202 K. G. HOSKINS 



pressure which charcteristically results from suitable doses of epinephrin. 

 When, however, the medulla was destroyed, this depressor reaction was 

 converted to pressor. But in spite of this reversal the dilator mechanism 

 in both the limb and the intestine was found to be functional. Destroy- 

 ing the spinal cord at successive levels failed to abolish the dilator response, 

 and Hartman concluded that, contrary to his previous belief, the mechan- 

 ism through which the dilatation was mediated lay outside the central 

 nervous system proper. 



By exclusion, then, it would appear that the mechanism is located 

 in the sympathetic ganglia. Direct experimentation indicated that such 

 is the case. In 6 dogs the intestine was independently perfused. Epi- 



Fig. 3. Graph showing the arterial pressure reaction and leg volume expansion 

 in a dog following the injection of 0.5 c.c. 1:10,000 epinephrin by jugular vein. The 

 leg was perfused with oxygenated Ringer's solution and isolated from the body circula- 

 tion. The nervous connections were intact. (Reduced one-half.) (After Hartman 

 and Fraser, Am. J. Physiol.) 



nephrin injected by jugular vein caused dilatation. When, however, the 

 splanchnic fibers peripheral to the ganglia were sectioned the dilator re- 

 action was abolished. Similarly, it was abolished by painting the ganglia 

 with nicotin, thereby blocking the connection between the preganglionic 

 and postganglionic neurons. 



The location of the vasodilator mechanism for the hind-limbs was 

 then determined. Since, as earlier shown, it is not in the spinal cord, 

 it must be in either the ganglia of the sympathetic chain or of the dorsal 

 roots. The hind-limb of a dog was placed in a plethysmograph. The 

 last five lumbar and the first sacral sympathetic ganglia were destroyed on 

 the corresponding side. The limb was then completely isolated from the 

 body circulation and perfused. Injection of epinephrin into the jugular 

 vein evoked marked dilatation. Similar results were obtained in other 

 animals, though not uniformly. In some cases destruction of the sympa- 

 thetic ganglia left the dilator mechanism functioning, but destruction of 

 the dorsal root ganglia abolished it. It appeared 'then that the dilator 

 mechanism for the limb may be located in either the dorsal root ganglia 



