1992 Fiscal Year Final Research Report Summary
Does denervation supersensitivity develop after brain death ?
| Project/Area Number |
03670832
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Ophthalmology
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| Research Institution | Saga Medical School |
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Principal Investigator |
OONO Shinji Saga Medical School Ophthalmology Professor, 医学部, 教授 (60050390)
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| Co-Investigator(Kenkyū-buntansha) |
INOUE Tomohiro Saga Medical School Research Associate, 医学部, 助手 (80223262)
NAGAHAMA Masahiro Saga Medical School Research Associate, 医学部, 助手 (50148821)
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| Project Period (FY) |
1991 – 1992
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| Keywords | Brain death / Internal carotid ligation / Vertebral artery clipping / Ciliospinal reflex / Auditory brainstem response / Circulation arrest / Aqueous turnover / Denervation supersensitivity |
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| Research Abstract |
Adult cats both sexs were used in this experiment In order to obtain experimental brain death, the bilateral internal carotid arteries were ligated and the vertebral arteries were clipped under Nembutal anesthesia. We emolyed this because of its reliability and simplicity after comparison of several procedures. Cats were always left on a respirator after discontinuation of blood circulation to the brain.
The pupil became gradually dilated after the discontinuation of circulation to the brain. It moderately dilated and fixed around 2 hours later. Reflex pupillary dilatation to the sciatic nerve stimulation and the light reflex usually discernible during this transitional stage. Reflex pupillary dilatation is the ciliospinal reflex in a wide sense. It disappeared after the completion of brain death. This result strongly suggests that reflex pupillary dilatation could be an adjuvant diagnostic tool of brain death. Auditory brainstem response also disappeared in this experiment.
Supersensitivity to the autonomic drugs, 0.125% pilocarpine in this experiment, was not proven at least 48 hours after brain death. Supersensitivity observed in human brain death does not appear to be caused by true denervation supersensitivity. It is known that the blood circulation in the brain discontinues or almost ceases under brain death. It is, therefore, reasonable to assume that supersensitivity observed in brain death is due to delay or stasis of the aqueous turnover, and accumulation or metabolic delay of the drugs in the iris and its surrounding tissues.
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