Profound hypothermia was achieved in 45 dogs by extracorporeal perfusion with heat exchanger and autogenous [lung oxygenation. The dogs were anesthetized with penthotal sodium and hyperventilated with oxygen through the endotracheal tube. Right thoracotomy through the 4th intercostal space was performed for cardiac cannulazation. Heparin (3mg/kg) was infused before cannulazation and polybrene (2.7mg/kg) after decannulazation.
During the first step of cooling, blood drained by gravity via the left atrial cannula into the reservoir was pumped into the heat exchanger by DeBakey type pump, then into the femoral artery. Ventricular fibrillalion occurred at the esophageal temperature of 25° to 30°C., after which the second step of cooling was started by the right heart perfusion. Venous. blood was drained from the right atrium by gravity and pumped into the pulmonary artery via the cannula inserted across the right ventricular outflow tract. When the esophageal temperature fell, to I5°C. cooling was stopped and circulatory arrest carried out by occlusion of vena cavae and clamping of the aorta.
The dogs were divided into two groups: in group I, pre-perfusion cooling of the blood in the heat exchanger and pump system was not carried out, whereas pre-perfusion cooling was done in group II. Circulatory arrest time in group I and lI was 10 and 30 minutes respectively. The right atriotomy for group I and the right ventriculotomy for group II were-performed during circulatory arrest.
After circulatory arrest the first step of rewarming was started, the procedure being essentially the same as that of the second step of cooling. When the body temerature reached 30° to 32°C., spontaneous regular beats appeared in some dogs and in the others electrical defibrillation was attempted. As soon as the heart beat became regular and strong the right heart perfusion was discontinued. As the esophageal temperature reached 35° C., left heart perfusion was also stopped, leaving the dogs in the room temperature.
Physiological and histological changes were studied and the results are summarized as follows. 1) Perfusion blood flow was 48 to 73 cc per kilogram of the body weight per minute during cooling and rewarming. 2) Cooling time to the esophageal temperature of 15°C. in group I and group II was 76 and 31 minutes respectively. Rewarming time to 32° C. in group I was 63 minutes and 32 minutes in group II. The esophageal temperature was reduced at a rate of 0.4°C/min. in the first step of cooling and 0.2"C. /min. in the second step in group I. In group II, cooling rate in the first and second. steps of cooling was 1°C./min. and 0.5°C/min. respectively. The rewarming rate of the two groups for the first and second steps were almost the same.
3) Ventricular fibrillation occurred as cooling progressed. it occurred at the mean, esophageal temperature of 26.3°C. in group I and 23.5°C. in group II. Ventricular fibrillation became more fine as body temperature approached 15°C. and they were so fine that in most of the dogs no visible motion was noted during circulatory. arrest. Ventricular fibrillation became coarse when body temperature increased. In half of the dogs of group I and about 15% of the dogs of group II spontaneous normal beating appeared at the mean esophageal temperature of 30° to 32°C. Except 3 dogs of group II, electrical defibrillation was successful in the others.
4) Arterial blood pressure fell as cooling progressed and returned to normal range on rewarming. Venous pressure did not change significantly during cooling and rewarming.
5) Formed elements of blood showed various changes: hemoglobin, hematocrit, and red and white blood cell counts decreased below the esophageal temperature of 25°C. and failed to resume normal range after rewarming.. Polymorphonuclear neutrophiles played an important role in changing the white blood cell count. Platelets count also decreased on cooling but did not recovered on rewarming.
6) The mean value of 02 and CO2 content of arterial blood showed no change at the esophageal temperature of 15°C. However the mean value of 02 saturation of the arterial blood at 15°C. was 103.9% whereas the control value was 93%.. The mean value of 02 content of the venous blood at i5°C. increased so that a-V 02 difference increased at this temperature.
7) The dogs were hyperventilated throughout the experiment. Respiratory alkalosis at the pre-cooling state was -changed to metabolic acidosis when the body temperature dropped to 15°C., then to mixed acidosis when the body temperature increased to 3G° C.
8) Blood electrolytes, Na and K stayed ;unchanged. Amylase and lipase activity were depressed by cooling and returned to normal level on rewarming.
9) Prolongation of P-R interval, QRS complex and width of P wave occurred as the body temperature
decreased and returned to normal range on rewarming. Elevation of S-T segment and flattening or inversion of T wave were constant findings during cooling and returned to normal as the body was rewarmed.
10) Nearly all dogs died within 24 hours following termination of the experiments.
11) Among the histological changes of the various organs edema of the brain was considered as the cause of death.
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