Thrombocyte

Comparable with red blood cells, desialylation of platelets leads to a rapid removal from the circulation (Choi et al. 1972, Greenberg et al. 1979). Despite contradictory results (Nurden and Caen 1976, Gartner et al. 1977, Patschke et al. 1977), there are valid indications that membrane-bound sialic acid does play an important role in the adhesion and aggregation of thrombocytes. (For further details see section IV, Blood Clotting.) 

Desialylated lymphocytes lose their orientation in the organism, show an increased agglutinability and are reversibly trapped in the liver (Woodruff and Gesner 1969). After resialylation during the following two days the lymphocytes leave the liver again and show normal behaviour in the circulation (Woodruff 

Recent studies have shown that T-lymphocytes of peritoneal origin possess both NeuSAc and Neu5Gc on their surface (Kaufmann et al 1981). Since this is the first demonstration of Neu5Gc on murine lymphocytes, it would be of special interest to learn, whether this derivative has the same properties in respect to migration behaviour and life span of cell. 

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The formed elements consist primarily of red blood cells, ie, erythrocytes. Less than 1 /600 of the total volume of the formed elements is composed of white blood cells, ie, leukocytes, and less than 1/800 are platelets, ie, thrombocytes. Table 1 gives the typical constitution of human blood. 

Primary blood components iaclude plasma, red blood cells (erythrocytes), white blood cells (leukocytes), platelets (thrombocytes), and stem cells. Plasma consists of water dissolved proteias, ie, fibrinogen, albumins, and globulins coagulation factors and nutrients. The principal plasma-derived blood products are siagle-donor plasma (SDP), produced by sedimentation from whole blood donations fresh frozen plasma (FFP), collected both by apheresis and from whole blood collections cryoprecipitate, produced by cryoprecipitation of FFP albumin, collected through apheresis and coagulation factors, produced by fractionation from FFP and by apheresis (see Fractionation, blood-plasma fractionation). 

There are undifferentiated stem cells of the blood elements in the bone marrow that differentiate and mature into erythrocytes, (red blood cells), thrombocytes (platelets), and white blood cells (leukocytes and lymphocytes). The production of erythrocytes is regulated by a hormone, erythropoietin (see the section on kidney toxicity), that is synthetized and excreted by the kidney. An increase in the number of premature erythrocytes is an indication of stimulation of erythropoiesis, i.e., increased production of erythrocytes in anemia due to continuous bleeding. 

Animal cells can modify arachidonic acid and other polyunsaturated fatty acids, in processes often involving cyclization and oxygenation, to produce so-called local hormones that (1) exert their effects at very low concentrations and (2) usually act near their sites of synthesis. These substances include the prostaglandins (PG) (Figure 25.27) as well as thromboxanes (Tx), leukotrienes, and other hydroxyeicosanoic acids. Thromboxanes, discovered in blood platelets (thrombocytes), are cyclic ethers (TxBg is actually a hemiacetal see Figure 25.27) with a hydroxyl group at C-15. 

MANAGING HONE MARROW SUPPRESSION. Bone marrow suppression is a potentially dangerous adverse reaction resulting in decreased production of blood cells. Bone marrow suppression is manifested by abnormal laboratory test results and clinical evidence of leukopenia, thrombocytopenia, or anemia For example, there is a decrease in the white blood cells or leukocytes (leukopenia), a decrease in the thrombocytes (thrombocytopenia), and a decrease in the red blood cells, resulting in anemia Fhtients with leukopenia have a decreased resistance to infection, and the nurse must monitor them closely for any signs of infection. 

In Section 24.3, use of electrosorption for effluent purification was mentioned. The same principle of an electrochemically controlled hemosorption (sorptive blood purification) is used in modem toxicology to extract toxins from blood. By appropriate potential control of the carbon sorbent, particular toxins can be removed selectively without traumatizing the blood, that is, without removing essential blood components such as the thrombocytes. 

The third of the cellular elements within the blood are the platelets (thrombocytes). Platelets are actually small, round or oval cell fragments. They are about 2 to 4 pm in diameter and have no nuclei. Platelets are formed in the red bone marrow as pinched-off portions of the very large megakaryocytes. Each megakaryocyte, which is confined to the bone marrow, can produce... 

Hematological Effects. Routine blood parameters (hemoglobin, erythrocyte, leukocyte and thrombocyte levels) measured in 11 hexachloroethane workers did not differ from those of the controls (Selden et al. 1994). Plasma hexachloroethane levels in these workers, who wore protective equipment, were 7.3 + 6.04 pg/L at the time of the hematological analysis and 0.08 0.14 gg/L before production resinned (Selden et al. 1993). Mild skin and mucous membrane irritation were reported in the exposed group, suggesting that exposure may have been through either the inhalation or dermal routes of exposure. 

Blood is the transport medium of the body. Plasma, which accounts for approximately 60% of the total volume, carries a wide range of small and medium-sized metabolites some are simply dissolved in solution (93% of the plasma is water), others are carried by specific carrier proteins. The chemical composition of the plasma is complex and reflects the chemical composition inside cells, which is why blood tests are so commonly used in diagnosis to see the biochemical events occurring in tissues. The formed cellular elements of the blood perform several functions defence against blood loss from bleeding (platelets, also called thrombocytes), defence against infection and immune surveillance (white cells, leucocytes), and gas transport and pH buffering (red cells, erythrocytes). 

Platelets (also called thrombocytes), the smallest of the formed elements of the blood, are formed by fragmentation of megakaryocytes. Each megakaryocyte (mega = big , karyo = nucleus ) can produce approximately 3000 individual platelets and a total of about 2 x 1011 platelets are formed each day. 

In addition to erythrocytes, blood contains white blood cells, called leukocytes, of several types, and platelets, also called thrombocytes, which control blood clotting. Hematopoiesis (from the Greek, haimo, for blood, and poiein for to make ) is the process by which the elements of the blood are formed. The marrow of bone contains so-called stem cells which are immature predecessors of these three types of blood cells. Chemicals that are toxic to bone marrow can lead to anemia (decreased levels of erythrocytes), leukopenia (decreased numbers of leukocytes), or thrombocytopenia. Pancytopenia, a severe form of poisoning, refers to the reduction in circulatory levels of all three elements of the blood. One or more of these conditions can result from sufficiently intense exposure to chemicals such as benzene, arsenic, the explosive trinitrotoluene (TNT), gold, certain drugs, and ionizing radiation. Health consequences can range... 

The fats also have a plastic function as they are included in cell membranes and other cell structures. The central and peripheral nervous systems are rich in lipids. PNFA are included in cell membranes, with their most significant function being the synthesis of cell hormones — prostaglandins. The properties of cell membranes as well as their interaction with external factors depend on the relation of PNFA concentration in cell components. In humans, prostaglandins are created not only in tissues but also in thrombocytes (thromboxanes) and in leucocytes (leukotrienes). The biological action of thrombocytes is extremely variant and depends on PNFA type which are the basis for fatty acid creation. 

Medicinal thrombocytopenia can emerge under the use of different medicines, including interferon. The main mechanism of medicinal thrombocytopenia pathogenesis is assisted by the destruction of thrombocytes by the complement which is activated during antibody preparation. On withdrawal, the content of thrombocytes in blood is normalized. The formation of antibodies to thrombocytes in patients with viral hepatitis C occurs due to the destruction of membrane glycoproteins by the viruses. 

Variant 1. The patients with the absence of thrombocyte number changes are recommended prophylactic doses of Griitization (Grin Mix — from 5-10 mL per day, Grin Pro — from 3-7 capsules per day or the 2.5-5 mg of the powder per day). While the number of thrombocytes is dimiitished slightly, the dose of Grinization is being increased. 

Variant 2. The patients with small thrombocyte number in the blood (not less than 100 x 10 in liter) are recommended, during the antiviral therapy, medium doses of Grinization (Grin Mix — 15 mL per day. Grin Pro — 10 capsules per day, or 7 g of the powder per day). With the tendency of decreasing thrombocyte number, the dose should be diminished to the prophylactic level. 

Variant 3. The patients with a serious decrease of thrombocytes number in blood (less than 90 x 10 in 1 L) before antiviral therapy application during 14 days are recommended to use high doses of Grinization (Grin Mix — from 25 to 33 mL, Grin Pro — from 12 to 16 g per day), till the number of thrombocytes is increased up to 100 x 10 in liters or more. For the period of antiviral therapy application, Grinization is recommended in medium doses. While the thrombocyte number is stabilized, the Grinization doses should be diminished up to the prophylactic ones. 

Variant 4. The patients with the thrombocytes number s decrease up to 80 X 10 in liter and less, without the antiviral therapy stop, the Grinization is recommended in high doses and with the thrombocytes number increase, the treatment is still performed at the background of high Grinization doses. While the number of thrombocytes is stabilized in the range of 100-150 x 10 in liter, the Grinization dose is diminished to a medium level if the thrombocytes number decrease, the dose should be increased. 

The positive influence of the Grinization on thrombocyte number is caused by the immune-modulating, cytoprotecting, antioxidant and apoptosis-modulating action of the biologically active components of the Grinization multi-nutrient complex. 

Ketanserin is an antagonist at 5-HT2A receptors and produces antihypertensive effects, as well as inhibition of thrombocyte aggregation. Whether 5-HT antagonism accounts for its antihypertensive effect remains questionable, because ketanserin also blocks a-adren-oceptors. 

Upon vascular injury, the coagulation system is activated thrombocytes and fibrin molecules coalesce into a plug ... 

Massive use of diuretics entails a hazard of adverse effects (A) (1) the decrease in blood volume can lead to hypotension and collapse (2) blood viscosity rises due to the increase in eryth-ro- and thrombocyte concentration, bringing an increased risk of intravascular coagulation or thrombosis. 

Thrombocytes are cell fragments that arise in the bone marrow from large precursor cells, the megakaryocytes. Their task is to promote hemostasis (see p. 290). 

The solid elements in the blood are the erythrocytes (red blood cells), leukocytes (white blood cells), and thrombocytes (platelets). 

Following injury to blood vessels, hemostasis ensures that blood loss is minimized. Initially, thrombocyte activation leads to contraction of the injured vessel and the formation of a loose clot consisting of thrombocytes (hemostasis). Slightly later, the action of the enzyme thrombin leads to the formation and deposition in the thrombus of polymeric fibrin (coagulation, blood clotting). The coagulation process is discussed here in detail. 

Both pathways depend on the presence of activated thrombocytes, on the surface of which several reactions take place. For example, the prothrombinase complex (left) forms when factors Xa and 11, with the help of Va, bind via Ca "" ions to anionic phospholipids in the thrombocyte membrane. For this to happen, factors 11 and X have to contain the non-proteinogenic amino acid y-carboxygluta-mate (Gla see p. 62), which is formed in the liver by post-translational carboxylation of the factors. The Gla residues are found in groups in special domains that create contacts to the Ca "" ions. Factors Vll and IX are also linked to membrane phospholipids via Gla residues. 

Acetylsalicylic acid and related non-steroidal anti-inflammatory drugs (NSAIDs) selectively inhibit the cyclooxygenase activity of prostaglandin synthase [2] and consequently the synthesis of most eicosanoids. This explains their analgesic, antipyretic, and antirheumatic effects. Frequent side effects of NSAIDs also result from inhibition of eicosanoid synthesis. For example, they impair hemostasis because the synthesis of thromboxanes by thrombocytes is inhibited. In the stomach, NSAIDs increase HCl secretion and at the same time inhibit the formation of protective mucus. Long-term NSAID use can therefore damage the gastric mucosa. 

Hormone-controlled lipases Thrombocyte aggregation Pain production Inflammatory response... 

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