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Chapter: Medical Physiology: Hemostasis and Blood Coagulation

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Anticoagulants for Clinical Use

In some thromboembolic conditions, it is desirable to delay the coagulation process. Various anticoagulants have been developed for this purpose.

Anticoagulants for Clinical Use

In some thromboembolic conditions, it is desirable to delay the coagulation process. Various anticoagulants have been developed for this purpose. The ones most useful clinically are heparin and the coumarins.

Heparin as an Intravenous Anticoagulant

Commercial heparin is extracted from several differ-ent animal tissues and prepared in almost pure form.

Injection of relatively small quantities, about 0.5 to 1 mg/kg of body weight, causes the blood-clotting time to increase from a normal of about 6 minutes to 30 or more minutes. Furthermore, this change in clotting time occurs instantaneously, thereby immediately pre-venting or slowing further development of a throm-boembolic condition.

The action of heparin lasts about 1.5 to 4 hours. The injected heparin is destroyed by an enzyme in the blood known as heparinase.

Coumarins as Anticoagulants

When a coumarin, such as warfarin, is given to a patient, the plasma levels of prothrombin and Factors VII, IX, and X, all formed by the liver, begin to fall, indicating that warfarin has a potent depressant effect on liver formation of these compounds. Warfarin causes this effect by competing with vitamin K for reactive sites in the enzymatic processes for formation of prothrombin and the other three clotting factors, thereby blocking the action of vitamin K.

After administration of an effective dose of war-farin, the coagulant activity of the blood decreases to about 50 per cent of normal by the end of 12 hours and to about 20 per cent of normal by the end of 24 hours. In other words, the coagulation process is not blocked immediately but must await the natural consumption of the prothrombin and the other affected coagulation factors already present in the plasma. Normal coagu-lation usually returns 1 to 3 days after discontinuing coumarin therapy.

Prevention of Blood Coagulation Outside the Body

Although blood removed from the body and held in a glass test tube normally clots in about 6 minutes, blood collected in siliconized containers often does not clot for 1 hour or more. The reason for this delay is that preparing the surfaces of the containers with silicone prevents contact activation of platelets and Factor XII, the two principal factors that initiate the intrinsic clot-ting mechanism. Conversely, untreated glass contain-ers allow contact activation of the platelets and Factor XII, with rapid development of clots.

Heparin can be used for preventing coagulation ofblood outside the body as well as in the body. Heparin is especially used in surgical procedures in which the blood must be passed through a heart-lung machine or artificial kidney machine and then back into the person.

Various substances that decrease the concentrationof calcium ions in the blood can also be used for pre-venting blood coagulationoutside the body. For instance, a soluble oxalate compound mixed in a very small quantity with a sample of blood causes precipi-tation of calcium oxalate from the plasma and thereby decreases the ionic calcium level so much that blood coagulation is blocked.

Any substance that deionizes the blood calcium will prevent coagulation. The negatively charged citrate ion is especially valuable for this purpose, mixed with blood usually in the form of sodiumammonium, or potassium citrate. The citrate ion combines withcalcium in the blood to cause an un-ionized calcium compound, and the lack of ionic calcium prevents coagulation. Citrate anticoagulants have an important advantage over the oxalate anticoagulants because oxalate is toxic to the body, whereas moderate quan-tities of citrate can be injected intravenously. After injection, the citrate ion is removed from the blood within a few minutes by the liver and is polymerized into glucose or metabolized directly for energy. Consequently, 500 milliliters of blood that has been rendered incoagulable by citrate can ordinarily be transfused into a recipient within a few minutes without dire consequences. But if the liver is damaged or if large quantities of citrated blood or plasma are given too rapidly (within fractions of a minute), the citrate ion may not be removed quickly enough, and the citrate can, under these conditions, greatly depress the level of calcium ion in the blood, which can result in tetany and convulsive death.

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