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Biomedical subjects

M Saetta

Publications and source records attributed to M Saetta.

100 records · Page 6Linked to original sources
PubMed1985

Mechanical aspects of chest wall distortion.

During passive inflation of the respiratory system, the rib cage (RC) expands because the pressure applied to it [approximately equal to abdominal pressure (Pab)] increases. Similar Pab-tidal volume (VT) relationships between passive and spontaneous inspirations would occur only if 1) Pab acts on RC equally in the two situations (no distortion) or 2) the extradiaphragmatic inspiratory muscles expand RC, compensating for distortion. In anesthetized adult rats and in sleeping human infants the passive relationships between VT and Pab or abdomen motion (AB) were constructed by occluding the airways during expiration. For a given Pab (or AB) in active breathing VT averaged 55% (rats) and 49% (infants) of the passive volume change. With phrenic stimulation in rats VT was only slightly less than during spontaneous breathing, indicating that, in the latter case, the respiratory system was essentially driven only by the diaphragm. In both species occasional breaths with large RC expansion occurred, and VT was then equal to or larger than the passive volume at iso-Pab. We conclude that 1) RC distortion decreases VT to approximately half of the passive value and 2) being on the relaxation curve reflects "compensated" distortion and not absence of it.

Abdomen↗
PubMed1985

Destructive index: a measurement of lung parenchymal destruction in smokers.

Destruction of alveolar walls is considered by most observers to be the most important part in the definition of emphysema, yet it has never been precisely defined and quantitated. We therefore attempted to devise a reliable microscopic technique to quantitate alveolar destruction that would be both sensitive to disease and easy to perform. Using a point-count system, we obtained an index of parenchymal destruction that represents the percentage of destroyed space as a fraction of the total alveolar and duct space. We have called this measurement the destructive index (DI). In the lungs of 8 nonsmokers and 23 smokers, we quantitated the DI and compared it with the mean linear intercept (Lm) and with pulmonary function in smokers. Although Lm was not significantly different in the 2 groups, significant differences between the DI of smokers and nonsmokers (p less than 0.005) were found. In addition, the DI correlated with FEV1(-0.43, p less than 0.05), MMEF (r = -0.44, p less than 0.05), and recoil pressure at 90% TLC (r = -0.61, p less than 0.05) in smokers. These findings suggest that the destructive component of emphysema can be easily quantitated microscopically, occurs in smokers before dimensional changes are evident (i.e., increased Lm), and influences lung function. Therefore, the quantitation of this destruction (DI) could add greatly to the microscopic definition of emphysema, complementing the information given by the dimensional component of emphysema (Lm).

Aged↗
PubMed1985

Reference equations for the single-breath diffusing capacity. A cross-sectional analysis and effect of body size and age.

A longitudinal study was implemented in an unpolluted rural area of northern Italy (near Venice), before the start of the operation of a large oil-burning thermoelectric power plant, in order to investigate the effects of the future exposure to air pollution and to elucidate the natural history of obstructive airways diseases. During the first cross-sectional survey, a sample of the general population (n=3,300, 8 to 64 yr of age) performed several lung function tests, and information on risk factors and on the presence of respiratory symptoms were obtained by a standardized questionnaire. There were 712 subjects who were classified as normal on the basis of rigid criteria and who were able to perform satisfactorily a single-breath CO diffusing capacity (DLCOsb) test. The DLCOsb values showed an increase with height and age early in life and a later decrease with age. Two age groups were selected to determine an age at which DLCOsb stopped increasing and began to decline. Reference equations were computed (using age and height) in these 2 different age groups in each of the sexes. Similar equations were calculated for the total lung capacity derived from single-breath helium dilution measurements. The DLCOsb values in this study were higher than reported by other investigators. The method of selection of the study population, the strict criteria for normal, as well as technical, differences probably explain this finding. Reference equations for diffusing capacity corrected to lung volume (DL/VA) were computed only for adults (much greater than 20) in both sexes, because age and height coefficients in young subjects were insignificant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Loss of alveolar attachments in smokers. A morphometric correlate of lung function impairment.

We studied post-mortem 9 nonsmokers' lungs and 9 smokers' lungs as well as 14 surgical smokers' lungs to examine the possible relationship of the number of alveolar attachments with airways inflammation and with lung function. Alveolar attachments are the alveolar walls radially attached to the small airways, and any discontinuity or rupture of these alveolar walls was considered abnormal. Normal and abnormal attachments were counted in nonsmokers and smokers and expressed as number of attachments, distance between attachments, and percentage of abnormal attachments. Although internal small airways diameter and mean linear intercept were not significantly different between smokers of either group and nonsmokers, significant differences in number of attachments (p less than 0.001), distance between attachments (p less than 0.01), and percentage of abnormal attachments (p less than 0.01) were found. The 3 indexes of alveolar attachments correlated significantly with the score for airways inflammation and with the elastic recoil pressure in smokers. No significant correlation with any other lung function test was found. We conclude that smokers have fewer alveolar attachments than do nonsmokers, and that the loss of alveolar attachments represents an early stage in the destruction of lung parenchyma, and is probably linked to inflammation of the small airways. Because of the strategic situation of this lesion, it could be responsible in part for the loss of elastic recoil seen in the initial stages of chronic obstructive pulmonary disease.

Aged↗
PubMedDate not supplied

Exponential analysis of the lung pressure-volume curve in newborn mammals.

The compliance of the lung (per unit of lung weight) is less in newborn mammals than in adults. This could result from a smaller volume of airspaces per unit weight and/or a lower lung distensibility. The isolated role of lung distensibility was evaluated by using a mathematical description of the pressure-volume (P-V) curve during lung deflation. Deflation limbs of static P-V curves in newborns of six species (four experimentally obtained and two taken from the literature) ranging from total lung capacity to the resting volume (Vr) were fitted by a monoexponential function of the type V = B - Ae-KP, where B equals Vmax at infinite P, A equals the difference between Vmax and V at P = O, and K is a constant representing lung distensibility. Unlike in adults, in newborns the monoexponential fitting provided an adequate description of the P-V curve for only a relatively small range of transpulmonary pressure (from P at Vr to 10-15 cm H2O). The K value of this portion of the curve was similar among species but higher than in adult mammals, averaging 0.240 cm H2O-1. This suggests a similar lung structure in the different species. Since lung distensibility in newborns is larger than in adults, the fact that a unit mass of lung in the newborn is less compliant should be due to the smaller volume of its airspaces.

Age Factors↗
PubMedDate not supplied

Why does airway obstruction persist in asthma due to low-molecular-weight agents? A Pathologistís view.

The pathology of occupational asthma, which is similar to that of nonoccupational asthma, is characterized by airway infiltration of eosinophils, mast cells, and T-lymphocytes associated with thickening of the subepithelial reticular basement membrane. Since occupational asthma is caused by exposure to a sensitizing agent present in the working environment, it might be expected that cessation of occupational exposure leads to complete recovery from the disease. Unfortunately, this fa orable prognosis is observed in only a small percentage of patients with occupational asthma; in most of them, symptoms and bronchial hyperresponsiveness persist, although often at a decreased level. The few longitudinal studies performed on airway pathology in subjects with occupational asthma have shown that, after cessation of exposure to the sensitizing agent, some of the pathologic alterations (such as the subepithelial collagen deposition) improve, whereas others (such as the airway eosinophilia) persist. This latter finding suggests a role for eosinophils in the persistence of symptoms and bronchial hyperresponsiveness in the majority of asthmatic subjects even several months after removal from exposure.

Airway Obstruction↗
PubMedDate not supplied

Reference values for vital capacity and flow-volume curves from a general population study.

A longitudinal epidemiological respiratory study has been started in the North of Italy to investigate the natural history of obstructive airways disease and the long-term effect of SO2 exposure. The first cross-sectional study was completed in this unpolluted area before the activation of a thermoelectric power plant (500 tons of SO2 produced daily). Follow-up surveys are planned after pollution emission starts for a period of ten years. A sample (n = 3289) representative of the general population was drawn from the villages of the area according to the different risks of pollution exposure. Subjects completed questionnaires and performed lung function tests, including forced expiratory (FVC) manoeuvres. For 801 'normal' subjects, prediction equations have been derived in age/sex groups for slow vital capacity (VC) and variables from the FVC manoeuvre. Comparisons with predictions of other studies are reported. Differences among FVC predictions were found, indicating that the use of different criteria for determination of the FVC manoeuvre end-point can affect results. In 'normals' VC was higher than FVC in older subjects. The difference between VC and FVC may be hypothesized as an epidemiological indication of the ageing effect on the mechanical properties of the ventilatory system.

Adolescent↗