽

2006 ◽

Vol 35 (1) ◽

pp. 41-44 ◽

Cited By ~ 5

Author(s):

Klein-Weigel ◽

Pillokat ◽

Klemens ◽

Köning ◽

Wolbergs ◽

...

Keyword(s):

Venous Thrombosis ◽

Deep Venous Thrombosis ◽

Femoral Artery ◽

Superficial Femoral Artery ◽

Rare Complication ◽

Femoral Vein ◽

Vein Thrombosis ◽

Explicit Information ◽

Life Threatening ◽

Legal Consequences

We report two cases of femoral vein thrombosis after arterial PTA and subsequent pressure stasis. We discuss the legal consequences of these complications for information policies. Because venous thrombembolism following an arterial PTA might cause serious sequel or life threatening complications, there is a clear obligation for explicit information of the patients about this rare complication.

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Crush implantation of a self-expanding interwoven stent over a subintimally recanalized standard stent in a TASC D lesion of the superficial femoral artery

VASA ◽

10.1024/0301-1526/a000238 ◽

2012 ◽

Vol 41 (6) ◽

pp. 458-462 ◽

Cited By ~ 4

Author(s):

Vogel ◽

Strothmeyer ◽

Cebola ◽

A. Katus ◽

Blessing

Keyword(s):

Femoral Artery ◽

Superficial Femoral Artery ◽

Popliteal Artery ◽

Duplex Ultrasound ◽

Stent Fracture ◽

Nitinol Stent ◽

Nitinol Stents ◽

Walking Capacity ◽

Radial Strength ◽

Good Treatment Option

We demonstrate feasibility of implantation of a self-expanding interwoven nitinol stent in a claudicant, where recanalization attempt of a heavily calcified, occluded superficial femoral artery (TASC D lesion) was complicated by a previously implanted, fractured standard stent. Wire passage through the occlusion and beyond the fractured stent could only be achieved through the subintimal space. A dedicated reentry device was used to allow distal wire entry into the true lumen at the level of the popliteal artery. Despite crushing of the fractured stent with a series of increasingly sized standard balloons, a significant recoil remainded in the area of the crushed stent. To secure patency of the femoro-popliteal artery we therefore decided to implant the novel self-expanding interwoven nitinol stent (Supera Veritas (TM), IDEV), whose unique feature is an exceptional high radial strength. Patient presented asymptomatic without any impairment of his walking capacity at three month follow up and duplex ultrasound confirmed patency of the stent. Subintimal recanalizations can be complicated by previously implanted stents, in particular in the presence of stent fracture, where intraluminal wire passage often can not be achieved. Considering the high radial strength and fracture resistance, interwoven nitinol stents represent a good treatment option in those challenging cases and they can be used to crush standard nitinol and ballonexpandable stents.

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Impact of thrombin injection in femoral artery pseudoaneurysms with AV-fistula

VASA ◽

10.1024/0301-1526/a000734 ◽

2018 ◽

Vol 47 (6) ◽

pp. 437-438

Author(s):

Oliver J. Müller ◽

Norbert Frey

Keyword(s):

Femoral Artery ◽

Thrombin Injection ◽

Av Fistula

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Post-operative Staphylococcus aureus infection of a superficial femoral artery stent

VASA ◽

10.1024/0301-1526/a000306 ◽

2013 ◽

Vol 42 (5) ◽

pp. 382-386

Author(s):

Karim Gariani ◽

Marc Righini ◽

Marco Roffi ◽

Gino Gemayel ◽

Damiano Mugnai ◽

...

Keyword(s):

Staphylococcus Aureus ◽

Femoral Artery ◽

Superficial Femoral Artery ◽

Aureus Infection

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P550 Comparison of intravascular ultrasound and colour coded duplex sonography for the evaluation of femoral artery stenoses

European Heart Journal ◽

10.1016/s0195-668x(03)93988-1 ◽

2003 ◽

Vol 24 (5) ◽

pp. 90

Author(s):

J RIEBER

Keyword(s):

Intravascular Ultrasound ◽

Femoral Artery ◽

Duplex Sonography

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Comparative Arterial Antithrombotic Activity of Clopidogrel and Acetyl Salicylic Acid in the Pig

Thrombosis and Haemostasis ◽

10.1055/s-0038-1646307 ◽

1992 ◽

Vol 68 (05) ◽

pp. 500-505 ◽

Cited By ~ 32

Author(s):

Ch M Samama ◽

Ph Bonnin ◽

M Bonneau ◽

G Pignaud ◽

E Mazoyer ◽

...

Keyword(s):

Platelet Aggregation ◽

Femoral Artery ◽

Bleeding Time ◽

Ex Vivo ◽

Flow Reduction ◽

Cyclic Flow ◽

Left Femoral Artery ◽

Before And After ◽

The Right ◽

Induced Aggregation

SummaryWe investigated the comparative antithrombotic properties of clopidogrel, an analogue of ticlopidine, and aspirin, using the Folts' model on femoral arteries in 22 pigs. On each animal, clopidogrel or aspirin were used to treat the thrombotic process on the left femoral artery and to prevent this process on the right femoral artery. Sequentially: an injury and stenosis were carried out on the left femoral artery; the thrombotic process was monitored with a Doppler during a 30-min observation period for cyclic flow reductions or permanent cessation of flow; after the first cyclic flow reduction occurred, clopidogrel (5 mg kg-1) or aspirin (2.5, 5, 100 mg kg-1) were injected intravenously; if cyclic flow reductions were abolished, epinephrine (0.4 µg kg-1 min-1) was injected to try to restore cyclic flow reductions and/or permanent cessation of flow; then injury and stenosis were applied on the right femoral artery. Before and after injection of clopidogrel or aspirin, ear immersion bleeding times and ex-vivo platelet aggregation were performed. Clopidogrel (n = 7) abolished cyclic flow reductions in all animals and epinephrine did not restore any cyclic flow reduction. On the right femoral artery, cyclic flow reductions were efficiently prevented, even for two injuries. Basal bleeding time (5 min 28) was lengthened (>15 min, 30 min after clopidogrel and remained prolonged even after 24 h). ADP-induced platelet aggregation was inhibited (more than 78%). Comparatively, aspirin had a moderate and no dose-dependent effect. Aspirin 2.5 mg kg-1 (n = 6) abolished cyclic flow reductions in 2 animals, CFR reoccurred spontaneously in one animal and epinephrine restored it in a second animal. Aspirin 5 mg kg-1 (n = 6) abolished cyclic flow reductions in only 3 animals and epinephrine always restored it. Aspirin 100 mg kg-1 (n = 3) was unable to abolish cyclic flow reductions. On the right femoral artery, aspirin did not significantly prevent cyclic flow reductions which occurred in all animals after one (n = 14) or two injuries (n = 1), except for one animal. Basal bleeding time was lengthened but it shortened rapidly, reaching its basal value after 24 h. ADP-induced aggregation was not significantly inhibited, whereas arachidonic acid induced aggregation was always inhibited. Clopidogrel appears as a more potent antithrombotic drug than aspirin in this model, in treating and preventing spontaneous or epinephrine-induced cyclic flow reductions and lengthening bleeding time.

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