Irradiation and Blood Vessel Prostaglandin Metabolism

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.

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Cancer Research Highlights: Blood Vessel Membrane Proteins Help Target Imaging Agents and Drugs

PsycEXTRA Dataset ◽

10.1037/e380682004-004 ◽

2004 ◽

Author(s):

Keyword(s):

Cancer Research ◽

Membrane Proteins ◽

Blood Vessel ◽

Imaging Agents ◽

Target Imaging

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

Thrombosis and Haemostasis ◽

10.1055/s-0038-1647259 ◽

1990 ◽

Vol 64 (01) ◽

pp. 091-096 ◽

Cited By ~ 6

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.

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

Thrombosis and Haemostasis ◽

10.1055/s-0038-1651902 ◽

1977 ◽

Vol 38 (04) ◽

pp. 0831-0849 ◽

Cited By ~ 1

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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Blood Vessel Tissue

10.32388/gpd4kf ◽

2020 ◽

Author(s):

Keyword(s):

Blood Vessel

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COMPARISON OF ANTIHYPERTENSIVE EFFECT OF MOXONIDINE VERSUS CLONIDINE IN RENAL FAILURE PATIENTS.

Journal of Drug Discovery and Therapeutics ◽

10.32553/jddt.v6i9.440 ◽

2018 ◽

Vol 6 (9) ◽

Author(s):

DR.MATHEW GEORGE ◽

DR.LINCY JOSEPH ◽

MRS.DEEPTHI MATHEW ◽

ALISHA MARIA SHAJI ◽

BIJI JOSEPH ◽

...

Keyword(s):

Blood Pressure ◽

Renal Failure ◽

Blood Flow ◽

Blood Vessel ◽

Blood Vessels ◽

High Blood Pressure ◽

Antihypertensive Effect ◽

The Body ◽

Ability To Work ◽

Blood Flows

Blood pressure is the force of blood pushing against blood vessel walls as the heart pumps out blood, and high blood pressure, also called hypertension, is an increase in the amount of force that blood places on blood vessels as it moves through the body. Factors that can increase this force include higher blood volume due to extra fluid in the blood and blood vessels that are narrow, stiff, or clogged(1). High blood pressure can damage blood vessels in the kidneys, reducing their ability to work properly. When the force of blood flow is high, blood vessels stretch so blood flows more easily. Eventually, this stretching scars and weakens blood vessels throughout the body, including those in the kidneys.

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