Thus the leucocytes clear a channel to the 

 exterior; and through this channel the pus 

 and other contents of the abcess may finally 

 be discharged. 



The functions of the other leucocytes 

 (small and large lymphocytes, basophils, and 

 eosinophils) are not clearly understood al- 

 though probably they have some relationship 

 to disease resistance. In different infections 

 different kinds of leucocytes tend to accu- 

 mulate in the blood, and consequently the 

 physician must obtain a differential white 

 cell count, in seeking the diagnosis of an un- 

 known infection. 



PLATELETS 



RED CELL 



Fig. 17-5. Human blood platelets, or thrombocytes. 

 A red blood cell is shown for comparison. 



Thrombocytes. The thrombocytes, or blood 

 platelets (Fig. 17-5), are smaller and less regu- 

 larly shaped than erythrocytes, although they 

 resemble erythrocytes in that they are abun- 

 dant (about 250 thousand per cu mm) and 

 they lack nuclei. The thrombocytes are 

 formed from the cytoplasm of certain very 

 large cells in the bone marrow, by a process 

 of fragmentation. Platelets cannot be seen in 

 ordinary shed blood because they disintegrate 

 immediately, liberating a substance that par- 

 ticipates in clotting. 



Blood Coagulation. Victims of hemophilia 

 — a rare hereditary defect of the blood — 

 bleed very profusely even from the slightest 

 wound. Hemophilic blood fails to clot in the 

 normal time (6 to 8 min), but takes an hour 

 or more to coagulate. In the absence of a nor- 

 mal clot to stop the bleeding, blood con- 

 tinues to flow from any ruptured vessel, and 



The Circulatory System - 323 



the life of the "bleeder" may be endangered. 



The clotting of a sample of normal blood 

 involves a series of chemical reactions that 

 starts as soon as the blood comes into contact 

 with a damaged tissue or with some other 

 foreign surface. The main reaction involves 

 the conversion of the soluble protein, fibrin- 

 ogen, into the insoluble protein, fibrin. The 

 fibrin precipitates in the form of a sub- 

 microscopic network of interlacing fibrils, 

 which holds the other blood components 

 within a colloidal mesh (Fig. 17-6). At first 

 the clot, or thrombus, is a semisolid mass 

 with a gelatinous consistency. But in time the 

 fibrin framework shrinks, squeezing a straw- 

 colored fluid, the serum, to the surface of the 

 clot, which now becomes hard and tough. 

 The serum is almost totally lacking in fibrin- 

 ogen and displays no further tendency to clot. 



The fibrinogen — »■ fibrin reaction depends 

 upon a specific enzyme, thrombase, which is 

 also called thrombin. Thrombase itself is not 

 present in the circulating blood, but blood 

 contains an inactive precursor of the enzyme, 

 which is called prothrombase (prothrombin). 

 Prothrombase must be converted into throm- 

 base before the blood can clot. In the ab- 

 sence of ionic calcium, prothrombase can- 

 not be activated (except very slowly); and 

 this accounts for the fact that coagulation 

 does not occur when calcium-precipitating 

 reagents (for example, oxalate compounds) 

 are added to the blood. 



The conversion of prothrombase to throm- 

 base occurs only when another substance, 

 thromboplastin, is available. Thrombo- 

 plastin is not present in circulating blood, 

 but the precursory protein, thromboplastin- 

 ogen, has been identified recently as one of 

 the normal globulin components of plasma. 

 Clotting does not begin, therefore, until 

 thromboplastinogen has been transformed 

 into thromboplastin. This reaction requires 

 the presence of another enzyme (thrombo- 

 plastinogenase) which is liberated, in shed 

 blood, by the disintegration of the platelets. 

 Thus, the platelets, which disintegrate when 

 blood escapes from a vessel and makes con- 



