No abstract

Senile lungs are characterized by a homogeneous enlargement of the alveolar airspaces, without fibrosis or destruction of their walls. Study of the functional characteristics of excisea senile lungs showed an increase in minimal air and a shift to the left of the elastic recoil pressure-volume curves, less pronounced than in emphysematous lungs. Maximal expiratory volumes and flows were normal. Total lung capacity was not significantly increased, but this may be a consequence of preagonal edema. Comparison of normal, senile, and emphysematous lungs showed a close relationship between recoil pressures and mean linear intercept, Lm, and between forced expiratory volume in 1 s and diameter and density of the membranous bronchioles. It is concluded that airspace enlargement may precede emphysema and may be responsible for changes in lung elasticity. In this respect, senile lungs are an example of the functional changes caused by an isolated airspace enlargement.

We partitioned pulmonary resistance (RL) in excised normal, senile, and emphysematous human lungs at various distending pressures; peripheral resistance (Rp) was measured by means of retrograde catheters and lung tissue resistance (Rti) by means of pleural capsules. By subtracting Rp from RL and Rti from Rp, we obtained, respectively, central (Rcaw) and peripheral (Rpaw) airway resistance. We determined also lung volumes, the elastic recoil pressure-volume curve, and the forced expiratory volume in 1 s-to-vital capacity ratio (FEV1/VC). The functional data were related to morphometry: mean linear intercept (Lm), diameter (d), and density (n/cm2) of membranous bronchioles. In the three groups of lungs, Rti demonstrates a marked negative frequency dependence and increases with transplumonary pressure. In emphysematous lungs, the increase of RL is mainly due to an increase of Rpaw; in addition, Rcaw and Rti are higher than normal. In the group of senile lungs, airway resistances are within normal range, but Rti is slightly increased. FEV1/VC is related to Rpaw and elastic recoil pressure; Rpaw is related to d and n/cm2, and Rti is related to dynamic elastance and to Lm.

We report here on a new case of L. buccalis bacteraemia. To our knowledge 16 other cases of L. buccalis bacteraemia have been reported in the literature, most of them in neutropenic patients. However L buccalis endocarditis does occasionally occur in non-neutropenic patients. The identification of L. buccalis is based on well known phenotypic features and confirmed by the detection of a large peak of lactic acid by gas chromatography for non volatile organic acids. L. buccalis is sensitive to a wide range of antibiotics including beta-lactam antibiotics, but it is resistant to aminoglycosides and macrolides.

In 54 patients with interstitial lung diseases and no signs of airway obstruction we measured lung volumes, maximal expiratory flows, diffusing capacity (DLCO), total respiratory resistance (Rrs) and reactance (Xrs) between 4 and 26 Hz by means of the forced oscillation technique. In all patients DLCO was less than 75% of the expected value. Patients were classified into two groups depending on total lung capacity (TLC): group A with TLC less than 80% of expected, and group B with TLC of 80% or more. Group A demonstrated a decrease of Xrs especially at low frequencies, with small, not significant changes in Rrs. In the patients in this group with the lowest values of TLC (less than 50%), we observed an increase of Rrs at low frequencies causing a negative frequency dependence of Rrs. In group B no distinct changes of Rrs and Xrs occurred. Canonical correlation analysis between routine lung function data and forced oscillation parameters, showed tight correlations between TLC in absolute value or VC in percent of the predicted value on the one hand and average level of Xrs and average slope of Xrs (and Rrs) vs frequency curves on the other hand. Measurements of lung mechanics in five additional patients and comparison with a model of the respiratory system suggest that the changes of Rrs and Xrs are not explained totally by the observed increase in lung tissue resistance and decrease in lung compliance. The observed changes in Rrs and Xrs are not specific for restrictive lung disorders; similar changes are met also in moderately advanced obstructive diseases.