| Project/Area Number |
61480267
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | Department of Traumatology, Osaka University Hospital |
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Principal Investigator |
SUGIMOTO Tsuyoshi Professor of Osaka University, 医学部・特殊救急部, 教授 (10028342)
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| Co-Investigator(Kenkyū-buntansha) |
KINOSHITA Yoshihiro Lecturer of Osaka University, 医学部・特殊救急部, 助手 (30195341)
UENISHI Masaaki Lecturer of Osaka University, 医学部・特殊救急部, 助手 (90176610)
SUGIMOTO Hisashi Assistant Professor of Osaka University, 医学部・特殊救急部, 講師 (90127241)
YOSHIOKA Toshiharu Associate Professor of Osaka University, 医学部・特殊救急部, 助教授 (60127313)
横田 順一朗 大阪大学, 医学部, 助手 (10166879)
渋谷 正徳 大阪大学, 医学部, 助手 (90187419)
阪本 敏久 大阪大学, 医学部, 助手 (50178571)
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| Project Period (FY) |
1986 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥6,600,000 (Direct Cost: ¥6,600,000)
Fiscal Year 1988: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1987: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1986: ¥4,100,000 (Direct Cost: ¥4,100,000)
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| Keywords | Brain death / Arginine vasopressin / Epinephrine / Heart / Liver / Kidney / Pituitary gland / 病理 / 抗利尿ホルモン(ADH) / 心機能 / 肝機能 / 腎機能 / 膵機能 / 骨髄機能 / 循環動態 |
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| Research Abstract |
In twenty-eight brain death patients simultaneous intravenous administration of arginine vasopressin at an average dose 0.3mU/kg/min and an additional small dose of epinephrine could steadily control not also systemic mean arterial pressure over 80 mmHg, but also diabetes insipidus for more than a week. Through the analysis of circulatory parameters both cardiac output and systemic vascular resistance were maintained in the normal level with the support of vasopressin and epinephrine. ECG revealed ST depression frequently in the first two days, but became normal gradually. The cardiac biopsy specimens were obtained from right ventricular septum. They showed atrophy and hypertrophy of myofilaments and interstitial edema in light microscopy. Severity of mitochondrial ianjury was various in every case, but it was supposed becoming worse gradually in electron microscope. Clinical data in our study showed normal renal function and progressive jaundice in most cases. Histopathologically norm
… More
al glomeruli and desquamation of epithelial cells of tubulus were observed in the specimens of kidney at autopsy. Normal hepatocytes and cholangiolitic changes were observed in the liver specimens. Severity of cholangiolitis depended on the furation from brain death to asystole. These histopathologic findings were comparable to the clinical data. We also studied the change of pituitary galnd after brain death. Basal serum levels of anterior pituitary hormones like ACTH, HGH, LH, FSH, TSH and prolaction were all detectable for seceral days after brain death. TSH and prolaction were both increased in response to added load of TRH. This remaining function of anterior pituitary gland was explained by the two anatomical peculiarities. Firstly, pituitary gland is protected from the direct compressive force of cerebral herniation in the bony structure. Inferior pituitary arteries and capsular arteries run into pituitary galnd through extradural approach. It was suggested that anterior lobe of pituitary gland still survived at least partially after brain death. Less
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