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HYPOXIA and ischemia are well documented as causal agents of cerebral edema and irreversable brain damage.1-7 Since the permanent deleterious effects of lowered O2 tension can, to some extent, be protected against by hypothermia, it was of interest to explore the influence of low temperature on the development of cerebral edema during circulatory arrest. In the experiments on rats presented here, deep hypothermia was induced by the closed vessel method of Andjus and resuscitation was accomplished with ul-$ trashortwave diathermy in the early stage of rewarming.8-11 Significant brain edema was not observed after one hour of circulatory arrest with hypothermia of 3 to 5 C, while moderate hypothermia of 20 C without hypoxia was observed to cause a contraction of the brain. Materials and MethodsForty-six male, Sprague-Dawley rats weighing 150 to 200 gm were used. Twelve of these had hypothermic circulatory arrest while under hypercapnic hypoxic anesthesia. Parameters such as blood gas tension and pH, brain water content, and survival were recorded and com¬ pared with those from control groups which underwent selected parts of the entire protocol.The treatment of all groups is summarized below. The rats subjected to the complete cir¬ culatory arrest protocol were placed in a closed two-liter vessel in a refrigerator at 4 C where they remained for 90 to 100 minutes. When removed, they had slow respiration and their rectal temperature was 17 to 20 C. They were then submerged in ice water with the nose and mouth protruding above the surface. They con-tinued to breathe slowly for several minutes until their colonie temperature dropped below 16 C. While in ice water, the animals cooled at a rate of about 1.3 C/min until going into cardiac standstill which was determined by an electro¬ cardiogram recording. After cardiac arrest, temperatures dropped slowly downward to less than 2 C. After 50 minutes of circulatory ar¬ rest, the rats were taken from the ice, damp dried, and placed on a 7 mm thick glass plate suspended between two diathermy electrodes (Fig 1). (This electrode configuration was sug¬ gested in a personal communication from Dr.Herman P. Schwan of the Moore School of Electrical Engineering, University of Pennsyl¬ vania.) The electrodes were connected to a 27 mega Hz (27 X 10e cycles per second) diather¬ my unit which delivers a maximum output of 440 watts (Fishertherm) in a capacitance configuration. It was not possible to measure the effective output to the animal but thermis¬ tor measurements of colonie temperature, made during intermittant power off periods, indicated a rise of 1 C/min. Positive pressure respiration with 100% 02 was administered from the start of rewarming. When the temperature reached 15 C, the diathermy was stopped and the ani¬ mals transferred to a 40 C water bath. ECG recordings at this time showed an average heart rate of 60 beats per minute, and spontaneous respiration appeared between 27 and 30 C, with a heart rate of 240 and 180 beats per minute.When the temperature of the animals reac...
HYPOXIA and ischemia are well documented as causal agents of cerebral edema and irreversable brain damage.1-7 Since the permanent deleterious effects of lowered O2 tension can, to some extent, be protected against by hypothermia, it was of interest to explore the influence of low temperature on the development of cerebral edema during circulatory arrest. In the experiments on rats presented here, deep hypothermia was induced by the closed vessel method of Andjus and resuscitation was accomplished with ul-$ trashortwave diathermy in the early stage of rewarming.8-11 Significant brain edema was not observed after one hour of circulatory arrest with hypothermia of 3 to 5 C, while moderate hypothermia of 20 C without hypoxia was observed to cause a contraction of the brain. Materials and MethodsForty-six male, Sprague-Dawley rats weighing 150 to 200 gm were used. Twelve of these had hypothermic circulatory arrest while under hypercapnic hypoxic anesthesia. Parameters such as blood gas tension and pH, brain water content, and survival were recorded and com¬ pared with those from control groups which underwent selected parts of the entire protocol.The treatment of all groups is summarized below. The rats subjected to the complete cir¬ culatory arrest protocol were placed in a closed two-liter vessel in a refrigerator at 4 C where they remained for 90 to 100 minutes. When removed, they had slow respiration and their rectal temperature was 17 to 20 C. They were then submerged in ice water with the nose and mouth protruding above the surface. They con-tinued to breathe slowly for several minutes until their colonie temperature dropped below 16 C. While in ice water, the animals cooled at a rate of about 1.3 C/min until going into cardiac standstill which was determined by an electro¬ cardiogram recording. After cardiac arrest, temperatures dropped slowly downward to less than 2 C. After 50 minutes of circulatory ar¬ rest, the rats were taken from the ice, damp dried, and placed on a 7 mm thick glass plate suspended between two diathermy electrodes (Fig 1). (This electrode configuration was sug¬ gested in a personal communication from Dr.Herman P. Schwan of the Moore School of Electrical Engineering, University of Pennsyl¬ vania.) The electrodes were connected to a 27 mega Hz (27 X 10e cycles per second) diather¬ my unit which delivers a maximum output of 440 watts (Fishertherm) in a capacitance configuration. It was not possible to measure the effective output to the animal but thermis¬ tor measurements of colonie temperature, made during intermittant power off periods, indicated a rise of 1 C/min. Positive pressure respiration with 100% 02 was administered from the start of rewarming. When the temperature reached 15 C, the diathermy was stopped and the ani¬ mals transferred to a 40 C water bath. ECG recordings at this time showed an average heart rate of 60 beats per minute, and spontaneous respiration appeared between 27 and 30 C, with a heart rate of 240 and 180 beats per minute.When the temperature of the animals reac...
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