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.

Experimental Study of the Effect of Nimodipine on CSF Formation

The author has performed an experimental study in order to investigate the effect of nimodipine on the production of CSF in 12 cats. The cats were divided into 2 groups, one for nimodipine intravenous infusion and the other for its vehicle infusion group. Using ventriculo-cisternal perfusion method, nimodipine and its vehicle were examined for their effects on CSF formation rate respectively. Baseline CSF formation rate was 22.5+/-2.9 microliter/min(S.E.) and it gradually reduced to 17.0+/-3.4 microliter/min(S.E.) after final infusion of nimodipine at 60 microgram/kg/min. Vehicle infusion revealed no significant change in CSF formation rate. Although the nimodipine insuion revealed declining tendency in CSF formation rate along with increment of nimodipine concentration, it was not statistically different from that of vehicle infusion group. Systolic blood pressure was significantly reduced after nimodipine infusion(133+/-31.8mmHg at baseline, 93.9+/-19.1mmHg at the end of the experiment) on oneway ANOVA test and it was significantly different from that in vehicle infusion group(p<0.01).

The Effects of Acetazolamide and Fluphenazin on CSF Formation

The purpose of this study was to invstigate the effect of acetazolamide and fluphenazine on the formation of CSF. Studis were performed in 12 cats those were divided into 2 groups;A-F group included animals received initial acetazolamide infusion and additional infusion of fluphenazine to the initial infusion and the F-A group for vice versa. The rate of CSF formation was measured at 3cm above zero outflow pressure by force transducer which connected to personal computer. After obtaining steady value of CSF formation rate, the drugs were infused intravenously according to the protocol. Base line CSF formation rate, 18.87+/-6.52 microliter/min. is reduced to 6.67+/-2.45 microliter/min after acetazolamide infusion and further reduced to 3.48+/-4.06 microliter/min after additional fluphenazine. In fluphenazine group, the base line CSF formation rate, 16.34+/-4.58 microliter/min is reduced to 9.63+/-4.58 microliter/min after initial infusion of fluphenazine and further to 6.45+/-3.64 microliter/min. after additional infusion of acetazolamide. Mean reduction of CSF formation after initial intravenous infusion of acetazolamide and fluphenazine were 59% and 37% respectively. Although statistically insignificant, the CSF formation reduction in A-F group revealed more even and profound value comparing with that of F-A group. These date suggest that in addition to the effect of acetazolamide to reduce the formation of CSF, some other mechanism may exist in CSF formation that major tranquilizer exert the effect on CSF formation.