Shock and Related Plienomena 135 



medulla) of a physiological nature and need not be discussed here. 

 Decompensation of peripheral vessels however is a suitable criterion 

 of shock on which to base an account of its chemistry. 



THE ROLE OF VASOCONSTRICTOR AND 

 VASODILATOR AMINES 



One of the most popular views of the pathogenesis of vascular 

 decompensation was that which suggested a massive release of the 

 vasodilator histamine. This theory went out of favour for a variety 

 of reasons, including the sustained nature of the circulatory collapse 

 and the failure of antihistamine drugs as a therapeutic measure. 

 Nevertheless, there is no doubt that release of histamine does occur 

 (Bloom, 1944). 



It is equally clear that release of the vasoconstrictor amines 

 adrenaline, nor-adrenaline and 5-H.T. also takes place. These vaso- 

 constrictor amines are also implicated in the sense that a cardinal 

 feature of shock is the inability of vessels in a state of decompensa- 

 tion to respond to adrenaline and nor-adrenaline in the normal 

 fashion. The infusion of large doses of adrenaline or nor-adrenaline 

 leads paradoxically to phenomena suggestive of massive histamine 

 release and to a state of peripheral circulatory collapse resembling 

 shock. This latter observation seemed to indicate that decompensa- 

 tion in shock might be due to the development in certain parts of 

 the vascular bed of a refractory state in which the vessels, because of 

 over-stimulation with adrenaline or nor-adrenaline, lost the ability 

 to respond to these vasoconstrictor amines or indeed to any stimulus 

 leading towards a restoration of vascular tone (Zweifach, 1958) . 



Schayer (I960) has recently shown the way towards a possible 

 reconciliation of the histamine and adrenaline hypothesis in shock 

 by demonstrating that adrenaline causes increased activity of the 

 enzyme histidine decarboxylase and presumably therefore in- 

 creased production of histamine. This finding suggests that these 

 two amines might form part of a balance governing vascular tone. 

 The results also indicate that a mechanism exists for prolonged 

 histamine effects and for the paradoxical vasodilator actions of 

 large doses of adrenaline. 



Further support for the role of amines in shock comes from the 



