| Co-Investigator(Kenkyū-buntansha) |
KUWAGATA Yasuyuki Osaka University, Traumatology, Research Fellow, 医学部, 医員
YAHATA Kouhei Osaka University, Traumatology, Research Fellow, 医学部, 医員
KINOSHIA Yoshihiro Osaka University, Traumatology, Assistant, 医学部, 助手 (30195341)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1991: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1990: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1989: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Research Abstract |
We found another two important facts during our series of studies in the brain dead patients with long-term stable circulation maintained by our vasopressin(ADH)and catecholamine method. One fact is that hypothalamic hormones still present in the serum of brain dead patients, though they met all the criteria of brain death, even several days after the diagnosis. The other is that body movement induced by painful stimuli and/or various types of voluntary movement are seen in brain dead patients. These two facts might contradict to the definition of the brain death ; "irreversible cessation of all functions of entire brain". In this study, we aimed to explain the meaning of these two facts.
We have got following results through this study :
## Results I ## Hypothalamic hormones, such as CRH, GRH and LH-RH, were detected in the serum of brain dead patients as long as 17 days after brain death. All brains, however, showed necrotic autolysis at most 7 days after brain death. This suggests the
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se hormones should be derived from any other tissues than the hypothalamus. Hypothalamic stimulation tests by insulin-induced hypoglycemia and arginine infusion showed absence of reacting secretion of CRH, ACTH, cortisol or GRH from hypothalamus. The serum endogenous ADH level decreased rapidly just after the brain death and had never increased in spite of abnormally high serum osmotic pressure. This means neither production of ADH in the hypothalamus nor commands from the upper nervous system to the pituitary gland is seen after brain death. These results do not contradict to the concept of brain death.
## Results 2 ## Various spinal reflexes disappeared temporally just after the brain death but were frequently observed again 5 to 10 days after brain death. Autopsy showed necrotic autolysis of the spinal cord which started from the upper cervical cord and developed downward to various level. All of them, however, were thought to be derived from the residual intact cord. We found a new autonomic reflex elicited by passive neck flexion for the first time in the world which is characterized by hemodynamic response such as marked increase of blood pressure and tachyeardia. This reflex was seen frequently in brain death(in 10 of 12 cases)and never seen in any other patients than brain death. Furthermore, this reflex was seen even in patients whose upper thoracic cord were degenerated, and depressed completely by a ganglion blocker. This reflex, therefore, is considered specific for brain death and to be a peripheral autonomic reflex including sympathetic ganglia. In the somatosensory evoked potential by stimulating the nervus medianus, the N13 peak, which was initially seen obviously, became dull gradually and disappeared 7 to 10 days after brain death. The N13 peak is thought to be derived from the upper cervical spinal cord. This suggests that the necrotic autolysis of the spinal cord is caused within 2 or 3 days after brain death and that of the lower cord 7 to 10 days later. Less
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