EFFECTS OF TEMPERATUKE: CELLULAR SYSTEMS 781 



after an interval that depends on the type of cell and the temperature, 

 the cell will be unable to recover when oxygen is again supplied. 



The detrimental processes that occur during anoxia proceed at slower 

 rates when the temperature is lowered and hence the interval required 

 for irreversible damage is lengthened. Fundamentally the same damage 

 will be produced by anoxia under normothermic or hypothermic conditions, 

 but the times necessary to reach a given level of disturbance will be different. 

 It is evident that this may be unrelated to effects on tissue function; that 

 is, hypothermia may protect against anoxic damage but will not necessarily 

 decrease the effects of anoxia on cellular activity. Similar reasoning may 

 be applied to the actions of certain inhibitors. 



Both hypothermia and anoxia alone cause a decrease in the K/Na ratio 

 of muscle cells (Gollan, 1956,) but together there is essentially no change. 

 In atria the drop of the K/Na ratio is faster under both conditions, and 

 when the tissue is both anoxic and hypothermic the rate of decrease is 

 less than during anoxia alone. Since the K/Na ratio is not only indicative 

 of disturbances in ion transport but also is important in determining the 

 physiological changes that occur, these results provide some experimental 

 evidence for the protection afforded by hypothermia. When the K/Na 

 ratio falls to a sufficiently low level, the operation of the sodium pump 

 or the selective permeability properties of the membrane are irreversibly 

 altered so that recovery does not occur upon reintroduction of oxygen. 



The respiration of several mammalian tissues at 20° is approximately 

 30% of what it is at 37° (Fuhrman, 1956). The functional activities of tis- 

 sues or whole organisms often change with temperature to about the same 

 degree as the respiration (Crozier, 1924). However, the situation is some- 

 times more complex and the various functions of a single tissue may be 

 modified by temperature changes in quite different ways. The heart may 

 be taken as an example (Hoffman, 1956; Brooks, 1956). The rate of the 

 heart beat will usually drop to a level between 15-25% as the temperature 

 is decreased from 37° to 20°; for the isolated rabbit atrium the fall is to 18% 

 of the rate at body temperature (Webb. 1950 b). The rate of impulse con- 

 duction over the myocardium generally decreases even more. In the rat 

 atrium the conduction rate at 20° is only 7% of the normal value (Hol- 

 lander and Webb, 1955). On the other hand the contractile tension may 

 rise as much as 45% as the cardiac tissue is cooled to the same degree, 

 even though the rate of beating is kept constant by electrical stimulation 

 (Hollander and Webb, 1955). The resting membrane potential of rat atrium 

 increases around 28% upon cooling to 20^. while the magnitude of the 

 action potential is not significantly altered, although the action potential 

 may be greatly prolonged due to slower rates of depolarization and repo- 

 larization. In this tissue a change of the temperature thus brings about a 

 variety of effects and it is obvious that there is no necessary correlation 

 between metabolic and functional variations. One might conclude from 



