| Project/Area Number |
61480332
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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 |
麻酔学
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| Research Institution | Nagoya University School of Medicine |
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Principal Investigator |
SHIMADA Yasuhiro (MIYAMOTO Yoshihiro) Nagoya University School of Medicine, 医学部, 教授 (50028669)
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| Co-Investigator(Kenkyū-buntansha) |
KAINUMA Motoshi Nagoya University School of Medicine, 医学部, 講師 (90135335)
ISHIKAWA Naohisa Nagoya University School of Medicine, 医学部, 助教授 (80109321)
SHIGEI Tatsuro 名古屋大学, 名誉教授 (60013786)
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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 |
¥6,800,000 (Direct Cost: ¥6,800,000)
Fiscal Year 1988: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1987: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1986: ¥3,300,000 (Direct Cost: ¥3,300,000)
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| Keywords | Pulmonary Edema / Neurogenic Pulmonary Edema / Anesthetic Depth / Vagus Nerve / Cardiopulmonary Nerve / Carbon Dioxide Concentration / Schwann cells / Dorsal root ganglia / Neurite outgrowth / Fibroblasts / Sciatic nerves / 星状神経節 / 神経原性肺水腫 / 気管支循環 / 血管透過性亢進 / セロトニン,ケタンセリン / 人工呼吸 / PEEP |
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| Research Abstract |
There is a controversy on the pathophysiology of neurogenic pulmonary edema (NPE), namely hydrostatic and permeability mechanisms. When ischemia develops in the central nervous system, hemodynamic changes occur both in systemic and pulmonary circulation, which would further complicate the study on NPE. The authors devoloped canine in situ model using two extracorporeal circulation systems and separating pulmonary circulation from systemic circulation. In situ lungs were perfused in the presence or absence of the cardiopulmonary nerves (CPN). A right-heart bypassed preparation was made first. It was then switched to a lung perfusion preparation and the lungs received all influences of sudden cessation of the brain and systemic circulation via the CPN. Hydrostatic mechanisms causing pulmonary edema were excluded by adjusting the pulmonary arterial preaaure less than 24mmHg. Accumulation of the extravascular lung water and rate of reaervoir blood loss were significantly lower in the CPN-severed group compared to the CNP-intact group. The result. indicates a CPN-mediated mechanism of permeability edema. Effects of the depth of anesthesia and intervention in the vagus nerves on the development of fibrin-induced NPE were examined in rats. Solutions of fibrinogen and thrombin were injected into the cisterna magna. Rats were anesthetized with an intraperitoneal injection of sodium pentobarbital, either 25 or 50mg/kg. Intervention in the vagus nerves consisted of intravenous atropine 1mg/kg or bilateral vagotomy. Lung water ratio was calculated as a ratio of the difference between wet and dry lung weight to dry lung weight. Incidence of pulmonary edema and lung water ratio were significantly decreased under deep anesthesia compared to light anesthesia. Lung water ratio was significantly increased in the vagotomized rats under light anesthesia compared to other groups. The results indicate the effects of anesthetic depth and vagus nerve on the development of NPE.
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