BACKGROUND AND OBJECTIVES: Smoking is regarded as one of the factors that bring about nonspecific hypersensitivity in allergic nasal mucosa. But it is uncertain how chronic smoking affects hypersensitivity in nasal mucosa. This study was designed to evaluate the relationship between smoking and nasal hypersensitivity. In this study, histamine is used since it is commonly used to evaluate nasal hypersensitivity. MATERIAL AND METHODS: Twelve smokers and 9 nonsmokers were participated in this study. Nasal mucosae of each subjects were stimulated by thiorphan followed by substance P. After stimulation, several dilutions of 10 to 5X104 ng/ml of histamine was instilled to both nasal cavity at intervals of 10 minutes. We measured the volume of nasal cavity by acoustic rhinometry in each step and counted the number of sneezing and nasal blowing at every 10 minute intervals. Changes in volume after each dillutions of histamine instillations were compared with the values measured after the stimulation by thiorphan and substance P., and this value was expressed as the percentage volume change. RESULTS: The nasal volume of smoker group was increased upto 100 ng/ml of histamine and decreased from 1000 ng/ml of histamine. The nasal volume of nonsmoker group decreased more than the smoker group with each dilution of histamine. The number of sneezing and nasal blowing increased in each group with each dilution of histamine. CONCLUSIONS: Chronic smoking may decrease susceptibility of hypersensitivity to histamine in nasal mucosa.
Histamine ; Hypersensitivity* ; Nasal Cavity ; Nasal Mucosa ; Rhinometry, Acoustic ; Smoke ; Smoking ; Sneezing ; Substance P ; Thiorphan

Impaired angiogenesis is a common pathological characteristic of chronic wounds. Therefore, the regulation of angiogenesis is important for proper tissue repair. It was reported that substance P (SP) accelerates wound healing in a skin injury model. SP is degraded by neutral endopeptidase (NEP). Our study shows that systemic co-treatment of SP and thiorphan, an inhibitor of NEP synergically increased the number of α-smooth muscle actin positive-blood vessels in skin wounds. However, there was no synergic improvement in wound contraction and extracellular matrix deposition. Therefore, inhibition of endogenous NEP activity by thiorphan treatment might modulate the effects of SP treatment specifically on accelerating angiogenesis during wound healing. However, the molecular mechanism(s) of the synergic increase in angiogenesis by SP and thiorphan treatment is still unknown.
Actins ; Extracellular Matrix ; Neprilysin ; Skin ; Substance P* ; Thiorphan* ; Wound Healing* ; Wounds and Injuries*

The mucus secretion of airway glands is known to be controlled by the various autonomic neurotransmitters such as noradrenalin and acetylcholine. However, a recent study suggests that non-adrenergic, non-cholinergic (NANC) nerves may contribute to the secretory activity of glands. Substance P (SP) has been proposed as a neurotransmitter of the NANC nervous system. SP is present within nerve fibers innervating the airway mucosa and is known to be released from sensory nerves via an axonal reflex. SP activity is controlled by neutral endopeptidase (NEP) which degrades SP. In this study, we evaluated the effects of NEP inhibitor (thiorphan) and substance P on nasal mucosa and histamine on the nasal mucosa in healthy males. In the thiorphan-substance P experimental group, the nasal volume decreased after nebulization of substance P in proportion to the concentration of histamine. In the thiorphan-substance P experimental group, the frequency of sneezing increased in proportion to the concentration of histamine, but there was no increased frequency of sneezing from thiorphan, SP and normal saline. The results of this study suggest that axonal reflexes can play a role in the pathogenesis of nasal mucosal hypersensitivity and neurogenic inflammation.
Acetylcholine ; Axons* ; Histamine ; Humans ; Hypersensitivity* ; Male ; Mucous Membrane ; Mucus ; Nasal Mucosa ; Neprilysin ; Nerve Fibers ; Nervous System ; Neurogenic Inflammation ; Neurotransmitter Agents ; Reflex* ; Sneezing ; Substance P* ; Thiorphan