EFFECTS ON NER\'OUS SYSTEM— ^IcQUEEN 247 



ticulaiiy because of the many variahles introduced l)y this method of animal prepara- 

 tion. If this relationship exists in the intact animal, it may well indicate a rather 

 precise rant^e of temperatures for minimal cerebral damage during anoxia. This 

 range, which forms the lower portion of their curve, is from 28°- 33° C. 



Fazekas and Hiniwich" were first al)le to prove directly the diminution of 

 cerebral metabolism during general refrigeration. This was done in 9 dogs by 

 establishing a fall in the arteriovenous oxygen difference in the presence of a 

 reduced cerebral IjKxkI How. 



Field, Fuhrman. and Martin" later showed in vitro with the Warburg apparatus, 

 that the cerebral oxygen consumption varied as a constant function of temperature. 

 This same group^^ further studied the rates of oxygen consumption of rat cerebral 

 cortex slices measured at 2>7.7° C. following one hour at 0.2° C. and noted full 

 recovery. These findings were confirmed /;; vivo by RosomofT and Holaday^^ in the 

 dog. They found the cerebral blood flow and oxygen consumption to fall linearly 

 and equally with the temperature. An estimated 6.7% decrease of blood flow per 

 degree of temperature decline in the range 35°- 25° C. was established. The mini- 

 mal changes noted in arteriovenous oxygen differences is surprising. 



Credit must go to Lougheed and Kahn-' for establishing a method of prediction 

 for the protection offered by cold to the brain threatened by ischemia. These pre- 

 dictions were made on the dog with a detailed analysis of the cerebral metabolic 

 rate and confirmed by clinical evaluations, microscopic examination of the Ijrains 

 and by the analyses of lactate-pyruvate ratios and electroencephalographic data. 

 They found that during the cooling, the total body oxygen consumption generally 

 coincided with the cerebral metabolic rate. The fundamental work of Bigelow^ on 

 oxygen consumption was thus extended to the brain. At 25° C. they noted the 

 cerel)ral metabolic rate to be reduced to between 23 and ZS% of control values. 

 The rate at 30° C. is approximately 50%. They were successful in safely cooling 

 7 of 8 dogs to a temperature of 23.6°- 25° C. with a 15-minute period of anoxia 

 One animal did show evidence of neurological damage. Further work by Lougheed, 

 Sweet, White and Brewster-* proved the value ^of this guide for neural survival 

 periods in the human. In one of 2 cases studied, ischemia was tolerated for periods 

 as long as 14 minutes 25 seconds (at 25.8° C). This 15-minute period would 

 appear to represent more than a maximal safe time limit. However, should it be 

 halved (to 8 minutes at 26° C. ), the brain would still be undamaged for a time 

 more than double that permissible at normal temperatures. 



Comparatively little attention has been directed toward studv of the degree of 

 protection afforded the spinal cord under conditions of hypoxia. Recently Beattie 

 et al} have evaluated such protection in normothermic and hypothermic dogs whose 

 spinal cords were endangered by ischemia produced by a thoracic aortic occlusion. 

 Hind-quarter paralysis was produced in 4 of 10 animals at rectal temperatures of 

 35°- 29° C. with aortic clamping of 60 minutes. Ten dogs were cooled with the 

 aorta clamped for 60 minutes and 5 similarly treated for 40 minutes. Questionable 

 weakness was noted in one animal in the first group. Those of the second group 

 displayed no weakness. Unfortunately, although the rectal temperatures are known 

 to be below 30°, the specific temperatures for each occlusion were not given. How- 

 ever, cooling to a level much lielow 30° is indicated because of the high incidence 



