TANI UCHI Tamiki Saitarna Medical School, Medicine, Assistant Staff, 医学部, 助手 (30275888)
海津 啓之 埼玉医科大学, 医学部, 助手 (30204308)
MORIMOTO Tadashi Saitama Medical School, Medicine, Associate Professor, 医学部, 講師 (20230154)
MATSUI Toru Saitama Medical School, Medicine, Assistant Professor, 医学部, 助教授 (70199735)
MORIKAWA Eiharu Saitama Medical School, Medicine, Assistant Professor, 医学部, 講師 (90251256)
|Budget Amount *help
¥3,200,000 (Direct Cost : ¥3,200,000)
Fiscal Year 1999 : ¥1,100,000 (Direct Cost : ¥1,100,000)
Fiscal Year 1998 : ¥700,000 (Direct Cost : ¥700,000)
Fiscal Year 1997 : ¥1,400,000 (Direct Cost : ¥1,400,000)
Whether brain hypothermia is established as a tool for the clinical treatment of the permanent focal cerebral isehemia remains to be yet. The first study aimed at comparing the effects of the 6 hour of selective brain hypothermia on final outcome of the experimental stroked animals.which were killed 6 (Experiment 1-1), 24 (Experiment l-2), 48 (Experiment 1-3) and 168 (Experiment 1-4) hours after occlusion ofleft middle cerebral artery.
A total of 116 Sprague-Dawley rats were divided into the above 4 groups, each of which included control animals (Group B)and sham-operated ones (Group C). They were endotracheally intubated and ventilated artificially. The proximal portion of the middle cerebral artery (MCAo) was electrically coagulated and then cut.
Our original methodology of the surface coil which perfused ice water enabled us to start selective brain hypothermia (SBH) immediately after MCAo during a period of 6 hours under general anesthesia (Group A). In the animals subjected to Group
s B and C, the brain temperature was kept normal during the anesthesia. During the experiment, the brain temperature, the rectal temperature, blood pressure and blood gas were continually recorded. Each animal was extubated after the rewarming, and bred in the cultivating cage at room temperature until they were killed. At the end of experiments, the brain was perfused transcardially and removed. The brain slices were stained for measuring an infarction volume.
In the second experiment, our methodology was refined on, providing the less invasive method. The difference between these two methods is to keep anesthesia by mask and spontaneous respiration and only 4 hour of brain hypothermia immediately after MCAo in the refined one. The effects of SBH on infarct size at 168 hours of MCAo were compared among the SBH-, control and sham-operated groups.
The brain temperature of the SBH-group reached 32℃ within 20 minutes after the MCAo, and then stayed around 30 during the SBH. A complete rewarming needed only one hour. No abnormal finding was demonstrated in the systemic parameters. The infarction volume (mm3 mean ± standard deviation) was as follows. Experiment 1-1 (n=27) A (n=16)60 ±28, B (n=8) 130±6, C (n=3) 11±2; Experiment 1-2 (n=25) A (n=14) 84±25, B (n=6) 137±27, C (n=5) 4 ± 4; Experiment 1-3 (n=21) A (n=8) 33±11, B (n=8) 96±25, C(n=5) 7±7; Experiment 1-4 (n=l0) A (n=5) 41±20, B(n=3) 86±23, C(n=2) 6±7; Experiment 2 (n=33) A (n=11) 25±18, B (n=13) 100±41, C (n=9) 2±2
The present type of SBH is shown to significantly reduce the infarction volume up to 168 hours after the onset of ischemia, from the analysis of variance with the p-value of less than 0.05. The present results open up a new promising therapeutic strategy against the brain stroke. Less