The Changes of Cortical Spreading Depression During Hypothermia and Rewarming in Rat

The present study was carried out to evaluate the effect of hypothermia and rewarming on the pattern of Cortical Spreading Depression(CSD) and predict the resultant vulnerability of the brain. Thirty four Sprague-Dawley rats, either sex, weighing 250-350gm, were used. They were devided into 4 groups, according to the degree of hypothermia and speed of rewarming, Profound Hypothermia & Slow Rewarming(G I), Profound Hypothermia & Rapid Rewarming(G II), Moderate Hypothermia & Slow Rewarming(G III), Moderate Hypothermia & Rapid Rewarming(G IV). CSD was elicited by local application of KC1 and identified by Direct Current Potential(DCP). We estimated the Frequency of DCP, Recovery time of negative shift of DCP, Area of negative shift of DCP according to the change of body temperature. The frequencies of DCP increased after rewarming compared with the normothermic state in all groups, statistical significance(P<0.05) was specially evident in Group II(Profound Hypothermia & Rapid Rewarming group), 5.1+/-0.3/30min.(mean+/-standard error) in normothermic state, while 9.3+/-0.8/30min in rewarming state. Recovery time(width) of DCP was delayed with hypothermia but decreased with rewarming but delayed state compared with normothermic state in all groups, i.e. 34.7+/-1.0sec at normothermic state, 59.9+/-4.3sec at 27.5 degrees C, 40+/-1.4sec at rewarming state in Group II. We can predict that the vulnerability of the brain tissue may be increased during the rewarming state following hypothermia in all groups. Such evidence is more significant in Group II(Profound Hypothermia & Rapid Rewarming) during the period of certain time(30-60min) after rewarming.

Influence of Hypoglycemia and Hypothermia on Direct Current Potential During Cortical Spreading Depression in Rats

The object of this study was to investigate the influences of hypoglycemia and hypothermia on the direct current(DC) pontetial changes during cortical spreading depression(CSD) in rats. The induction of CSD was achieved by the application of KCI solution on the cortex of the frontal lobe. Hypoglycemia and hypothermia were induced respectively by insulin injection and the application of an ice pack. The DC potential changes during progressive hypoglycemia and hypothermia were measured with microelectrodes from the cortex of the parietal lobe of rats. Under contril condition, the rate of CSD was one per 5-10 min and the negative shift of DC potential was about 30 mV. The recovery time from negative shift to base line of DC potential was about 40 sec. In rats treated with insulin, the amplitude of DC potential shift was unaffected by hypoglycemia. The recovery time of DC shift was 40+/-2.26 sec at normoglycemia and it was delayed progressively as the blood glucose level lowered. The mean of it was 63+/-8.02 sec at 30 mg/dl and 77.1+/-22.0 sec with the blood glucose falling below 20 mg/dl. The same delay in the recovery time as seen in the hypogylcemia group was observed in rats treated with hypothermia. The recovery time of DC shift was 39.4+/-3.02 sec in normothermia(36.5degrees C), but it was delayed to 61.15+/-4.15 sec at 30degrees C and 96.67+/-14.92 sec at 26degrees C body temperature. This study suggested that each condition of profound hypoglycemia below 30 mg/dl and hypothermia below 30degrees C was to be harmful to the ion homeostasis and the integrity of the cell membrane and it may lead neurons to death.