352 



PHYSIOLOGY OF INDUCED HYPOTHERMIA 



TABLE V 



Experience with Treatment of Coronary Air Embolism and Ventricular Fibrillation in 



Hypothermic Dogs Subjected to Right Ventriculotomy and Placement of Sutures 



IN Ventricular Septum by Cardiac Massage, Intracardiac Epinephrine, 



AND Electric Shock 



(Surgery, Nov., 1955) 



Sinoauiicular node injection after onset of fibrillation 



" Before the last successful defibrillation sinoauricular node was injected. 



onset of fibrillation, while it occurred repeatedly in half the others. In one, fibrilla- 

 tion developed 10 times and lasting conversion followed procaine injection. 



Using the information derived from these experiments, we were able to produce 

 and repair ventricular septal defects in a series of dogs without mortality.^ 



Recent experiments have demonstrated that the period of safe venous inflow 

 occlusion in moderately hypothermic dogs can be markedly prolonged by perfusion 

 of the coronary arteries, or the coronary and carotid arteries, with oxygenated 

 blood. ^ These animals were cooled to a body temperature of from 24° to 28.5° C. 

 Of 12 dogs with coronary perfusion subjected to venous inflow occlusion of from 

 25 to 29.5 minutes, an ultimate normal recovery was made by 11. The exceptional 

 animal died of hemorrhage. One of the animals exhibited hind leg weakness for 

 two days, five were stuporous the day following surgery, and one for three days. 

 The behavior and function of all, however, appeared normal thereafter. Fifteen ani- 

 mals with coronary and carotid artery perfusion were sul)jected to right ventric- 

 ulotomy and venous inflow occlusion of from 26 to 35 minutes. All recovered 

 without any evidence of cord or brain damage. Three, however, died later of 

 hemorrhage. One with an occlusion period of 38 minutes died after five days of 

 stupor. In some animals in both groups ventricular fibrillation occurred after re- 

 lease of caval occlusion but in all conversion was easily accomplished. All had been 

 protected by procaine blockade of the superior vena cava-atrial junction. Transient 

 neurologic sequelae were noted in some of the animals with coronary perfusion 

 alone and in none with coronary and carotid perfusion subjected to comparable 

 periods of venous inflow occlusion. The fact that eventual recovery took place in 



