Kaneko K, Shimanuki T, Komoda T, Kase Y, Iinuma T
Department of Otorhinolaryngology, Saitama Medical School.
Nihon Jibiinkoka Gakkai Kaiho. 2000 Sep;103(9):986-92. doi: 10.3950/jibiinkoka.103.986.
Most of the nitric oxide (NO) in expiratory air is produced by the nose and its accessory sinuses, and nasal allergies related to NO have been often reported. In the present study, we postulated that nose bleeds may be somehow related to reactive oxygen species. The expression of NO synthase (NOS) by the nasal mucosa was evaluated using the RT-PCR method, and the concentration of NO in air expired through the nose was measured. The activity of superoxide dismutase, which scavenges superoxide anions, was also evaluated. The genetic expression of iNOS was observed in the nasal mucosa, and a significantly lower level of expression was noted in subjects with a nosebleed, compared to that of the controls. This result was interpreted as indicating a decrease in NO levels as a result of the nosebleed, leading to an elevation in blood pressure. Transient elevations in blood pressure caused by oxidative stress may lead to the rupture of nasal vessels if hypertension preexists. Serum levels of superoxide dismutase increased significantly in subjects with nose bleeds. This finding might be related to the activity of the superoxide anion, which is released in large amounts during nose bleeds. Serum superoxide dismutase levels increase in response to the high concentration of superoxide anions. The concentration of NO in air expired through the nose was significantly lower in subjects with nose bleeds, compared to that of the control subjects. We suggest that NO production decreases in subjects experiencing nose bleeds and that this reduction is induced by preexisting hypertension and injury from reactive oxygen species, contributing to the resulting nose bleed.