Blood Vessel Mechanics

2008 ◽  
pp. 392-402
Author(s):  
Ruth Okamoto
Keyword(s):  
Blood Vessel ◽  
Vessel Mechanics

The Influence of Initial Stresses on Blood Vessel Mechanics

2003 ◽  
Vol 03 (02) ◽  
pp. 215-229 ◽  
Author(s):  
Paola Nardinocchi ◽  
Luciano Teresi
Keyword(s):  
Blood Flow ◽  
Stress State ◽  
Blood Vessel ◽  
Mechanical Behavior ◽  
Large Deformations ◽  
Blood System ◽  
Initial Stresses ◽  
Small Deformations ◽  
Vessel Mechanics

In order to account for the in vivo conditions of blood vessels, we investigate the mechanical behavior of a stressed tube-like membrane when small deformations are superimposed on large deformations: the latter simulate the stretches present in the in vivo arteries while the superimposed deformations account for the small — but essential for the blood propagation — deformations due to the pulsatile nature of the blood flow. Our aim is to discuss how a stress state influence the response of the vessel-blood system.

An alternate formulation of blood vessel mechanics and the meaning of the in vivo property

1995 ◽  
Vol 28 (6) ◽  
pp. 679-687 ◽  
Author(s):  
Louis J. Brossollet ◽  
Raymond P. Vito
Keyword(s):  
Blood Vessel ◽  
Vessel Mechanics

An Ultrastructural Study of Pericytes

1968 ◽  
Vol 26 ◽  
pp. 66-67
Author(s):  
T. M. Murad ◽  
E. von Haam
Keyword(s):  
Plasma Membrane ◽  
Endothelial Cell ◽  
Basement Membrane ◽  
Blood Vessel ◽  
Vascular Endothelial Cells ◽  
Myoepithelial Cells ◽  
Capillary Blood ◽  
The Body ◽  
Capillary Blood Vessel ◽  
Outer Plasma Membrane

Pericytes are vascular satellites present around capillary blood vessels and small venules. They have been observed in almost every tissue of the body and are thought to be related to vascular smooth muscle cells. Morphologically pericytes have great similarity to vascular endothelial cells and also slightly resemble myoepithelial cells.The present study describes the ultrastructural morphology of pericytes in normal breast tissue and in benign tumor of the breast. The study showed that pericytes are ovoid or elongated cells separated from the endothelial cell of the capillary blood vessel by the basement membrane of endothelial cell. The nuclei of pericytes are often very distinctive. Although some are round, oval, or elongated, others show marked irregularity and infolding of the nuclear membrane. The cytoplasm shows mono-or bipolar extension in which the cytoplasmic organelles are located (Fig. 1). These cytoplasmic extensions embrace the capillary blood vessel incompletely. The plasma membrane exhibits multiple areas of focal condensation called hemidesmosomes (Fig. 2, arrow). A variable number of pinocytotic vesicles are frequently seen lining the outer plasma membrane. Normally pericytes are surrounded by a basement membrane which is found more consistently on the outer plasma membrane separating the pericytes from the stromal connective tissue.

Effect of Ridogrel on Vascular Contractions Gaused by Vasoactive Substances Released during Platelet Activation

1990 ◽  
Vol 64 (01) ◽  
pp. 091-096 ◽  
Author(s):  
W J Janssens ◽  
F J S Cools ◽  
L A M Hoskens ◽  
J M Van Nueten
Keyword(s):  
Smooth Muscle ◽  
Blood Vessel ◽  
Platelet Activation ◽  
Prostaglandin F2α ◽  
Thromboxane A2 ◽  
Femoral Arteries ◽  
Vasoactive Substances ◽  
Caudal Artery ◽  
Isolated Rat ◽  
Rat Platelets

SummaryRidogrel (6.3 × 10−6 to 10−4 M) inhibited contractions of isolated rat caudal arteries and rabbit femoral arteries caused by U-46619. The slope of an Arunlakshana-Schild plot (pA2-value: 3.4 × 10−6 M) on the caudal artery was slightly higher than one (1.14). This effect was maximal within}D min of incubation of the blood vessel with the compound and easily reversible. Ridogrel antagonised contractions of isolated rabbit femoral arteries caused by prostaglandin Fzo2α in the same concentration range. Ridogrel also inhibited contractions induced by aggregating rat platelets on isolated rat caudal arteries (itt the presence of ketanserin 4 × 10−7 M) and on isolated rabbit pulmonary and femoral arteries (in the absence of ketanserin). Ridogrel had no effect on Ca2+-induced contractions in depolarised isolated rabbit femoral arteries, and at 10−4 M antagonised serotonin-induced contractions in this blood vessel. Its effect on serotonin-induced contractions was statistically significant but very small on isolated rat caudal arteries. These observations indicate that ridogrel is an antagonist of prostaglandin endoperoxide/thromboxane A2 and prostaglandin F2α raCeptors on vascular smooth muscle.

The Intravascular Generation of Fibrinogen Derivatives and the Blood Vessel Wall in Venous Thrombosis and Disseminated Intravascular Coagulation

1977 ◽  
Vol 38 (04) ◽  
pp. 0831-0849 ◽  
Author(s):  
Gwendolyn J. Stewart
Keyword(s):  
Blood Vessel ◽  
Venous Thrombosis ◽  
Vessel Wall ◽  
Fluid Phase ◽  
Primary Site ◽  
Blood Vessel Wall ◽  
Fibrin Deposition ◽  
Tissue Destruction ◽  
Fibrin Formation ◽  
Rich Material

SummaryBoth deep venous thrombosis and DIC are intermediate mechanisms of disease – both are a consequence of the deposition of fibrin-rich material in blood vessels some distance from the primary site of tissue destruction. The great difference in the sites of fibrin deposition may depend on the extent and site of activation of the clotting mechanism. DIC likely occurs in the fluid phase of the blood as a consequence of massive fibrin formation while thrombosis results from limited fibrin formation at the interface between blood and vessel wall. Leukocytes may be essential for attaching thrombi to the vessel wall in many places.

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