30 



PHYSIOLOGY OF INDUCED HYPOTHERMIA 



tained there for three and one-half hours. The first tracing is taken with the heart at 

 2!i7° at 2 : 40 p.m., soon after perfusion was liegun. At 3:11 p.m. the temperature had 

 fallen to 20° and a very slow heart rate is noted. At 3 : 40 p.m. the temperature was 

 14.8° and visible and electrical systole had ceased. At 3 : 54 p.m. the temperature 

 reached 10° and remained between 8 and 10° until 7 : 29 p.m. when warming began. 

 At 7 : 52 p.m. a visible beat was noted and simultaneously resumption of electrical 

 systole appeared. At 8: 20 p.m., the temperature was again 20° and a regular beat 

 was recorded. At 9 : 42 p.m. the temperature was 36.9° and return to a rate near the 

 original was observed. 



Table III summarizes in tabular form the results of experiments with the isolated 

 heart preparation. The notable features are ( 1 ) cessation of heart beat between 12° 

 and 15° in all preparations except that of 12-10-54 in which isolated contractions 

 were observed at 8° ; (2) the spontaneous resumption of heart beat in all prepara- 

 tions when the temperature returned again to 12° or 15° even in preparations with 

 hypothermic asystole of over eight hours duration; and (3) no significant loss of 

 myocardial potassium to the medium even at low temperatures. 



These perfusion experiments show clearly for the rat's heart that hypothermic 

 asystole is completely reversible and are evidence that for this animal, hypothermia 

 is not lethal because of a direct effect upon the myocardium. Perhaps the most im- 

 portant difference between the perfused preparation and the heart in the intact hypo- 

 thermic animal is that in the former, perfusion and oxygenation of the coronary 

 circulation is independent of the contraction of the ventricles, while in the latter, 

 myocardial anoxia must ensue as soon as the pumping action of the heart ceases, 

 thus complicating the possibly reversible effects of hypothermia with the known 

 lethal effects of anoxia. 



In contrast with diaphragmatic muscle and the other tissues cited at the outset 

 of this paper, the perfused hypothermic heart does not undergo potassium loss. This 

 was an unexpected observation, and corresponds in superficial respects at least to 

 the observations of Dr. Renkin on the perfused hind leg, of which you will hear 



