Mechanism of nasal obstruction in patients with allergic rhinitis

Abstract

Summary Nasal obstruction is a crucial symptom in allergic rhinitis (AR) patients and may affect the quality of life. It is caused mostly by nasal mucosal obstruction, and to a lesser extent, fluid secretion. Mucosal congestion is primarily a vascular phenomenon comprising vasodilatation of capacitance vessels (cavernous sinus) and oedema formation due to plasma leakage from post‐capillary venules. The nose has a complex microvascular anatomy consisting of capacitance vessels, arteriovenous anastomosis, and subepithelial and periglandular capillaries. Nasal congestion is explained by the effects of local mediators exerting potent vasodilatation or increasing permeability of nasal blood vessels and nerves. Capacitance vessels usually constrict because of constant sympathetic tone. They distend by a variety of stimuli such as loss of continuous sympathetic stimulation on the sinusoids, direct vasodilatation by vasoactive substances, contraction of cushion veins, and compression of venules by distended arteries in the intraosseous bony canals of periosteal space. Although topical application of histamine can cause vasodilatation and oedema, histamine is not likely a major mediator causative of nasal congestion in AR. Nasal vascular dilatation elicited by cysleukotriene 1 (cysLT1) may be induced by nitric oxide produced through cysLT1 receptor activation. Thromboxane A2 may cause capacitance vessel dilatation through a contraction of cushion veins. Potentiation of vasoconstrictor action of steroids has been reported since the 1950s. Glucocorticoids (GCs) have two fundamentally different vascular effects: classic action modifying the transcription of pro‐inflammatory genes and acute non‐genomic action (within minutes) that increases the vasomotor tone. The non‐genomic effect is likely related to binding of GCs to the plasma membrane and inhibition of extraneuronal monoamine transporter on vascular smooth muscle cells, thereby increasing noradrenaline concentrations at α1‐adrenoceptors. Genomic vascular effects include the reduction of vessel density, decrease of hyperperfusion, reduction of inflammatory microvascular hyperpermeability, and decreased influx and activation of inflammatory cells. These effects require hours to manifest themselves physiologically.

8‐ iso ‐prostaglandin E 2 induces nasal obstruction via thromboxane receptor in murine model of allergic rhinitis

“…Capillaries are present in the surface layer while venous sinusoids are abundant in the anterior part of the inferior septum (Figure 5A,C). 3 As shown in Figure 5B, α-SMA-negative/CD31-positive capillaries were broadly present on the surface are of septum mucosa (Figure 5B, left picture). α-SMA-positive/CD31-negative elastic fibers were observed at high-magnification (Figure 5B, right picture).…”

“…*p < .05; **p < .01 3.4 | The effect of 8-iso-PGE 2 on TP-mediated endothelial barrier disruption Vasodilation of sinusoid vein and plasma leakage due to vascular hyperpermeability in post-capillary vessels are mainly involved in the induction of nasal obstruction. 3 We previously demonstrated that endothelial TP activation results in vascular hyperpermeability both in vitro and in vivo. 14 To examine whether the 4 candidates mediate TP-induced vascular hyperpermeability, we measured trans endothelial resistance (TER), indexed as vascular permeability, by using BAECs.…”

15‐hydroxy eicosadienoic acid is an exacerbating factor for nasal congestion in mice

“…Nasal congestion is a difficult symptom to treat and manage in AR. Mucosal engorgement, edematous swelling due to increased blood flow, and vascular hyperpermeability cause nasal congestion 11 . The nasal mucosa is covered by large, sinusoidal veins, most of which possess thin walls and store a large amount of blood.…”

Reliability Assessment of the Endoscopic Examination in Patients with Allergic Rhinitis

“…9 Nasal tk;1obstruction is noted to be the most commonly presenting and debilitating symptom of allergic rhinitis, and it is caused by vasodilation of arterioles, venules, and capillaries as well as an increase in vessel permeability that leads to edema. 10 …”

“…9 Nasal tk;1obstruction is noted to be the most commonly presenting and debilitating symptom of allergic rhinitis, and it is caused by vasodilation of arterioles, venules, and capillaries as well as an increase in vessel permeability that leads to edema. 10 Allergic rhinitis was traditionally classified as either seasonal or perennial based on the time of occurrence of symptoms. This classification has ceased to be used since the development of new Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines for the diagnosis and classification of allergic rhinitis.…”