| Project/Area Number |
05671263
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | Tottori University Faculty of Meddicine |
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Principal Investigator |
ISHIBE Yuichi Tottori University Faculty of Medicine Dept.of Anesthesiology, Assistant Professor, 医学部, 助教授 (40122014)
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| Co-Investigator(Kenkyū-buntansha) |
OHSHIMA Yoshiaki Tottori University Faculty of Medicine Dept.of Anesthesiology Assistant, 医学部附属病院, 助手 (90233105)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1994: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1993: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | nitric oxide / inhalation / hypoxia / pulmonary hypertension / N^<omega>-L-nitro-arginine methyl ester / methylene blue / acethylcholine / N^ω-L-nitro-arginine methyl ester / 一酸化窒素(NO) / 低酸素性肺血管収縮(HPV) / 血管内皮傷害 |
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| Research Abstract |
Since nitric oxide (NO) has been recognized as the endothelium-derived relaxing factor, inhalation of NO gas is applied for therapy of pulmonary hypertension in varieties of lung disease. We examined the mechanism of inhaled NO-induced vasodilation of hypoxic pilmonary vasoconstriction (HPV) using the perfused rabbit lung, and then investigated the effect of inhaled NO on pulmonary hypertension during acute lung injury in dogs. The results showed that inhaled NO (0-30ppm) dose-dependently inhibited HPV response, and inhibition of endogenous NO with NO synthase inhibitor did not affect the dose-response relationship between NO concentration and HPV response, although NO synthase inhibition augmented HPV response per se. Furthermore, methylene blue (MB) that inhibits guanylate cyclase (GC) and blocks signal transduction of NO,partially blocked the effect of inhaled NO,although MB completely inhibited ACh-induced vasodilation. In the dogs with oleic acid-induced lung injury, inhaled NO reduced pulmonary hypertension by 50%, but did not improve systemic oxygenation. These results suggest that inhaled NO may dilate the pulmonary vessels through guanylate cyclase-cyclic GMP system and act as a vasodilator even in the condition with deteriorated signal transduction system. Further studies are required to clarify the effect of inhaled NO during lung injury such as sepsis or ARDS.
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