Biomedical subjects
Takao Okubo
Publications and source records attributed to Takao Okubo.
Tachykinins via Tachykinin NK(2) receptor activation mediate ozone-induced increase in the permeability of the tracheal mucosa in guinea-pigs.
1. Acute exposure to ozone is known to cause airway hyperresponsiveness, which, at least in part, seems to result from an increase in the permeability of the airway mucosa. Recently, we demonstrated that depletion of sensory neuropeptides inhibits the ozone-induced increase in the permeability of the tracheal mucosa in guinea-pigs. The aim of this study was to determine whether tachykinins mediate ozone-induced increase in the permeability of the tracheal mucosa in guinea-pigs. 2. Anaesthetized guinea-pigs were exposed to either 3 p.p.m. ozone or filtered air for 30 min. Immediately after exposure, a tracheal segment was isolated in vivo and administered with horseradish peroxidase (HRP). The permeability was assessed by monitoring the appearance of HRP in the blood. 3. A low dose of NKA increased the permeability of the tracheal mucosa, whereas a low dose of SP was without effect. Low and high doses of the selective NK(3) receptor agonist, senktide, were also without effect. The effect of a low dose of NKA was abolished by the NK(2) receptor antagonist, SR-48,968. A high dose of SP increased the permeability in a manner reversible by the NK(1) receptor antagonist, CP-96,345. 4. Pretreatment with SR-48,968 completely inhibited the ozone-induced increase in the permeability, whereas CP-96,345 had no effect. 5. It is thus concluded that endogenous tachykinins mediate the ozone-induced increase in the permeability of the tracheal mucosa in guinea-pigs mainly via NK(2) receptor activation.
Analysis of exhaled nitric oxide by the helium bolus method.
STUDY OBJECTIVES: The precise anatomic sites contributing to exhaled nitric oxide (eNO) are still unknown. The present study was designed to analyze profiles of eNO by referring to the He exhalation curve and examining the effects of breath-holding and expiratory flow rates on eNO. PARTICIPANTS: Healthy volunteers and patients with stable asthma. MEASUREMENTS AND RESULTS We used the He bolus method of the closing volume, and simultaneously analyzed the concentrations of exhaled He and nitric oxide (NO). By referring to the He exhalation curve, the expired gas was divided into three parts: airway dead space (phase 1), a mixture of airway and alveolar gas (phase 2), and alveolar gas (phase 3 and phase 4). The eNO profiles showed a peak in phase 2 (peak eNO) and decreased gradually to a plateau in the latter half of phase 3 (plateau eNO). The levels of peak eNO were higher than those of plateau eNO in both normal subjects and asthmatic patients. Breath-holding increased levels of peak eNO 2.5-fold in both normal subjects and asthmatic patients, but it did not affect the levels of plateau eNO. The levels of peak eNO increased as the expiratory flow rate decreased, and the levels of plateau eNO showed a similar flow dependency. CONCLUSION: A peak value of eNO concentration profiles may directly express the production of NO in the airway.