354 PHYSIOLOGY OF INDUCED HYPOTHERMIA 



necessary to inject lignocaine in the sinus node from the superior vena cava to the 

 inferior vena cava in three or four points. With this method we obtain, first, a very 

 marked bradycardia; second, sometimes brief cardiac arrest (30 seconds) ; third, a 

 nodal rhythm. It also seems that the contraction of the ventricle begins only after 

 the acute dilation of the auricle. There is a mechanical contraction which is the re- 

 sult of the autonomic rhythm imposed to the heart after the sino-atrial blockade. 



The benefit, I think, is not only in the diminution of the cardiac excitability, but 

 in the slow heart rate. When the heart is clamped, the metabolism of the heart is 

 very different in spite of hypothermia : the metabolism of the heart is an anoxic 

 metabolism ; and the immediate reaction of the heart in those anoxic conditions is 

 first, the outpouring of potassium, second, the use of glycogen as the only emer- 

 gency fuel. It seems that the heart cannot use more than a certain quantity of its 

 own glycogen ; the slower the heart rate the more economical is the use of glycogen 

 and the longer can l)e the duration of the arrest of the circulation. 



On the other hand, in the same period of arrest of the blood circulation we still 

 have coronary flow. We were surprised to see that during 12 to 14 minutes we still 

 had coronary flow in spite of the occlusion of both vena cava and azygos. Cer- 

 tainly the coronary flow is diminishing gradually during those 12 to 14 minutes, and 

 after 15 minutes of clamping the coronary flow is about 1 per cent of its value at 

 the beginning of the clamping. 



At the same time there is a reduction in the oxygen supply, and there is also a 

 reduction in all the metabolite supply to the heart. 



What are our results with this method in surface cooling and in artificial hiber- 

 nation? In surface cooling we could arrest the blood circulation in dogs cooled l)e- 

 tween 23 and 24° C. during 22 and 30 minutes without any cases of ventricular 

 fibrillation in 22 dogs. In artificial hibernation we did the same work, and the arrest 

 of the blood circulation was also from 17 to 28 or 30 minutes. We have had about 

 2 per cent of ventricular fil)rillation. 



In 16 monkeys we did the same experiment in surface cooling and in artificial 

 hibernation with exactly the same results: No cases of ventricular fibrillation in 

 spite of 16 to 25 minutes of arrest of the blood circulation. 



REFERENCES 



1. Cahn, J., Melon, J. M., and Dubrasquet, M. : Excitabilite cardiaque et hibernation artificielle, 



Compt. rend. See. biol. ]47: 1193-1196, 1953. 



2. Melon, J. M., Cahn, J., and Dubrasquet, M. : Protection cardia(|ue en chirurgie cardiovascu- 



laire experimentale, Anesth. et analg. 10: 426-434, 1953. 



