By Mark R. Stein
Addressing the relationships among gastroesophageal reflux and airway illnesses, this pioneering reference is the one unmarried resource that serves as a radical assessment of the topic, delivering a wide spectrum of knowledge facilitating right prognosis and therapy of GERD and GERD-related problems. targeting dentition, top airway affliction, cough, and decrease airway sickness, and provided in a layout perfect for basic care companies and experts, Gastroesophageal Reflux ailment and Airway illness
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Additional resources for Gastroesophageal Reflux Disease and Airway Disease
In a study of the relaxant innervation of the guinea pig airways, for example, stimulation of capsaicin-sensitive vagal afferent nerves innervating the esophagus elicited relaxations of airway smooth muscle that were abolished by tachykinin receptor antagonists (116). A series of physiological and pharmacological analyses revealed that these relaxations were mediated by the tachykinins activating, via peripheral reflex, parasympathetic ganglion neurons that innervate the airways but have cell bodies in the esophageal myenteric plexus (which is densely innervated by tachykinin-containing nerves.
In the skin and in other tissues innervated by somatic nerves, other cardinal signs of inflammation are persistent pain (‘‘dolor’’) and hyperalgesia and thus altered physiology (‘‘functio laesa’’) in the tissues proximal to the inflamed area (85,145). It seems likely that the hyperalgesia mediated by somatic afferent nerves and the exag- Table 3 Tachykinin Receptor–Mediated Regulation of the Airways and Lungs End organ effects Tachykinin receptors involveda Vasodilatationb Plasma extravasation Inflammatory cell recruitment and activation Airway smooth muscle contraction Mucus secretion CNS-mediated reflexesc Modulation of parasympathetic neurotransmission NK1 NK1, NK1, NK2, NK1 NK1, NK3, a NK2 NK2 NK1 NK2, NK3 NK1 Ref.
One such reflex mediated by the tachykinin-containing sensory nerves is inflammation. Lundberg and Saria (102) were the first to systematically characterize the role of sensory nerves in pulmonary inflammation. , cigarette smoke, histamine, bradykinin, and mechanical irritation) elicits marked plasma extravasation from the vasculature in the airway mucosa of rats. However, following chemical desensitization of the tachykinin-containing sensory nerves with capsaicin (an unmyelinated afferent nerve-selective neurotoxin), nearly all proinflammatory stimuli delivered to the lung were rendered ineffective at eliciting plasma extravasation.