Physical reactive rhinitis, also known as vasomotor rhinitis, can be divided into three clinical types, with some patients often having specific nasal reactions to certain rational stimuli. For example, episodes of sneezing, accompanied by more watery nasal discharge, occur whenever there is exposure to cold air, sudden temperature changes, humidity, etc. Patients can often clearly state the trigger. Patients can often clearly state the trigger for the onset. This type of rhinitis may also be classified as reverse hyperactivity rhinitis. Vasomotor rhinitis is a hyperreactive rhinopathy caused by imbalance of neuroendocrine regulation of the vascular and glandular functions of the nasal mucosa. The pathological mechanism of this disease is complex and many aspects are still not well understood, thus posing certain difficulties for the exact clinical diagnosis and effective treatment. There are no significant gender differences in the onset of the disease, and vasomotor rhinitis rarely occurs in children.
The nasal mucosa contains a large number of glands, a rich vascular bed and many sources of innervation, constituting a delicate, sensitive and active end organ that performs various physiological functions at the gateway to the respiratory tract. It relies on neurovascular, neuroendocrine and other activities to maintain the balance between the nasal cavity and the internal and external environment. This equilibrium surface depends on two pathways from the hypothalamus: the humoral regulation of nasal mucosal function through the pituitary gland with the help of the endocrine chain, and the direct neural regulation through the autonomic nervous system. A functional change in one of these pathways can cause dysfunction and increased reactivity of the nasal mucosal vessels and glands, which is the main pathophysiological basis for the development of vasomotor rhinitis.
The etiology of over-intense reverse rhinitis: 1. Autonomic dysfunction Under normal circumstances, when sympathetic nerves are excited, their terminals release norepinephrine and neuropeptide y, through the corresponding receptors on the vessel wall to maintain nasal mucosal vascular tone. When the parasympathetic nerve is stimulated, its terminals release acetylcholine, which causes vasodilation and glandular secretion through M receptors in the vessel walls and glands. Recent studies have also revealed the presence of vasoactive intestinal peptide (VIP) immunoreactive fibers in the parasympathetic nerves of the nasal mucosa. Uddman (1987) suggested that the glandular secretion caused by parasympathetic excitation is due to acetylcholine, whereas the vasodilation is due to the non-cholinergic vasodilator -VIP. -VIP. Repeated sympathetic stimulation (overwork, irritability, anxiety, nervousness, etc.) can deplete excess neurotransmitter synthase and transmitters that have been synthesized and stored in nerve endings, resulting in a corresponding decrease in the number of α1 and β receptors, which can cause hyposympathetic tone. Some anti-hypertensives, non-selective beta-blockers and antidepressants are sympathetic blockers, and repeated application can also cause reduced sympathetic tone. When sympathetic tone is reduced, parasympathetic excitability increases, which can cause vasodilation and glandular secretion, resulting in the clinical symptoms of vasomotor rhinitis. As early as 1943 Fowler found that cervical sympathetic ganglion removal could cause patients to develop vasomotor rhinitis. Removal of the superior cervical sympathetic ganglion resulted in vasodilatation of the nasal mucosa, submucosal edema, and glandular hyperplasia in animals, and increased activity of cholinesterase was found around the glands. These changes are identical to those seen in the mucosal histopathology of patients with vasomotor rhinitis.
2. Endocrine disorders Endocrine disorders can also cause reactive changes in the nasal mucosa. Hypothyroidism can cause a decrease in autonomic sympathetic tone. Such patients often have nasal congestion as the main symptom. Changes in estrogen levels can also cause nasal symptoms. Many clinical studies have shown that some female patients have significant nasal symptoms during premenstruation or pregnancy, such as nasal congestion, excessive sneezing and clearing of the nose. Animal experiments have shown that increasing the level of estradiol in the body can increase the reactivity of the nasal mucosa, which can be seen as epithelial thickening, tissue edema, small blood vessel dilation and glandular hyperplasia. The mechanism of this effect of estradiol is not known. However, it has been found that increased levels of estradiol in the body increase cholinergic M-receptors and decrease α1-adrenergic receptors in nasal mucosa tissue. Estradiol also enhances the release of non-immune histamine from mast cells.
3. Non-immune release of histamine and other inflammatory mediators There are various factors that cause the non-immune release of histamine and other mediators, such as chemical (narcotics, salicylic acid preparations), physical (sudden changes in temperature, humidity, climate, dust), and neurological (emotional changes). The exact mechanism of non-immune release of histamine is unknown, but regardless of the precise mechanism, it is regulated by intracellular cAMP levels. Whenever a decrease in intracellular cAMP levels can be induced, the mast cells can be made to release the mediator.