| Project/Area Number |
09670700
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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 |
Circulatory organs internal medicine
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| Research Institution | University of Tokyo |
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Principal Investigator |
HIRATA Yasunobu (1998) Univ. of Tokyo, Internal Med. , Lecturer, 医学部・附属病院, 講師 (70167609)
百村 伸一 (1997) 東京大学, 医学部附属病院, 助手 (10190985)
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| Co-Investigator(Kenkyū-buntansha) |
MOMOMURA Shin-ichi Toranomon Hospital, Internal Med. , Chief, 沖中記念研究所, 部長 (10190985)
TAKENAKA Katsu Univ. of Tokyo, Internal Med. , Lecturer, 医学部・附属病院, 講師 (20188204)
SUGIURA Seiryo Univ. of Tokyo, Internal Med. , Assist. Prof., 医学部・附属病院, 助手 (10272551)
AOYAGI Teruhiko Univ. of Tokyo, Internal Med. , Assist. Prof., 医学部・附属病院, 助手 (10251240)
MATSUMOTO Akihiro Univ. of Tokyo, Internal Med. , Clin. fellow, 医学部・附属病院, 医員
横山 郁夫 東京大学, 医学部附属病院, 医員
平田 恭信 東京大学, 医学部附属病院, 講師 (70167609)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1997: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Nitric Oxide / Exhaled gas / plasma NOx / Exercise test / hypertension / hyper lipidemia / diabetes mellitus / renal disease / 慢性心不全 / 慢性閉寒性肺疾患 |
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| Research Abstract |
This study was performed to establish nitric oxide(NO) measurement iii the exhaled air in humans and to assess whether endogenous NO production of the lungs is abnormally regulated at rest amid during exercise in patients with various kinds of diseases such as congestive heart failure (CHF), hypertension (HT), hypercholesteremia (HL), diabetes mellitus (DM), lung diseases, chronic glomerular nephritis (CGN), and chronic renal failure (CRF). Plasma concentrations or nitrite plus nitrate (NOX) were measured by lime Griess method as indicators of systemic NO production.
1) Patients with CHF (n=14) had higher exhaled NO concentration and output than controls. Exercise increased NO output about 3 times in controls, but the increase was smaller in the patients. These findings suggest that abnormal regulation of NO production may cause the attenuated exercise-induced vasodilation iii heart failure.
2) Patients with HT, HL, and DM had the similar levels of exhaled NO concentration amid output co
… More
mpared with normal controls at rest. Although exercise increased NO output in both groups, the increase was less in these patients than was normals. Plasma NOX concentrations in the normals increased during exercise, but not in patients with HT.These findings suggested that exercise-induced increase of NO production, most likely as a consequence of increased shear stress, was impaired in these patients.
3) Patients with lung diseases such as idiopathic pneumonitis and collagen diseases, had a higher exhaled NO concentration amid output. These results suggest that endogenous NO production is increased in the lungs of patients with mining imflamation of collagen diseases, and it may play some pathophysiological roles in these patients.
4) Patients with CGN (n=21) exhaled higher concentrations of NO and output than did controls. Plasma NOX concentrations were also significantly greater in the patients than in the controls. In patients with CGN, exhaled NO output correlated negatively with creatinine clearance. These findings suggested that endogenous NO production is increased in patients with CGN.Increased endogenous NO production may play sonic pathophysiological role in these patients.
5) Patients with CRE (n=40) had a higher exhaled NO concentration and output, and a higher plasma NOX concentration than did controls. These values did not differ between patients on hemodialysis amid those on continuous ambulatory peritoneal dialysis. The increase in exhaled NO with the simultaneous increase in circulating cytokines suggests that NO synthase seems to be induced significantly in these patients. increased endogenous NO production may have sonic pathophysiological role in uremic patients. Less
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