Platelet-Vessel Wall Interactions in Hemostasis and Thrombosis

2010 ◽  
Vol 2 (1) ◽  
pp. 1-75 ◽  
Author(s):  
Rolando E. Rumbaut ◽  
Perumal Thiagarajan
Keyword(s):  
Vessel Wall ◽  
Wall Interactions

Platelet-vessel wall interactions: Implication of 5-hydroxytryptamine. A review

1984 ◽  
Vol 15 (5-6) ◽  
pp. 612-626 ◽  
Author(s):  
F. Clerck ◽  
J. M. Nueten ◽  
R. S. Reneman
Keyword(s):  
Vessel Wall ◽  
Wall Interactions

Effects of ovariectomy on aggregation, secretion, and metalloproteinases in porcine platelets

2003 ◽  
Vol 284 (5) ◽  
pp. H1679-H1685 ◽  
Author(s):  
Muthuvel Jayachandran ◽  
Whyte G. Owen ◽  
Virginia M. Miller
Keyword(s):  
Platelet Aggregation ◽  
Vessel Wall ◽  
Atp Release ◽  
Ovarian Hormones ◽  
Reticulated Platelets ◽  
Tissue Inhibitors Of Metalloproteinase ◽  
Atp Secretion ◽  
Sexually Mature ◽  
Wall Interactions ◽  
Expression And Activity

Differences in the aggregation and release of growth factors including matrix metalloproteinases (MMPs) after loss of ovarian hormones could contribute to an exaggerated response to injury in arteries of ovariectomized animals. Therefore, experiments were designed to compare aggregation, dense granular ATP release, expression of MMPs (MMP-2, MMP-9, and MMP-14) and tissue inhibitors of metalloproteinase (TIMP-1 and TIMP-2) in circulating platelets from sexually mature (7 mo old) gonadally intact and ovariectomized (4 wk) female pigs. Numbers of circulating platelets did not change after ovariectomy, but the percentage of reticulated platelets increased significantly. Platelet aggregation and dense granular ATP secretion also increased significantly with ovariectomy. In platelet lysates, active MMP-2 increased, whereas MMP-14 significantly decreased, after ovariectomy; the expression of TIMP-1, TIMP-2, and P-selectin did not change. These results suggest that platelet turnover, aggregation, and ATP secretion increase with ovariectomy. Also, ovarian hormones selectively regulate the expression and activity of MMPs in porcine platelets. Increased platelet aggregation and activity of MMP-2 would alter platelet-platelet and platelet-vessel wall interactions, contributing to an exaggerated response to injury with loss of ovarian hormones.

Endothelial glycocalyx thickness and platelet-vessel wall interactions during atherogenesis

2011 ◽  
Vol 106 (11) ◽  
pp. 939-946 ◽  
Author(s):  
Mirjam oude Egbrink ◽  
Viviane Heijnen ◽  
Remco Megens ◽  
Wim Engels ◽  
Hans Vink ◽  
...  
Keyword(s):  
Vessel Wall ◽  
Laser Scanning ◽  
Ex Vivo ◽  
Laser Scanning Microscopy ◽  
Endothelial Glycocalyx ◽  
Knock Out ◽  
Two Photon ◽  
Common Carotid Arteries ◽  
Wall Interactions

SummaryThe endothelial glycocalyx (EG), the luminal cover of endothelial cells, is considered to be atheroprotective. During atherogenesis, platelets adhere to the vessel wall, possibly triggered by simultaneous EG modulation. It was the objective of this study to investigate both EG thickness and platelet-vessel wall interactions during atherogenesis in the same experimental model. Intravital fluorescence microscopy was used to study platelet-vessel wall interactions in vivo in common carotid arteries and bifurcations of C57bl6/J (B6) and apolipoprotein E knock-out (ApoE-/-) mice (age 7 – 31 weeks). At the same locations, EG thickness was determined ex vivo using two-photon laser scanning microscopy. In ApoE-/- bifurcations the overall median level of adhesion was 48 platelets/mm2 (interquartile range: 16 – 80), which was significantly higher than in B6 bifurcations (0 (0 – 16), p = 0.001). This difference appeared to result from a significant age-dependent increase in ApoE-/- mice, while no such change was observed in B6 mice. At the same time, the EG in ApoE-/- bifurcations was significantly thinner than in B6 bifurcations (2.2 vs. 2.5 μm, respectively; p < 0.05). This resulted from the fact that in B6 bifurcations EG thickness increased with age (from 2.4 μm in young mice to 3.0 μm in aged ones), while in bifurcations of ApoE-/- mice this growth appeared to be absent (2.2 μm at all ages). During atherogenesis, platelet adhesion to the wall of the carotid artery bifurcation increases significantly. At the same location, EG growth with age is hampered. Therefore, glycocalyx-reinforcing strategies could possibly ameliorate atherosclerosis.

Platelet–Vessel Wall Interactions

2017 ◽  
pp. 1158-1162
Author(s):  
Thomas G. Diacovo
Keyword(s):  
Vessel Wall ◽  
Wall Interactions

Blood cell—Vessel wall interactions

1992 ◽  
Vol 12 (1) ◽  
pp. 55-58 ◽  
Author(s):  
Jean-Luc Wautier
Keyword(s):  
Blood Cell ◽  
Vessel Wall ◽  
Wall Interactions

Platelet-Vessel Wall Interactions in von Willebrand’s Disease

1979 ◽  
Author(s):  
M.I. Barnhart ◽  
R.M. Wilkins ◽  
J.M. Lusher
Keyword(s):  
Vessel Wall ◽  
Ex Vivo ◽  
Umbilical Vein ◽  
Vein Wall ◽  
Qualitative And Quantitative ◽  
Perfusion Model ◽  
Vascular Defect ◽  
Umbilical Cords ◽  
Wall Interactions ◽  
Scanning Electron

Adhesion of von willehrand (vW) platelets (P) from 12 patients was tested in an ex vivo human umbilical vein perfusion model. Experiments (42) employed twelve umbilical cords from Caesarian sections and P (fetal, adult and vW) either washed (with apyrase protection) or used as P rich plasma or whole blood. FVIII antigen (FVIII:ag), Ristocetin co-factor (RCF) and FVIII procoagulant were measured in blood and umbilical vein effluents. Either hypoxia or epinephrine pretreatment of vein released FVIII:ag and RCF into perfusates. Binding of a marker (latex linked anti-human FVIII:ag) demonstrated that FVIII:ag became exposed at endothelial surfaces. Scanning electron microscopy displayed vWP-vessel interactions. Although vWP adhered to injured vein wall, both qualitative and quantitative differences existed which related to the plasma RCF level. The vWP were less adhesive to exposed subendothelium than were control fetal or adult P. The vWP had less surface activity, spreading and fewer pseudopods. Vein pretreatment with FVIII antibody partly blocked P adhesion. Perfusion of cryoprecipitate with vWP improved their adhesion, activation and aggregation. These observations further establish the model's utility and validity for studies aimed at discovering the nature and extent of the vascular defect in various P disorders. The model seems especially well suited for testing impacts of P and/or endothelial cell reactive agents on platelet-vessel wall interactions.

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