CARDIOVASCULAR CHANGES DURING CEREBRAL ANEMIA 25 



3:05 Gasps return, pressure continues rising 



3:10 Pressure reaches 90 mm. Hg. again, regular waves in blood pressure curve, 

 respiration reestablished 



3 : 17 Section of cord at T 4, pressure drops to 70 mm. 



Corneal reflex, Occlusion: sharp rise of pressure to 100 mm. fall to 60 mm. 

 during vagus slowing, subsequent rise to 112 mm.; anemic increment 

 42 mm. 



3:23 Pressure released before spontaneous fail, drops sharply to 44 mm. but 

 immediately begins to rise again 



3:25 Gasps return 



3:33 Pressure at 84 mm. again, respiration reestablished 



3:39 Section of cord at T 2, pressure falls to 46 mm. Hg. total depression of pres- 

 sure, 84 mm. 



3:40 Corneal reflex, Occlusion: initial rise to 64 mm. Hg. fall to 30 mm, during 

 vagus slowing, second rise to 74 mm. Hg. anemic increment 28 mm. 



3:42 30 Head arteries released before spontaneous fall, pressure immediately 

 falls to 20 mm. but again regains level 



3:45 Pressure has reached 54 mm., gasps return, further rise to 60 mm. respira- 

 tion reestablished 

 Thorax opened, artificial respiration administered 



4:05 Sympathetic chain cut in midthoracic, pressure fall to 40 mm. total depres- 

 sion of pressure 90 mm. 



4:07 Corneal reflex: occlusion, rise to 52 mm. slight fall, rise to 48 mm. anemic 

 increment 12 mm. 



4:11 Release of head arteries, pressure drops to 30 mm. 



4:14 Gasps return, pressure rises to 40 mm. respiration reestablished 



4:55 Splanchnics cut in psoas muscles, no effect on blood pressure, no recovery 

 of level or return of respiration 



5:10 Artificial respiration intermitted, pressure drops to base line. 



Effect of the splanchnic constrictor fibers on the anemic rise. The bur- 

 den of the anemic response seems to lie in the vasomotor apparatus, 

 and, if the evidence of these experiments is adequate, almost exclusively 

 on the splanchnic constrictor fibers. Peripheral section of the splanch- 

 nic nerves, with its great depression of blood pressure, and the sub- 

 sequent inability to obtain any anemic increment whatever, speaks 

 strongly, almost unequivocally, for such an interpretation. Additional 

 evidence for the importance of the splanchnic pathway for the vaso- 

 motor changes during anemia is the relation of the level of blood pressure 

 after section within the splanchnic outflow to the anemic increment 

 elicitable on occlusion. The data show quite clearly that the greater 

 the initial depression, the less powerful the response. 



This very definite grading of the blood pressure level to the magni- 

 tude of the anemic rise gives a further insight into the anatomical 

 relations of the splanchnic outflow. In the cats examined the greatest 



