Activity In Rabbit Maxillary Sinus Research Articles

The influence of leukotrienes and platelet activating factor on mucociliary activity in the rabbit maxillary sinus

Inflammatory mediators released in the airways during allergic reactions can affect the mucociliary system. Leukotrienes and platelet activating factor have been shown to affect the mucociliary activity in various cell preparations. The in vivo effects of these inflammatory mediators on mucociliary activity in rabbit maxillary sinus were investigated using a photoelectric technique. Leukotrienes C4 and D4 in the dose range 0.01-10.0 nmol/kg did not alter mucociliary activity significantly, either when given as bolus injections or as intraarterial infusions. Platelet activating factor had no effect in the dose range 0.001-0.1 nmol/kg. A dose of 1.0 nmol/kg increased mucociliary activity by 20.2 +/- 5.5% but produced adverse respiratory and circulatory effects at the same time. It is concluded that the inflammatory mediators leukotrienes C4, D4 and platelet activating factor have no essential regulatory influence on mucociliary activity in the upper airways of the rabbit.

Effects of neurokinin A and calcitonin gene-related peptide on mucociliary activity in rabbit maxillary sinus

Substance P (SP) released from sensory C-fibers in the airways increases the mucociliary (m.c.) activity in the rabbit maxillary sinus. The purpose of the present study was to investigate the m.c. effects of two other neuropeptides, coexisting with SP in sensory neurones, neurokinin a (NKA) and calcitonin gene-related peptide (CGRP). NKA increased the m.c. activity dose-dependently (dose range 0.1–10.0 μg/kg, 88 pmol to 8.8 nmol/kg), the maximum increase being 41.9 ± 2.6%. The effect was inhibited by pretreatment with the tachykinin antagonist ( d-Pro 2, d-Trp 7,9)SP, but not with atropine or hexamethonium. Thus NKA released from sensory C-fibers may contribute to the non-cholinergic increase of m.c. activity observed after C-fiber stimulation. In contrast CGRP did not influence the m.c. activity. Neither did it influence the responses to NKA or SP. It is concluded that CGRP is unlikely to be involved in the control of m.c. function.

Influence of substance P on ciliary beat frequency in airway isolated preparations

The neuropeptide substance P (SP), which is released from sensory C-fibres after stimulation by chemical irritants, accelerates mucociliary activity in rabbit maxillary sinus in vivo. In order to investigate the mechanism behind this finding, we recorded ciliary beat frequency (CBF) in vitro from various respiratory explants by a photoelectric technique. It was noticed that ciliated cells from the maxillary sinus displayed a higher beating frequency than cells from the trachea and the bronchus, in that order. SP 10 −10-10 −4 M did not influence the CBF in explants from rabbit maxillary sinus, rabbit trachea and main bronchi, guinea-pig trachea and human adenoids. Neurokinin A (NKA) 10 −6-10 −5 M, which is also thought to be released from sensory C-fibres, did not influence the CBF in guinea-pig trachea. Neither did the C-fibre stimulant capsaicin 10 −8-10 −4 M increase CBF in explants from human adenoids. The present findings indicate that the mucociliary effect of SP in vivo is not mediated by an effect on the cilia themselves.

The Morphological Basis for the Effect of Substance P on Mucociliary Activity in Rabbit Maxillary Sinus

The mucociliary (m.c.) activity in rabbit maxillary sinus is accelerated by the neuropeptide substance P (SP). The morphological basis for this mechanism was investigated by immunocytochemistry using monoclonal antibodies directed against SP. SP-like immunoreactivity was found in nerve fibres in the subepithelial layer of the sinus mucosa, in the maxillary nerve, and in nerve endings close to nerve cell bodies in the sphenopalatine ganglion. Thus, there is morphological evidence in the rabbit that SP plays a role in the regulation of m.c. activity. The results also support the view that the rabbit maxillary sinus is a suitable experimental model for studying SP effects in the airway mucosa.