134 The Chemistry of the Injured Cell 



adrenocortical secretion interact to increase protein breakdown re- 

 mains obscure. 



THE CHEMISTRY OF SHOCK 



Shock is a state of peripheral circulatory collapse whose essential 

 feature is that the volume of circulating blood is too small relative 

 to the volume of the blood vessels. This discrepancy may follow 

 either a rapid reduction in the blood volume or a paralytic dilata- 

 tion of the peripheral vessels or both. Thus shock may occur as a 

 sequel to acute haemorrhage, severe physical, chemical or thermal 

 injury or overwhelming infection. The clinical picture of shock is 

 characteristic and familiar, the patient being cold, pale, sweating 

 and unconscious. The obvious treatment of shock is to increase the 

 blood volume by transfusion. This measure is usually successful, 

 but sometimes it fails. Shock which fails to respond to blood trans- 

 fusion is called irreversible and has led to much research and spec- 

 ulation on its nature, which nevertheless remains uncertain. Much 

 work on the haemodynamic disturbance of shock has been done 

 on both sides of the Atlantic, particularly during the last war. Ac- 

 counts of this aspect of the problem may be found elsewhere 

 (Cameron, 1958) . 



Shock is an almost perfect illustration of the truism that path- 

 ology is the interaction of injury and bodily reaction to injury. 

 When the volume of blood relative to that of the vessels falls sud- 

 denly the body reacts by a profound vasoconstriction in all those 

 organs which are not immediately essential for life, i.e. everywhere 

 except the heart, respiratory muscles and brain. Some ill effects may 

 follow this vasoconstriction alone, e.g. in the kidney where there 

 may be tubular necrosis. Elsewhere, particularly in the liver and 

 intestine, following prolonged vosoconstriction, the vessels may 

 develop a form of paralysis often termed decompensation in which 

 they suffer paralytic dilatation and become unable to respond to 

 vasoconstrictor stimuli. The failure of these vessels to regain their 

 normal tone is one of the essential features of irreversible shock. 



The compensatory phenomena of shock, e.g. changes in cardiac 

 output and peripheral vasoconstriction, may be attributed to 

 nervous and hormonal changes (especially concerning the adrenal 



