8 CORA SENNER WINKIN 



rises as great in magnitude and duration as those recorded by Stewart 

 (28) or those herein obtained. The relative volume of blood held in 

 these animals within the splanchnic system, as compared with that 

 controlled by the somatic innervation is, however, somewhat different 

 from that in cats. Little experimental attention was here given to 

 this problem. In one animal, however, curare was injected and a vigor- 

 ous anemic response was obtained. The occlusion time was normal (3 

 minutes) ; the anemic increment, however, was below the average, being 

 only 80 mm. In another cat, both sciatics and the brachial plexuses 

 on both sides were divided. Pressure did not fall after the lesions. 

 Both stellate ganglia were then removed. The animal gave an anemic 

 increment of 100 mm. Hg. 



It seems accordingly that the muscular factor is of no primary signifi- 

 cance in either the initiation or the maintenance of the anemic rise. 

 The fact that no great depression of the level of blood pressure results 

 in spite of extensive elimination of muscular innervation is interesting 

 in comparison with subsequent results, and effectively contrasts the 

 influence of skeletal innervation and visceral innervation on blood pres- 

 sure. 



b. The influence of the cardiac innervation on the anemic rise. The 

 influence of the cardiac nerves on the anemic rise may be exerted in 

 either of two ways. The change in rate and amplitude of the heart 

 beat may affect the output per minute as emphasized by Tigerstedt, (57) 

 or afferent impulses aroused within the heart may affect reflexly the 

 efferent cardio-vascular innervation as discussed by Hill (59). It is 

 conceivable that in either of these ways, or both, the heart may influence 

 significantly the level of blood pressure. 



Frank (57), mathematically, and Erlanger (58) by sphygmomano- 

 metric measurements, have attempted to show that the output of the 

 heart remained a constant, or in other words that pulse pressure times 

 pulse rate remains a constant. Wickwire (60) has shown that the 

 usual compensatory changes in heart rate to a change in the systemic 

 blood pressure may be absent in deep anesthesia or in cases of restric- 

 tion of the volume of blood flow to the brain. Under normal circum- 

 stances, Erlanger's statement probably holds true, but may not 

 necessarily apply under critical conditions. 



1. Effect of the vagus. Mosso (61), Gouty- and Stewart found that 

 following the first short rise in blood pressure (which in the intact ani- 

 mal is never very great) there is a considerable slowing of the pulse. 

 As long as this slowing of the pulse persists, pressure ceases to rise, and 



