372 PHYSIOLOGY OF INDUCED HYPOTHERMIA 



in the reservoir was warmed to 37° C. and reinfused via the femoral vein. Because 

 rapid transfusion precipitated ventricular fihrillation in the first two experiments, 

 the rate thereafter was restricted to 5 ml./min. At this rate, and with constant oh- 

 servation of the pulse and immediate cessation of transfusion on the first sign of 

 cardiac irregularity, ventricular fibrillation during transfusion was avoided. When 

 the arterial pressure had risen to 60 mm. Hg, the animal was immersed in a water 

 bath (40^5° C.) to hasten warming. After completion of the transfusion the dogs 

 were given 25 grams of glucose intravenously to counteract the development of 

 hypoglycemia. The blood pressure continued to rise concurrent with the rise in 

 rectal temperature until normal limits were restored. When the animals were re- 

 moved from the bath and dried, some struggling usually occurred. Occasionally 

 weakness or paralysis of the hind legs, especially of the leg with the cannulated 

 femoral artery, occurred and lasted about two days. 



Adequate spontaneous respiration persisted at all temperatures as low as 19° C, 

 so that artificial respiration was not required. 



Data were obtained on pulmonary ventilation, oxygen consumption, cardiac out- 

 put (Fick method), A-V oxygen difference and blood pH (Beckman glass electrode 

 pH meter). 



Three types of experiments were performed. Group I (14 dogs) were treated as 

 described above. Group II (9 dogs) received in addition one million units of crys- 

 talline potassium penicillin-G intravenously and 0.5 gram streptomycin intramus- 

 cularly at the time of transfusion, and twice daily for three days thereafter. From 

 the therapeutic point of view, it was necessary to determine the importance of the 

 time of application of the hypothermia. Accordingly, in Group III (10 dogs) the 

 cooling was started during shock when the level of hypotension was reached. The 

 rectal temperature fell to 28° C. within one hour. In these dogs antibiotic therapy 

 was given as in Group II. 



All dogs which died or were killed were submitted to gross postmortem examina- 

 tion. 



RESULTS 



Effect of hypothermia on tolerance to hypotension and on survival rate in 

 hemorrhagic shock {table II). Previous experiments on uncooled dogs, which 

 received no antibiotic or antibiotics as given in these experiments, provide the con- 

 trol data.'' These show that after about five hours of hypotension (30 mm. Hg) 

 40 per cent of the shed blood will have returned from the reservoir to the circula- 

 tion. At this time the rate at which the blood is returning spontaneously is insuffi- 

 cient to sustain the selected level of hypotension, so that the blood remaining in the 

 reservoir must be rapidly transfused to sustain the blood pressure. The resulting 

 immediate and substantial pressor response is transient, and death follows after an 

 average of six hours of shock. The survival rate is some 15 per cent or less. Sur- 

 vival in these experiments means survival in good condition for at least five days 

 after transfusion. 



In all three groups of experiments with hypothermia the capacity to tolerate 

 severe hypotension is distinctly greater than in uncooled animals. The volume of 

 blood returning to the dog from the elevated reservoir within the period of observa- 



