Biomedical subjects

Jens A Andersson

Publications and source records attributed to Jens A Andersson.

3 recordsLinked to original sources

PubMed2002

Heme oxygenase and nitric oxide synthase in human middle ear epithelium indicates local carbon monoxide and nitric oxide production.

The gas mixture of the middle ear differs from that of the atmosphere, a fact that has been attributed to gas exchange across the middle ear mucosa. Several diseases of the middle ear seem to be related to impaired ventilation together with conjunctional changes in pressure and gas composition. Carbon monoxide (CO) and nitric oxide (NO) have recently been shown to be endogenously produced in the human lung as well as in the nasal airways. The production of CO and NO is enzymatically regulated by heme oxygenase (HO) and NO synthase (NOS), respectively. These enzymes display isoforms that are both constitutively expressed [HO-2, endothelial NOS (eNOS), neuronal NOS (nNOS)] and inducible [HO-1, inducible NOS (iNOS)] following different types of stimulation. The present study was designed to investigate the presence of HO-1, HO-2 and eNOS in the middle ear epithelium, using immunocytochemistry. Specimens from human middle ear mucosa obtained at autopsy and during surgery revealed HO-1-, HO-2- and eNOS-like immunoreactivity, indicating the possibility of local CO and NO production in the middle ear. If this assumption is true, it may affect our understanding of middle ear physiology and give new insights into the mechanisms behind middle ear pathology.

Carbon Monoxide↗

PubMed2002

A decrease in maxillary sinus pressure, as seen in upper airway allergy or infection, results in an increase in upper airway nitric oxide levels.

The paranasal sinuses are connected to the nasal cavity via small osties. Ostial occlusion, caused by mucosal swelling, will result in a slowly increasing negative pressure inside the sinus cavity. In parallel, the oxygen content in the sinus will decrease, resulting in the development of relative hypoxia. Hypoxia is a powerful inducer of nitric oxide (NO) synthase, and inducible NO synthase has been shown to be present in considerable amounts in the upper airways, including the sinuses. The present study was designed to investigate whether a reduction in sinus pressure would affect upper airway NO production. Thirteen healthy volunteers were investigated. A pressure chamber was used to lower the ambient pressure to -4.9 kPa. NO was sampled from one nostril or via a drainage tube inserted into the maxillary sinus before, during and after the hypobaric exposure. When the pressure was decreased, NO levels increased from 256 +/- 15 to 316 +/- 19 ppb (n = 13, p < 0.001). The NO levels remained elevated (282 +/- 21 ppb; p < 0.05) when measurements were repeated 20 min after leaving the chamber. The nasal airway resistance (V2tot) also increased as a result of the chamber session (from 16 +/- 2 degrees before to 21 +/- 3 degrees after; p < 0.05). An increase in NO levels was also found when the experiments were repeated with NO sampled directly from the maxillary sinus (225 +/- 6 before and 265 +/- 9 ppb after; n = 6, p < 0.001). For control purposes the nasal analyses were repeated again, this time under hyperbaric conditions (+ 4.9 kPa). This resulted in a slight decrease in the NO levels (from 273 +/- 22 to 241 +/- 17 ppb; n = 10, p < 0.001), but there was no change in the nasal airway resistance. We conclude that a reduction in sinus pressure, as seen in upper airway allergy or infection, may result in an increase in upper airway NO production.

Adult↗

PubMed2002

The paranasal sinuses as reservoirs for nitric oxide.

OBJECTIVE: Nitric oxide (NO) is an important mediator and inflammatory marker in human upper airways. Enzymes responsible for NO production have been demonstrated both in the nose and in the paranasal sinuses, but NO levels in the sinuses are reported to be several times higher than those in the nose. It has been postulated that the paranasal sinuses may be the primary sites for NO production in the upper respiratory tract. The present study was designed to compare the NO levels sampled from the nose with those found in the paranasal sinuses. MATERIAL AND METHODS: NO levels in the maxillary sinus and nose were determined using a continuous chemiluminescence measuring technique in seven healthy volunteers. RESULTS: When NO was sampled, via a drainage tube inserted into the maxillary sinus, a transient peak in NO level was recorded. The maximal NO level (5,761 +/- 1,513 ppb; n = 7) was reached within 10 s and was followed by the establishment of a lower steady-state level (304 +/- 51 ppb). When NO was continuously sampled from the nose a steady-state level, similar to that found in the sinus, was immediately established (313 +/- 52 ppb). CONCLUSION: The data presented confirm previous findings of extremely high NO levels in the paranasal sinuses and suggest that these cavities may also function as reservoirs for NO.

Adult↗