294 THE CIRCULATION OP THE BLOOD 



the theory that shock is dependent upon an impairment of a higher 

 nerve mechanism as a result of overstimulation by afferent impulses. 



Cannon 35 has recently suggested that the engorgement of the splanch- 

 nic blood vessels may be the result of a constriction of the portal rad- 

 icles in the liver, which dams back the blood in the portal circulation. 

 He points out that these radicles have vasoconstrictor nerve fibers, as 

 evidenced by the fact that the rate of flow of fluid through the per- 

 fused liver decreases during asphyxia, as well as when the hepatic 

 nerve plexus is stimulated electrically or when epinephrine is injected 

 into the portal vein. He argues that, since the blood vessels in other 

 areas of the body are constricted in shock, so also will be those of the 

 liver, with the result that the blood of the portal vein, in which ordinarily 

 there is a very low blood pressure (10 mm.Hg), will become dammed 

 back in these veins and therefore removed from the systemic circulation. 

 It does not seem to the writer, however, that this explanation is likely 

 to be the correct one, for, although it is true that vasoconstrictor in- 

 fluences have been shown to exist in the hepatic radicles of the portal vein, 

 yet, since it is only under special experimental conditions that this can 

 be done, they must be very feeble in nature. As we have seen else- 

 where, portal vasoconstriction can not be demonstrated by stimulation 

 of the hepatic plexus with stimuli which are sufficient to produce marked 

 constriction of the hepatic artery radicles (see page 255). 



The engorgement of the splanchnic capillaries and venules is much 

 more likely to be dependent upon local influences acting on the vessels 

 themselves. When shock is produced by manipulation of the abdominal 

 viscera, it is easy to see how this local disturbance might be set up. 

 When shock is caused in other ways, as by violent stimulation of sen- 

 sory nerves, the atony of the splanchnic vessels is not so easily accounted 

 for unless we assume that it is a type of abnormal reciprocal vascular 

 innervation. For example, when stimuli are applied locally to sensory 

 surfaces under ordinary conditions, a distribution of the blood of the 

 body takes place, more being sent to the irritated region and less to 

 other parts of the body (see page 238). During the sensory stimula- 

 tion preceding shock, it is conceivable that this reciprocal innervation 

 acts in a faulty manner, causing at first a dilatation of the splanchnic 

 arterioles and thus allowing more blood to enter the splanchnic capil- 

 laries and venules, which being possessed of little tone are incapable 

 of responding by increased tonicity, so that they become overdistended 

 and the blood in them stagnates. 



In any case there is no doubt that the initial change is the stagnation 

 of blood in these vessels, and when once such stagnation has occurred, 

 the process goes on spontaneously probably on account of the accumula- 



