Blood aggregation

Iron-stimulated free radical-mediated processes are not limited to the promotion of peroxidative reactions. For example, Pratico et al. [188] demonstrated that erythrocytes are able to modulate platelet reactivity in response to collagen via the release of free iron, which supposedly catalyzes hydroxyl radical formation by the Fenton reaction. This process resulted in an irreversible blood aggregation and could be relevant to the stimulation by iron overload of atherosclerosis and coronary artery disease. 

Sweeney JD, Labuzzetta JW, Michielson CE, Fitzpatrick JE (1989) Whole blood aggregation using impedance and particle counter methods. Am J Clin Pathol 92 794-797 Turitto VT (1982) Blood viscosity, mass transport, and throm-bogenesis. Prog Hemost Thromb 6 139-177... 

Oura Y. The effects of platelet-activating factor (PAF) on the collagen-induced whole blood aggregation. Rinsho Byori-Japanese J Clin Path 1994 42 63-69... 

An aqueous extract of alfalfa inhibited ADP- and collagen-induced human platelet aggregation but had no effect on arachadonic acid- or thrombin-induced platelet aggregation. Alfalfa inhibited thromboxane B2 synthesis induced by ADP or collagen, and whole blood aggregation induced by collagen (Pierre et al. 2005). 

Physiological responses to prostaglandins encompass a variety of effects Some prostaglandins relax bronchial muscle others contract it Some stimulate uterine con tractions and have been used to induce therapeutic abortions PGEj dilates blood vessels and lowers blood pressure it inhibits the aggregation of platelets and offers promise as a drug to reduce the formation of blood clots... 

Barrier Phenomenon. In red cell filtration, the blood first comes into contact with a screen filter. This screen filter, generally a 7—10-) m filter, does not allow micro aggregate debris through. As the blood product passes through the deeper layer of the filter, the barrier phenomenon continues as the fiber density increases. As the path becomes more and more tortuous the cells are more likely to be trapped in the filter. 

The presence of hemoglohin-S (Hb-S) ia red blood cells leads to the formation of Hquid crystalline aggregates iaside the ceU under conditions of low oxygen tension (43,44). The morbid aggregates ultimately arrange themselves iato a gel-like material composed of long fibers that extend the entire length of the ceU and distort its usual shape. 

Gum-Saline. Gum is a galactoso—gluconic acid having molecular weight of approximately 1500. First used (16) in kidney perfusion experiments, gum—saline enjoyed great popularity as a plasma expander starting from the end of World War I. The aggregation state of gum depends on concentration, pH, salts, and temperature, and its coUoid oncotic pressure and viscosity are quite variable. Conditions were identified (17) under which the viscosity would be the same as that of whole blood. 

Dismption of the endothehal surface of blood vessels expose coUagen fibers and connective tissue. These provide surfaces that promote platelet adherence, platelet release reaction, and subsequent platelet aggregation. Substances Hberated from the platelets stimulate further platelet aggregation, eg, adenosine diphosphate maintain vasoconstriction, eg, serotonin and participate in blood coagulation, eg, platelet Factors III and IV. In addition, the release reaction modifies platelet membranes in a manner that renders phosphoHpid available for coagulation. The thrombin [9002-04-4] elaborated by the coagulation mechanism is a potent agent in the induction of the platelet release reaction. 

Platelet activating factor (PAF) was first identified by its ability (at low levels) to cause platelet aggregation and dilation of blood vessels, but it is now known to be a potent mediator in inflammation, allergic responses, and shock. PAF effects are observed at tissue concentrations as low as 10 M. PAF causes a dramatic inflammation of air passages and induces asthma-like symptoms in laboratory animals. Toxic-shock syndrome occurs when fragments of destroyed bacteria act as toxins and induce the synthesis of PAF. This results in a drop in blood pressure and a reduced... 

FIGURE 15.5 The cascade of activation steps leading to blood clotting. The intrinsic and extrinsic pathways converge at Factor X, and the final common pathway involves the activation of thrombin and its conversion of fibrinogen into fibrin, which aggregates into ordered filamentous arrays that become cross-linked to form the clot. 

Therapeutic Function Blood platelet aggregation inhibitor... 

The formation of a platelet aggregate requires the recruitment of additional platelets from the blood stream to the injured vessel wall. This process is executed through a variety of diffusible mediators which act through G-protein-coupled receptors. The main mediators involved in this process are adenosine diphosphate (ADP), thromboxane A2 (TXA2), and thrombin (factor Ila). These mediators of the second phase of platelet activation are formed in different ways. While ADP is secreted from platelets by exocytosis, the release of TXA2 follows its new formation in activated platelets. Thrombin can be formed on the surface of activated platelets (see Fig. 2). 

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