Disease relevance of Pulmonary Stretch Receptors

• 4. Addition of SO2 (300-400 p.pm.) to the inspirate, which others have shown preferentially blocks pulmonary stretch receptors, abolished the Breuer-Hering reflex, but had no significant effect on baseline levels of muscle vascular conductance or heart rate during normoxia, nor on the gradual increases in these variables during hypoxia (8% O2) [1].
• A proposed mechanism is secondary pulmonary stretch receptor activation due to hyperventilation, induced by direct stimulation of carotid body chemoreceptors by adenosine [2].

High impact information on Pulmonary Stretch Receptors

• 4. Intravenous veratrine caused similar effects to capsaicin before denervations, presumably due to stimulation of slowly adapting pulmonary stretch receptors [3].
• 2. Inhalation of CO2 depressed pulmonary stretch receptor discharge despite the absence of changes in arterial PCO2 [4].
• Heart rate variability (HRV) is mediated by at least three primary mechanisms: 1) vagal feedback from pulmonary stretch receptors (PSR), 2) central medullary coupling between respiratory and cardiovagal neurons (RCC), and 3) arterial baroreflex (ABR)-induced fluctuations [5].
• Effects of potassium channel and Na+-Ca2+ exchange blockers on the responses of slowly adapting pulmonary stretch receptors to hyperinflation in flecainide-treated rats [6].
• The effect of vagally and acetylcholine (ACh)-induced bronchoconstrictions was assessed by an increase in the slowly adapting pulmonary stretch receptor (SAR) activity during both inflation and deflation and the rise in total lung resistance (R(L)) [7].

Biological context of Pulmonary Stretch Receptors

• We studied the effects of aerosol administration of veratridine (a sodium channel opener) or nifedipine (a calcium channel blocker) on the responses of rapidly adapting pulmonary stretch receptors (RARs) and dynamic lung compliance (Cdyn) to aerosols of 2 and 4% ammonia solutions in anesthetized spontaneously breathing rabbits without intact vagi [8].
• Electromyographic patterns of the diaphragm and a posterior cricoarytenoid (PCA) muscle were evaluated in anesthetized rabbits with and without reversible blockade of pulmonary stretch receptors by inhalation of 200 ppm sulfur dioxide (SO2) [9].
• However, the inhibitory effect of CO2 on pulmonary stretch receptors seems to be enhanced by an increase in body temperature [10].

Anatomical context of Pulmonary Stretch Receptors

• Stimulation of CO2 sensitive chemoreceptors and pulmonary stretch receptors appear to have interactive effects on the central generation of ventilatory output in toads [11].
• To study the effect of bronchoconstriction on the activity of pulmonary stretch receptors (PSRs), acetylcholine aerosols (0.05% solution) were delivered continuously into the lungs while the afferent activity of a single PSR was recorded from a filament of the vagus nerve [12].
• The results indicate that the stimulation of rapidly adapting pulmonary stretch receptors by 5-HT is not caused by contraction of the airway smooth muscle [13].
• The inhibitory baroreceptor and pulmonary stretch receptor sympathetic reflexes, and the central excitatory effect of CO2 on renal sympathetic nerve firing were not altered [14].

Associations of Pulmonary Stretch Receptors with chemical compounds

• 6. In these conditions, the reflex response to CO2 could be simulated provided that the pulmonary stretch receptor had an end-expiratory discharge [4].
• 2. Capsaicin was injected intravenously to stimulate lung C-fibre receptors, and veratrine to stimulate pulmonary stretch receptors and cardiac receptors [3].
• Acetazolamide treatment (20 mg/kg) diminished the inhibitory responses of slowly adapting pulmonary stretch receptors to CO2 inhalation, which were not significantly influenced by pretreatment with nifedipine (1 mg/kg) [15].
• Cholinergic and H1-receptor influences of histamine on slowly adapting pulmonary stretch receptor activity in the rabbit [16].
• Effects of 5-hydroxytryptamine on rapidly adapting pulmonary stretch receptor activity in the rabbit [13].

Analytical, diagnostic and therapeutic context of Pulmonary Stretch Receptors

• 7. It is suggested that the vagally mediated tachypnoeic response to changes in airway CO2 seen in conditions of cardiopulmonary bypass is due to the effect of CO2 on the end-expiratory discharge of pulmonary stretch receptors [4].
• In other series of experiments, we also examined the responses of rapidly adapting pulmonary stretch receptors (RARs) and dynamic lung compliance (Cdyn) to intravenous injections of sodium cyanide (NaCN, 20 and 30 micrograms/kg) before and after administration of atropine (1 mg/kg) in spontaneously breathing rabbits with vagal efferent activities [17].
• Single units of slowly adapting pulmonary stretch receptors (PSRs) were investigated in anesthetized cats during spontaneous breathing on continuous positive airway pressure (2-5 cmH2O), before and after lung lavage and then after instillation of surfactant to determine the PSR response to surfactant replacement [18].
• We examined the responses of slowly adapting pulmonary stretch receptors (PSRs), total lung resistance (RL) and dynamic lung compliance (Cdyn) to administered veratridine before and after pretreatment with atropine or flecainide in anaesthetized, artificially ventilated rabbits with bilateral vagotomy [19].

References