12 CORA SENNER WINKIN 



functional the maximal anemic increment is not immediately obtained, 

 and cannot be reached in tlie early part of the occlusion unless the 

 vagi be sectioned. The same seems to follow also for the accelerators 

 since, when they are removed, the vagus cannot prevent the immediate 

 and considerable augmentation of pressure. In the earlier part of the 

 anemic response, the combined action of the entire cardiac innervation 

 seems to effect a considerable check on the rapid rise of blood pressure. 

 This may be due to afferent or efferent impulses, but the accelerators 

 seem to be involved as well as the vagi. 



The relations of the cardiac innervation to the second rise of pressure 

 are not so clear. Stewart (28) attributed this in part to accelerator 

 fibers in the stellate ganglion, and possibly in the vagus, but recently 

 Stewart and Rogofif (63) have demonstrated the possibility of producing 



Fig. 2. Cat 23; cerebral anemia. Splanchnic nerves sectioned at their entry 

 to coeliac ganglia. Occlusion time 3 minutes. Skeletal convulsions and res- 

 piratory spasms evident. The only factors in the vascular reaction recognizable 

 in the tracing are the changes in heart rate. This is accompanied by a very slight 

 change in level as the heart is breaking away at the usual time from its slow rate. 

 Two respiratory gasps are later imposed on the tracing. 



cardiac acceleration by sciatic stimulation even after the heart is com- 

 pletely denervated. In this series of experiments the rise appears very 

 definitely in cats with accelerators removed and vagus intact. It must, 

 therefore, be referable to vasomotor or endocrine effects under these 

 conditions. Ordinarily, there is no break in the curve after double 

 vagotomy, the fall due to vagus slowing being absent. In two cats, 

 however, such a second rise has also been seen when the heart was com- 

 pletely denervated. It seems that the cessation of the vagus effect, 

 while undoubtedly significant, is only one of the factors involved. 



In the absence of the influence of tne cardiac nerves on the initiation 

 and maintenance of the reaction to cerebral anemia, it seems that we 

 must look to the vasomotor mechanism itself. 



