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Biomedical subjects

H Mitsufuji

Publications and source records attributed to H Mitsufuji.

8 recordsLinked to original sources
PubMed2001

Antiinflammatory properties of inducible nitric oxide synthase in acute hyperoxic lung injury.

The objective of this study was to determine whether endogenous nitric oxide (NO), specifically the inducible NO synthase isoform (iNOS: NOS II), reduces or amplifies lung injury in mice breathing at a high oxygen tension. Previous studies have shown that exogenous (inhaled) NO protects against hyperoxia-induced lung injury, and that endogenous NO derived from iNOS inhibits leukocyte recruitment and protects against lung injury induced by lipopolysaccharide. In the present study, hyperoxia (> 98% O(2) for 72 h) induced acute lung injury in both wild-type and iNOS-deficient mice as determined by elevated albumin and lactate dehydrogenase levels in bronchoalveolar lavage fluid (BALF) and by increased extravascular lung water. Lung injury was greater in iNOS-deficient mice than in wild-type mice and was associated with an increased number of polymorphonuclear leukocytes in BALF. iNOS messenger RNA expression levels increased in the lungs of wild-type hyperoxic mice. Nitrotyrosine, a marker of reactive NO species, was expressed in both wild-type and iNOS-deficient mice in hyperoxia, indicating an iNOS-independent pathway for protein nitration. We conclude that iNOS is capable of reducing pulmonary leukocyte accumulation and lung injury. The data indicate that iNOS induction serves as a protective mechanism to minimize the effects of acute exposure to hyperoxia.

Acute Disease↗
PubMed2001

Acute changes in bronchoconstriction influences exhaled nitric oxide level.

In previous studies the exhaled nitric oxide (NO) level of asthma patients was investigated only in association with bronchial inflammation, and whether the degree of bronchoconstriction itself influences the exhaled NO level has never been investigated. We therefore evaluated the effect of inhalation of a bronchoconstrictor (methacholine) or a bronchodilator (salbutamol) on the exhaled NO level of healthy volunteers and asthma patients. The exhaled NO level of the healthy volunteers decreased after methacholine inhalation. The exhaled NO level of patients with mild or moderate persistent asthma, who had no asthma attacks on the day of measurement, increased after salbutamol inhalation, and the exhaled NO level of asthma patients during asthma attacks increased after salbutamol inhalation followed by intravenous drip infusion of aminophylline. It is suspected that large amounts of NO are trapped in the lung distal to the constricted airway, contributing little to the exhaled NO level at the mouth. However, we expect that the trapped NO is exhaled at a larger fraction after the dilatation of the constricted small airway, thereby increasing the exhaled NO level at the mouth. In conclusion, the results of this study suggest that acute changes in bronchoconstriction themselves influence the exhaled NO level independently of the change in NO synthase activity associated with airway inflammation.

Adult↗
PubMed1997

[A standard maneuver to measure the concentration of exhaled nitric oxide].

We measured the concentration of nitric oxide (NO) exhaled during a standard maneuver in 55 healthy subjects (nonsmokers: 23 men and 32 women). After two deep breaths, each subject exhaled from total lung capacity through the mouth at 2 L/min into a Teflon tube connected to a chemiluminescence analyzer. The concentration of exhaled NO was defined as the plateau value measured during the latter part of expiration. In nonsmokers, the concentration was 28.7 +/- 12.2 ppb (mean +/- S.D.), which did not differ from that in smokers. The logarithm of the NO concentration (logNO) was normally distributed; it was significantly related to expiratory flow rate, but not to age, height, weight, sex, or the number of cigarettes smoked per day. The 95% confidence interval for the concentration of exhaled NO in healthy nonsmokers was 10.2 to 64.6 ppb.

Adult↗
PubMed1995

[Basic evaluation of nitric oxide inhalation therapy].

We studied the site of action of nitric oxide (NO) and the dose-response relationship between inhaled NO and PaO2. We also measured nitrosyl-hemoglobin (Hb-NO) levels in arterial and mixed venous blood and NO2 levels in our NO inhalation system to confirm the safety of NO inhalation. In an ovine model of ARDS induced by lung lavage, pressure-flow plots indicated that the site of action of inhaled NO was close to the alveoli. During hypoxia, pulmonary artery pressure decreased as the concentration of inhaled NO increased; PaO2 peaked at 10-20 ppm NO. The levels of Hb-NO in arterial and mixed venous blood during inhalation of 40-60 ppm NO under hypoxic conditions were greater than the levels under normoxic conditions, but Hb-NO still accounted for less than 0.1% of the total Hb. Less than 0.1 ppm on NO2 was generated during inhalation of 5 ppm NO. In conclusion, inhaled NO can dilate pulmonary vessels near alveoli without lowering the O2 carrying capacity of blood. In the present system, only a negligible amount of NO2 was produced.

Administration, Inhalation↗
PubMed1994

[A case of aspirin-induced asthma which developed due to rubbing a lotion containing a non-steroidal anti-inflammatory drug, ketoprofen, on the skin].

A forty-year-old woman was admitted to our hospital because of a severe attack of bronchial asthma. The asthmatic attack developed 3 hours after her rubbing a large amount of a lotion containing a non-steroidal anti-inflammatory drug (NSAID), ketoprofen, over her skin. The patient had a past history of asthmatic attack induced by another NSAID (Sedes-G) given per os. The previous asthmatic attack developed about 3 hours after her rubbing the lotion containing the NSAID over her skin. The relatively long interval between the per cutaneous NSAID administration and the onset of the asthmatic attack indicates that the time delay is dependent on the absorption route of the administered NSAID. The severity of the attack is considered to be related to the amount of NSAID absorbed.

Administration, Cutaneous↗