120 The Chemistry of the Injured Cell 



gan (promethazine HC1) not only exert a general antagonism 

 to increased capillary permeability but also cause a general in- 

 hibition of electrolyte movements in damaged cells and mito- 

 chondria. This may possibly mean that increased capillary permea- 

 bility to protein is in some way secondary to, or at least associated 

 with, electrolyte disturbance in the vascular endothelium and that 

 capillary permeability factors such as histamine may act by alter- 

 ing the electrolyte and water balance of these cells. Such specula- 

 tions are rendered more plausible by recent electron microscopy 

 which has indicated that protein appears to leave histamine-treated 

 vessels by transport through the endothelial cytoplasm rather than 

 by passage through channels of molecular dimensions between the 

 cells, as was widely supposed (Alksne, 1960) . 



Because of many uncertainties it is appropriate to stress the 

 hypothetical and tentative nature of the scheme for the mechanism 

 of the vascular changes of inflammation presented in Figure 10. It 

 cannot be denied that anti-inflammatory compounds such as salicy- 

 late, quinine or monoamine oxidase inhibitors may act in other 

 ways, e.g. by stimulating the release of endogenous anti-inflamma- 

 tory substances. Adrenaline itself may stimulate the pituitary gland 

 to release adrenocorticotropic hormone (ACTH). However, in the 

 experimental systems on which the above scheme is based adrena- 

 line has a much more powerful anti-capillary permeability effect 

 than any known adrenal cortical or pituitary hormone. In addition, 

 careful studies have failed to provide evidence that these drugs, e.g. 

 salicylate, do in fact exert their effect by stimulation of the adrenal 

 cortex (Smith, 1959) . 



LEUCOCYTIC EMIGRATION 



One of the early changes of acute inflammation is the adhesion 

 of polymorphonuclear leucocytes of the blood to the luminal sur- 

 face of the lining endothelium of small blood vessels. This phe- 

 nomenon is followed in due course by the migration of polymorphs 

 through the vessel wall into the tissues. The adhesion of leucocytes 

 is associated in some way with the development of "stickiness" by 

 the vascular endothelium. "Stickiness" can be demonstrated by 

 the adhesion of colloidal particles injected into the circulation. It 



