What is All of the following affect resting ventilation except and explain in detail?
B i.e. J receptorTidal volume excessive load is prevented by (or lung maintains the tidal volume by) activation of slowly adapting pulmonary (or bronchial) stretch receptorsQ."Inflation of lungs induces fuher inflation" due to elastic recoil of alveoli. With inflation of the lungs, there is augmentation of respiratory effo= Head's paradoxical reflex.Excessive inflation of lungs cause reflex inhibition of inflation- this is Hering Breuer inflation reflex mediated by vagus. Conversely, excessive deflation of lungs cause reflex inhibition of expiration - this is Hering- Breuer deflation reflex.- Physiological role of J (juxta-capilary/alveolar) reflex is unceain but it occurs in pathological states such as pulmonary congestion, pulmonary edemaQ and embolism when the J recptors are stimulated by large lung hyper inflation, or intravascular chemicals like capsaicin, bradykinin & serotonin etc.- Slowly adapting pulmonary stretch receptors are stimulated by lung inflation (not hyper inflation) - Ganong p 632 table 37.2. Hyper inflation (over stretching) of lungs stimulate stretch receptors and lead to Hering - Breuer inflation reflex. However, more recent work indicates HB reflex may be impoant in new born babies but are largely inactive in adult human unless the tidal volume exceeds 1 liter (John west) /1.5 liter (Guyton), as in exercise. So we can extract inference that, although stretch receptors get stimulated by (normal-quiet) inflation, the HBI reflex occurs only after lung hyper inflation.Nonchemical Responses Mediated by Pulmonary Receptors and ReflexesReceptor TypeLocationImpulse travel in(i.e. Vagalinnervation)StimulusResponse/ ReflexSlowly adaptingAirwayMyelinated vagalLung inflationQ- Inspiratory timeStretch Receptorsmoothfibers shoening(pulmonary orbronchial stretchreceptors)muscle (?) - Hering-Breuerinflation & deflationreflexesQ - Bronchodilation - Hyperpnea - TachycardiaRapidly adaptingAirwayMyelinated vagal- Lung- Increased airwayIrritant Receptorsepithelial cellsfibersHyperinflationQresistance i.e. broncho(type of - Exogenous &constriction (egstretch/mechano- endogenousasthama)receptor) substances eghistamine andprostaglandins- Mucus secretion- Cough_ Hering-Breuerdeflation reflexJ (Juxta-In pulmonaryUnmyelinated- Lung Hyper- Apnea (d/t intensecapillary/alveolar)interstitial(pulmonaryinflationQ (large)stimulation) f/b rapid,Receptorsspace close tovagal)- Exogenous &shallow breathing(Juxta pulmonarybloodC fibersendogenous(tachypnea) andcapillary receptorcapillaries of agents egdyspneaor pulmonary Cfiber receptor)- Pulmonarycirculation- Bronchialcirculation capsaicin,bradykinin,serotonin,histamine,prostaglandins,phenyl diguanide-Pulmonary edema, embolism- Broncho constriction- Mucus secretion- Brady cardia-Hypotension(-pulmonarychemoreflex) & congestionQ * Bronchial C fiber receptors located in the airways and innervated by nonmyelinated fibers are activated bychemicals (notably bradykinin)injected into bronchial aery. Their stimulation gives rise to tachypnea, bronchoconstriction, and airway secretion. Along with type J (juxta pulmonary capillary) receptors, they contribute to air way defence reflexes.* Receptors in nose & upper airway (nasopharynx, larynx & trachea) responding to mechanical & chemical stimulation 1/t sneezing, coughing, broncho constriction and aryngospasm.* Impulses from joint & muscle receptors of moving limb stimulates ventilation during early exercise.* Gamma system or muscle spindle of thoracic intercostal muscles and diaphragm sense elongation of these muscles and reflexly control strength of contraction. For example dyspnoea is sensed by unusually large respiratory effos required to move the lung.* Pain cause apnea followed by hyperventilation. Heating of skin (or fever) result in hyperventilation (paly d/t stimulation of hypothalamic thermoreceptor).* Aerial (aoic & carotid sinus) baroreceptor stimulation by increased BP causes reflex hypoventilation or apnea; whereas decreased BP 1/t hyperventilation (thereby enhancing venous return following severe hemorrhage).