116 The Chemistry of the Injured Cell 



formation (thought to be due to histamine) much less than the 

 later stages possibly due to activated globulins or peptides 

 (Spector, 1958) . This interpretation may still be correct, but un- 

 fortunately from the point of view of simplicity, compounds that 

 inhibit globulin activation also cause a general suppression of 

 capillary permeability increased by a variety of compounds 

 (Spector and Willoughby, 1960a) , an action discussed in the pages 

 that follow. 



THE INACTIVATION OF VASOCONSTRICTOR AMINES 

 AS PART OF THE INFLAMMATORY REACTION 



The vascular events of acute inflammation may be regarded as 

 a temporary disturbance of the balance of forces normally govern- 

 ing the behaviour of vessels, the vasoconstrictor forces being for 

 the time in abeyance. So far only influences actively dilating vessels 

 and increasing their permeability have been considered. Recently, 

 however, evidence has come to light supporting a new concept, 

 namely that the vascular changes of acute inflammation are partly 

 due to the destruction of an amine that would otherwise constrict 

 and reduce the permeability of capillaries and oppose the action 

 of compounds such as histamine and kinins. 



The most important endogenous compounds with these "anti- 

 permeability" actions on blood vessels are, the catechol monoa- 

 mines adrenaline and nor-adrenaline, (epinephrine and nor- 

 epinephrine) . Amongst other situations, they are present in plate- 

 lets, leucocytes and vessel walls and at least two enzymes destroy 

 them in the body, monoamine oxidase and catechol-o-methyl 

 transferase. It has been found recently at University College Hos- 

 pital that the administration of specific inhibitors of monoamine 

 oxidase greatly reduces the increased capillary permeability conse- 

 quent on thermal or chemical injury. This result is explicable on 

 the basis that inflammatory phenomena are in fact partly due to 

 inactivation of vasoconstrictor amines by monoamine oxidase 

 (Spector and Willoughby, 1960b) . Administration of competitive 

 inhibitors of catechol-o-methyl transferase failed to modify the 

 inflammatory reaction. 



