248 PHYSIOLOGY OF INDUCED HYPOTHERMIA 



of ventricular fibrillation in other animals of this series. One can expect at normal 

 body temperature an incidence of paralysis of 50% or more with the thoracic 

 aorta clamped for one hour. These findings do, then, show this time limit to be 

 over maximum even with cooling, and they do establish the basic prolongation of 

 the survival period for the spinal cord during general hypothermia. 



One other group of experimental data seems pertinent, and points directly to 

 the innocuous character of limited hypothermia. Jeppson and Nielsen-^ have re- 

 cently found the number of lesions of the blood brain barrier induced with 50% 

 Diodrast to decline sharply with a fall in temperature. In comparable groups of 

 rabbits they found 8 lesions at 38° C, 5 lesions at 35° C, 4 lesions at 31° C, and 

 lesions at 25 ° C. 



Mention should be made of several reports of one untoward eft'ect. This is spe- 

 cifically a lowering of the threshold for the induction of cerebral seizures during 

 cooling. Noell and his group^^ first demonstrated this with recordings of the 

 electrical activity of the cortex and striatum of the rabbit in 1952. They found 

 parameters of electrical stimulation which were capable of producing widespread 

 and prolonged convulsive activity over and beneath the cortex during cooling, but 

 which were quite ineffective both before and after cooling. Similarly, normally 

 subconvulsive amounts of metrazol were productive of seizure patterns during the 

 period of hypothermia. The body temperatures for such change were not given in 

 detail but were below 30° C. These findings were confirmed in the dog by Ferrari 

 and Amantea^- in the temperature range 22°- 34° C, These authors detected pat- 

 terns which they identified as generalized and petit mal in type and which were 

 found to originate simultaneously in all cortical areas. The seizure patterns so 

 evoked recall the work of Bremer in 1935* on direct cooling of the cortex. He 

 noted a rapidly reversible weakening of the oscillations with brief periods of local 

 refrigeration. This depression phase persisted after the application of more intense 

 and prolonged cold (ice) and was then followed with a phase of what was called 

 intensification of cortical activity. Rewerts-''^ similarly on clinical grounds has in- 

 dicted the exposure to cold as a causal agent in the production of epilepsy and other 

 neurological abnormalities. 



Finally, at least four current problems seem to demand attention. First, a deter- 

 mination of the exact range of brain temperatures for maximal safety during 

 ischemia. Second, an assessment of the possibility of injury in the form of a lower- 

 ing of the threshold for seizures or other change even at temperatures as high 

 as 30° C. Third, a better understanding of the basic action of cold on the sympa- 

 thetic nervous system; and lastly, an investigation of thermosensitivity of periph- 

 eral nerve during clinical hypothermia. 



REFERENCES 



1. Bcattie, E. J., Adovasio, D., Keshishian, J. M., and Blades, B. : Refrigeration in experimental 



surgery of the aorta, Surg., Gynec. & Obst. 96: 711-713, 1953. 



2. Bigelow, W. G., Callaghan, J. C, and Hopps, J. A.: General hypothermia for experimental 



intracardiac surgery; the use of electrophrenic respirations, an artificial pacemaker for 

 cardiac standstill, and radiofrequency rewarming in general hypothermia, Ann. Surg. 132: 

 531-539, 1950. 



