We developed a prototype laser monitor, consisting of a single laser sensor, to observe chest wall displacement during respiration. With this monitor, respiratory waveforms are expressed as an anterioposterior motion of the chest wall. The purpose of this study was to examine the characteristics and performance of this prototype. Performance was assessed: 1) under static conditions; 2) using a lung model ventilated in both conventional and high frequency oscillation (HFOV) modes; and 3) during spontaneous breathing in normal adults.In vitro, the monitor performed well both under static conditions and during mechanical ventilation. Reliable "respiratory" wave forms, with no frequency-dependent change in the relationship between displacement and volume, were produced during both conventional ventilation and HFOV at 15 Hz. In vivo, abdominal displacement, measured in the midline, was linearly correlated with the tidal volume signal integrated from flow. The waveforms produced by the monitor were adequate for monitoring respiration and for calculating respiratory timing variables.While a single laser sensor is unlikely to be sufficient for monitoring respiration in spontaneously breathing subjects, the performance of the prototype monitor was sufficiently impressive to encourage further development and further study of this type of truly noninvasive respiratory monitor.

The influence of pulmonary vascular congestion on the response of the airways and lung tissue to low doses of inhaled methacholine (MCh) was studied by inflating a balloon catheter in the left atrium of the heart in six piglets, with an additional five piglets serving as control animals. Congestion alone resulted in small increased in baseline airway (Raw) (14.6 +/- 3.7%) and tissue (Rti) resistance (8. 1 +/- 6.5%). Low-dose inhaled MCh (0.3 mg/ml) increased Raw and Rti in the control group by 10.8 +/- 10.3% and 42.2 +/- 29.5%, respectively. The increase in Raw with MCh in the presence of vascular engorgement was significantly greater (67.8 +/- 18.9%) but the increase in Rti (38.1 +/- 13.2%) was similar to that seen in the control group. Morphometric measurements were performed on transverse sections of large and small airways from nine additional piglets (three congested only, three MCh only, and three congestion plus MCh). The thickness of the inner airway wall was similar in all groups. Compared with MCh only piglets, the thickness of the outer airway wall (between the outer border of the smooth muscle and the surrounding lung parenchyma) was increased (p < 0.05) in engorged only and engorged plus MCh piglets. Compared with MCh only and engorgement only, the amount of airway smooth muscle shortening was greater (p < 0.05) in all airway size groups in piglets that underwent engorgement plus MCh challenge. The results of this study demonstrate that pulmonary vascular engorgement, induced by increased left atrial pressure, selectively enhances the airway, but not the parenchymal, response to inhaled MCh. These changes are associated with increased thickness of the outer airway wall in response to vascular congestion, suggesting that uncoupling of the mechanical interdependence between the airway smooth muscle and the lung parenchyma may have occurred. Mechanical uncoupling may reduce the load opposing smooth muscle shortening resulting in increased airway narrowing in response to low doses of inhaled methacholine.

These data suggests that leflunomide can prevent primary allergic sensitization and prevent allergen-induced EAR by inhibiting production of allergen-specific IgE antibodies. Further studies in atopic conditions are warranted.

Eleven open-chest piglets were studied to examine the effects of vascular engorgement on partitioned airway and lung tissue mechanics, and to investigate the role of vagal denervation on lung function during engorgement. Alveolar pressure was measured using alveolar capsules. Pulmonary elastance (EL) and resistance (RL), airway (Raw), and tissue (Vti) resistance were calculated during mechanical ventilation. Acute fluid administration with polygeline (10 mL/kg boluses up to a total of 30 mL/kg) resulted in an increase of RL with increases in both Raw and Vti. Vti rose 2-3-fold in comparison with Raw. To increase left atrial pressure, a balloon catheter was inserted into the left atrium of the heart and inflated with different volumes. The responses of EL, RL, Raw and Vti were comparable to those with acute fluid load. Alterations in pulmonary mechanics were closely correlated to mean pulmonary artery blood pressure. In another six animals the effect of vagotomy on vascular engorgement was studied. Vagotomy did not alter baseline airway or tissue mechanics. Furthermore, vagotomy did not influence the change of pulmonary mechanics to fluid load or increase of left atrial pressure. Our data indicate that in young piglets vascular engorgement causes alterations in airway and lung tissue mechanics that are not dependent on vagal influences.

No abstract