702 PRINCIPLES OF GENERAL PHYSIOLOGY 



eight seconds should cause an appreciable accumulation of metabolites in a resting, 

 curarised leg. It is to be remembered that the blood was fully oxygenated. It 

 is desirable that compressions of still shorter duration should be tested. If, 

 however, we accept a reaction of the muscle cells of the arterial wall to- fall of 

 pressure, it is necessary to suppose that they must previously have been in a 

 state of contractile response to the normal high pressure. Further, if the 

 electrical change described by Carl Tigerstedt (page 687 above) be accepted as due 

 to arterial contraction, it shows that the larger arteries respond to the heart 

 beat by a contraction, although small. 



Kesson (1913) was unable to find any reaction in isolated arteries. 



Regulation of Supply to Organs. Summing up the facts of the previous pages, 

 we may say that the blood flow through an organ in activity is increased in the 

 following ways : 



1. By rise of general arterial pressure, produced by constriction in other 



parts. 



2. By vascular dilatation in the organ itself. These two effects are 



combined in the Loven reflexes. 



3. By the production of acid metabolites by cell activity. 



The natural tonus in arterioles is maintained in three, or perhaps four, 

 ways : 



1. The natural property of smooth muscle to be in a state of partial 



tonus. 



2. The continuous vaso-constrictor impulses sent out by the tonic excita- 



tion of the vaso-constrictor centre. 



3. The contraction set up by adrenaline in those arterioles supplied with 



sympathetic nerves when this substance is present in the blood. 

 (4. The contraction by which they respond to the normal stretching force 

 of the blood pressure, possibly.) 



THE COAGULATION OF THE BLOOD 



The fact that the blood, when it leaves the blood vessels and comes into 

 contact with the tissues or external objects, sets into a kind of jelly is familiar 

 to all. 



The value of this process to the organism appears to be to lessen loss of blood 

 when blood vessels are injured. 



It is impossible to give an account here of the great mass of work that has 

 been done on the process. In point of fact, it cannot be said that it is yet 

 understood. Much of the research done has led to little more than the multiplica- 

 tion of names given to supposed substances held to take part in it, but these have 

 not been isolated as chemical individuals, and the names really refer to aspects of 

 phenomena (see the remarks on pages 107 and 328 above). 



As an illustration, I would refer to the paper by Collingwood and MacMahon (1912), 

 where we find the following names used as applying to definite substances : fibrinogen, 

 prothrombin, prothrombokinase, anti-thrombokinase, thrombokinase, anti-thrombin, and anti- 

 prothrombin. These are supposed to be present before clotting. After clotting we have : 

 fibrin, thrombin, thrombokinase, anti-thrombin ?, anti-prothrombin, anti-thrombokinase, and 

 prothrombin. 



On the whole it appears that the point of view originally taken by Wooldridge 

 (1887-1893) and developed by Nolf (1906-1908) has the most evidence in its 

 favour. According to this theory, the phenomenon is essentially an interaction 

 of colloids under the influence of electrolytes, especially calcium salts. There is 

 reason to suppose that the so-called " fibrin-ferment " is not an enzyme, although 

 some enzymes of a proteoclastic nature may be concerned in the later liquefaction 

 of the clot. 



In invertebrates there are two kinds of processes, one associated with breaking 



