| Project/Area Number |
20592117
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Emergency medicine
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
ISOTANI Eiji Tokyo Medical and Dental University, 医学部附属病院, 講師 (90251529)
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| Co-Investigator(Kenkyū-buntansha) |
大友 康裕 東京医科歯科大学, 大学院・医歯学総合研究科, 教授 (40176946)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2009: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2008: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | subarachnoid hemorrhage / pulmonary edema / triple H therapy / cerebral vasospasm / extravasucular lung water index / 脳神経疾患 / PiCCO plus / 肺血管外水分量 / 胸腔内血液量 / 心機能 / くも膜下出血 / カテコラミン / BNP / 神経原性肺水腫 / CSWS / 血管内容量の再分布 |
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| Research Abstract |
Objectives : Volume management is crucial in intensive care, however, in some patients it is very hard to achieve optimal water balance. Subarachnoid hemorrhage (SAH) patient is a representative example. Cardiopulmonary complications are common after SAH : neurogenic pulmonary edema, cardiac failure, and so on. We have started the multicenter controlled trial about cardiopulmonary function after SAH. In this study we will present the effects of PiCCO plus monitoring after SAH. Methods : We analyzed the cardiopulmonary functions of 62 patients monitored by PiCCO plus during two weeks after SAH. Results : Output, contractility and afterload were essentially normal after SAH. Intrathoracic blood volume was slightly elevated and this fluid redistribution causes hydrostatic fluid retention in lung tissues on PiCCO monitoring after SAH. Conclusions : Persistent catecholamine release and the different sensitivity of blood vessels to catecholamine cause the blood volume redistribution and hydrostatic pulmonary edema. The cardiac preload due to catecholamine release leads to BNP release resulted in natriuresis. This is the underlying mechanism of so-called cerebral salt wasting syndrome.
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