1996 Fiscal Year Final Research Report Summary
Clinical Application of Nitric oxide (No) in Pulmonary Hypertension.
| Project/Area Number |
07670526
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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 |
内科学一般
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| Research Institution | University of Tokyo |
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Principal Investigator |
MURATA Ichiro University of Tokyo, Department of Medicine And PHysical Thefapy Assistant Professr, 医学部・附属病院, 助手 (30190911)
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| Co-Investigator(Kenkyū-buntansha) |
SATOU Makoto University of Tokyo, Department of Medicine And PHysical Thefapy Assistant Profe, 医学部・附属病院, 助手
TAKEUCHI Fujio University of Tokyo, Department of Medicine And PHysical Thefapy Assistant Profe, 医学部・附属病院, 講師 (70154979)
TAKIZAWA Hajime University of Tokyo, Department of Medicine And PHysical Thefapy Assistant Profe, 医学部・附属病院, 助手 (80171578)
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| Project Period (FY) |
1995 – 1996
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| Keywords | systemic sclerosis / pulmonary hypertension / pulmonary fibrosis / pulmonary arteriopathy / nitric oxide (NO) / NO in expired air / NO inhalation |
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| Research Abstract |
We attempted to diagnose pulmonary hypertension (PH) in 135 patients with systemic sclerosis and related disorders. PH was diagnosed in 28 patients by Doppler echocardiography and in 2 patients by right heart catheterlzation. PH was attributable to pulmonary fibrosis in 9 patients who had proximal scleroderma without SLE/polymyositis overlap. Pulmonary arteriopathy was the probable cause of PH in 7 patients with overlap and in 4 patients who had proximal scieroderma without overlap. We quantified nitric oxide (NO) in the exhaled air of these patients patients to obtain baseline data for NO inhalation therapy. Although the major source of NO in expired air is the nasopharynx, the quantity of NO could reflect NO production in the pulmonary vascular endothelium with the use of a mouthpiece and noseclip for collection of expired air. Eighteen clinically stable patients and 15 normal controls were studied. The cause of PH was pulmonary arteriopathy in 13 patients and pulmonary fibrosis in 5
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patients. Heasurements were made at rest with subjects sitting and during incremental cycle ergometry exercise (1 W/sec). Subjects breathed through a mouthpiece attached to a gas spectrometer for continuous measurement of expired air voiume. For measurement of NO concentration, exhaled air was directed through a sampling tube into an NO chemiluminescence analyzer. NO output was calculated by multiplyng NO concentration by minute ventilation. While NO production in control subjects more than doubled by peak exerclse, there was no significant rise with exercise in patients with arterlopathy (p<0.001). NO production was significantly reduced in patients with pulmonary fibrosis compared with controls and patients with pulmonary arteriopathy both at rest and during exercise (p<0.01). The low NO production in pulmoanty fibrosis may be due to loss of normal functional vascular endothelium. The failure to lucrease NO production in pulmonary fibrosis and arteriopathy may refiect an insufficient recruitment of the capillary bed during exercise. NO supplementation could reduce pulmonary vascular resistance in these patients. Less
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