PubMed · 5058515
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G M Ardran, F H Kemp. 1972. A function for adenoids and tonsils.. https://doi.org/10.2214/ajr.114.2.268
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Lymphadenopathy and nasal obstruction are very common in the HIV-positive patient and may or may not reveal a nasopharyngeal tumor. Biopsy is warranted if there is evidence suggestive of lymphoma or other neoplastic disease. This would include progressive rapid enlargement observed on examination or CT scan, an asymmetric growth pattern, and evidence of invasion of normal anatomic boundaries. It is certain that not all cases of adenoid hypertrophy that occurs early in the course of HIV disease represent a malignancy. Further study is needed to determine the proper timing for nasopharyngeal biopsy in the HIV-positive population. As the life span of the HIV-positive patient increases, so may the incidence of malignant degeneration.
On stimulation of trigeminal nerve endings, neuropeptides are released into the nasal mucosa. Among these neuropeptides is substance P(SP). In this study, we determined the effect in vitro of SP, as well as SP together with thiorphan, a blocker of the SP-degrading enzyme neutral endopeptidase, on the ciliary beat frequency (CBF) of the human upper respiratory tract. Ciliated epithelium of human adenoid tissue was used in the experiments. The CBF was measured by means of a computer-assisted photoelectric method. Substance P(10(-8) to 10(-5) mol/L, n = 7) showed a small but statistically significant dose-dependent decrease in CBF. On perfusion with SP (10(-8)) to 10(-5) mol/L, n = 8) in combination with thiorphan, no statistically significant effect was found. We conclude that SP does not have a direct effect on ciliary activity to such an extent that it will affect mucociliary transport in vivo.
Substance P is a neuropeptide released by afferent neurons in the respiratory tract during inflammatory reactions. It produces effects on blood vessels, bronchial smooth muscle, nasal glands, and respiratory cilia. We studied the in vitro effect of substance P on the ciliary beat frequency of human adenoid explants and its mechanism of action. Substance P was added to cultured adenoid at concentrations of 10(-10), 10(-8), 10(-6), and 10(-4) mol/L. Ciliary beat frequency was determined with phase-contrast microscopy and microphotometry. Substance P increased ciliary beat frequency a maximum of 11.9% +/- 3.8% (p < 0.01). Diclofenac (10(-6) mol/L) significantly blocked the ciliostimulatory effects of SP (p < 0.022), indicating that prostaglandin synthesis is an intermediate step in the action of substance P on ciliary beat frequency. The L-arginine analogs, NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arginine, inhibit nitric oxide synthesis from L-arginine. L-Arginine analogs (10(-4) to 10(-2) mol/L) inhibited the effect of substance P (p < 0.02 at the higher concentration). This inhibition was reversed by adding L-arginine, demonstrating that nitric oxide production is a required step in substance P-induced ciliostimulation. Substance P stimulates ciliary activity in human nasal mucosa as a result of secondary production and release of endogenous prostaglandins and nitric oxide. It is likely that inflammatory disease processes that stimulate release of substance P and subsequent prostaglandin and nitric oxide production modify mucociliary transport. Pharmacologic modification of substance P and its second messengers may eventually permit regulation of this important defense mechanism and control of neurogenic inflammation.