BRAIN COOLING— JENSEN, PARKINS and VARS 277 



prior to occlusion. Seven of 10 survived a 2-hour period of occlusion. None of 

 these were paraplegic. 



As additional normothermic controls, 37-degree saline was substituted for the 

 iced saline. Eight of 10 animals survived 1 hour of occlusion, thus suggesting a 

 beneficial effect of the saline alone. All survivors were paraplegic. None of 10, 

 however, survived the 2-hour occlusion. 



The integrity of the intestine appears to be a primary factor in survival follow- 

 ing temporary occlusion of the thoracic aorta. Direct visceral hypothermia was the 

 most effective procedure in prevention of this type of ischemic shock. 



Dr. Jean Calm: Figure 1 (page 226) shows the encephalographic control 

 during total arrest of the blood circulation. That is a usual encephalogram at 30° C, 

 regardless of the method of hypothermia employed. 



Silence of the brain is obtained 30 to 120 seconds after arrest of the blood cir- 

 culation (fig. 2), depending on the method of the hypothermia. It seems that 

 silence is obtained after only one or two minutes in hibernation, and is obtained in 

 30 to 60 seconds in surface cooling. After 20 or 25 minutes of circulatory arrest, 

 when the clamp is released and the heart rate and the blood pressure returned to 

 normal, silence in the brain persists for two to four hours after release of the 

 clamp (fig. 3). Twenty-four hours later, when the temperature has returned to 

 33° C, the electroencephalogram is normal (fig. 4). 



Silence is obtained after 120 seconds at 27° C, and after 80 seconds at 29° C. 

 After clamping, the number of slow waves of small amplitude is increased. In only 

 one case did we find fast waves. The return to the fast waves is about 120 seconds 

 to 200 seconds after the release of the clamping. I can't understand why, despite 

 the return to normal of the blood pressure, silence in the brain persists after 20 

 minutes of clamping. 



Dr. James D. McMurrey: We have been interested in a study of cerebral 

 physiology under hypothermia and in the possibility of occluding the cerebral 

 afferent circulation in monkeys. We have occluded the cerebral afferent circulation 

 under hypothermia in about 60 monkeys by an occlusion of the brachycephalic and 

 left subclavian arteries at the arch of the aorta. Almost invariably if the occlusion 

 were complete there was disappearance of the electroencephalographic tracing 

 within one minute. 



Figure 1 (page 278) is a reproduction of electroencephalographic tracings in a 

 monkey subjected to 15 minutes of cerebral afferent vascular occlusion vmder hypo- 

 thermia. We believe that occlusion of the brachycephalic and left subclavian vessels 

 is sufficient to completely occlude the cerebral afferent circuit. Almost invariably we 

 got the pattern demonstrated here, which is a marked depression to almost com- 

 plete absence of electrical activity during cerebral afferent vascular occlusion. 



In a series of monkeys with occlusion of the cerebral afferent circulation for 

 more than 20 minutes, the animals either died or, upon follow-up by clinical ex- 

 amination and encephalography, were found to be greatly damaged. 



Monkeys occluded for 15 minutes seem to tolerate the procedure moderately 

 well. We were able to produce multiple occlusions for as many as three periods of 

 occlusions, with five minutes' interruption of the occluding period, for periods of 

 12 minutes without damage. 



Studies of the cerebral oxygen consumption and cerebral blood flow demon- 



