The effect of chest wall vibration on dyspnea at rest was investigated in 15 patients with severe chronic respiratory diseases. The magnitude of their baseline dyspnea was 17.9 +/- SE 3.3 mm on a 150-mm visual analog scale. One hundred hertz out-of-phase vibration (OPV; inspiratory intercostal muscles vibrated during expiration and expiratory intercostal muscles vibrated during inspiration) increased dyspnea an average of 21.9 +/- SE 7.8 mm (p < 0.05). One hundred hertz in-phase vibration (IPV; inspiratory intercostal muscles vibrated during inspiration and expiratory intercostal muscles vibrated during expiration) decreased dyspnea an average of 6.9 +/- SE 2.8 mm (p < 0.05). Changes in the respiratory pattern and arterial blood gas determinations elicited by 5-min IPV were investigated in eight of the 15 patients. Tidal volume was significantly increased in all eight of these patients. Respiratory frequency was decreased in seven patients and increased in one. Functional residual capacity, measured before and during the application of IPV for a period of about 10 breaths, was increased in one patient and decreased in the remaining seven. PaCO2 decreased by 1.3 +/- 1.0 mm Hg (p < 0.05), from 49.6 +/- 8.4 mm Hg; PaO2 increased by 3.4 +/- 2.3 mm Hg (p < 0.05), from 67.7 +/- 12.7 mm Hg. The results indicate that in-phase chest wall vibration decreased pathologic dyspnea in patients with chronic respiratory disease and suggest that the effects on respiratory sensation are mediated by afferent information from chest wall respiratory muscles to supraspinal centers.

This study investigated the morphological changes of lungs in F344/N rats (9 -36 months old). We initially examined general and quantitative morphological changes, and then we used immunohistochemistry to detect distributional changes in collagen subtypes (types I, III, and IV) and smooth muscle cell (SMC) markers (␣-smooth muscle actin (ASMA), ␥-smooth muscle actin (GSMA), desmin, and vimentin) in the lungs. In 24-month-old rats, alveolar ducts and alveolar sacs were enlarged, and alveoli were wider and shallower than in younger animals. In old rats (Ն27 months), terminal and respiratory bronchioles and alveolar ducts were dilated and alveoli were more extended than in 24-month-old rats. No age-related distributional changes were observed for collagen types I, III, and IV as revealed by immunohistochemistry, or elastin as revealed by resorsin fuchsin. SMCs in the extra-and intrapulmonary bronchi were immunoreactive for ASMA, GSMA, and desmin, but not for vimentin at all ages. In old rats (Ն27 months), SMCs were loosely arranged in comparison with younger animals, and stainability for GSMA and desmin was decreased. In the respiratory bronchioles and alveolar ducts, a few cells immunoreactive for ASMA and vimentin were observed in the smooth muscle aggregations of the alveolar orifice in rats younger than 12 months. In older rats (Ͼ20 months), cells immunoreactive for ASMA and vimentin were increased in septal tips. In conclusion, extension of distal airways and immunohistochemical changes of SMC markers in F344/N rat lungs were evident by ϳ24 months of age, but there was no apparent change in connective tissue morphology. Anat Rec Part A 272A: 538 -547, 2003.

ABSTRACT. The aim of this study was to determine the effect of perineural capsaicin (CAPS) treatment on cardiopulmonary reflexes elicited by topical laryngeal instillation of CAPS and distilled water (DW) in sevoflurane-anesthetized dogs. Cardiopulmonary reflexes elicited by CAPS (10 µg/ml, 10 ml) were attenuated by perineural CAPS treatment to the superior laryngeal nerves (SLNs) (P<0.05), whereas those by DW (10 ml) remained unaffected (P>0.05). The reflex responses to DW that remained even after the perineural CAPS treatment were eliminated by laryngeal anesthesia with lidocaine. These results suggest that cardiopulmonary reflexes from the laryngeal mucosa elicited by CAPS instillation can be blocked by perineural CAPS treatment to the SLNs, which may result from inhibition of the laryngeal CAPS-sensitive C-fiber afferents.-KEY WORDS: canine, control of breathing, laryngeal afferents.The larynx is a potent reflexogenic region of the upper airway that is rich in sensory afferents and elicits various airway defence reflexes such as apnea, coughing, glottal closure, mucus hypersecretion, bronchoconstriction, bradycardia and hypertension [10]. Among several types of mechanoreceptors described in the larynx, capsaicin (CAPS)-sensitive C-fibers and water responsive rapidly adapting 'irritant' receptors are thought to have primary role in eliciting these airway reflexes. Whereas there are several studies which suggest the behavior of the CAPS-sensitive C -f i b e r s a n d w a t e r -r e s p o n s i v e r e c e p t o r s electrophysiologically [4,10], the reflex data to support their contribution is still lacking.In a recent report, we have demonstrated that perineural CAPS treatment to the SLNs can block C-wave afferent compound action potentials in anesthetized dogs [6]. We hypothesized that if the afferent information via the Cfibers were preferably blocked by the perineural CAPS treatment, then the resultant cardiopulmonary reflexes would be attenuated or extinguished without affecting other myelinated fiber components such as water-responsive receptors. Thus the purpose of this study was to determine t h e e ff e c t o f p e r i n e u r a l C A P S t r e a t m e n t o n cardiopulmonary reflexes elicited by topical laryngeal instillation of CAPS and distilled water (DW) in dogs.Animals and anesthesia: Six healthy beagles (3 females and 3 males) were studied. Their mean age was 13.5 (range, 10 to 15) months and mean body weight was 8.6

Nasal administration of halothane at concentrations generally used for mask induction of anesthesia induces reflex inhibition of breathing. Afferent fibers in the caudal nasal nerve appear to play an important role in the reflex inhibition of breathing induced by halothane administration.

Vibratory stimulation applied to the chest wall during inspiration reduces the intensity of breathlessness, whereas the same stimulation during expiration has no effect or may increase breathlessness. The purpose of the present study was to determine whether vibration reduced the intensity of breathlessness during progressive hypercapnia with and without the addition of an external resistive load. A second objective was to see whether the mouth occlusion pressure at 0.2 s (P0.2) was reduced by the vibratory stimulation. Hypercapnic ventilatory response was conducted in 10 healthy male volunteers with simultaneous measurement of visual analog scale, P0.2, and minute ventilation. Hypercapnic ventilatory response was performed and randomly combined with or without vibratory stimulation (100 Hz) as well as with or without inspiratory load. With inspiratory load, in-phase vibration did not cause any significant changes in the slopes of P0.2 and minute ventilation to CO2, whereas the slope of visual analog scale to CO2 significantly decreased from 0.47 +/- 0.15 to 0.34 +/- 0.11 (SE) cm/Torr (P < 0.05). We conclude that in-phase vibration could decrease the slope of breathlessness elicited by inspiratory load combined with hypercapnia without changing motor output.