Characterization of crackles from patients with fibrosis, heart failure and pneumonia.

The spectral analysis of crackles sounds has been carried out based on the assumption that they are stationary signals, and the majority of the work on the crackles was accomplished before the publication of the Computerized Respiratory Sound Analysis (CORSA) guidelines. This works characterizes crackles acquired from patients with fibrosis, heart failure, and pneumonia, breathing at a constant rate, with a system developed according to the CORSA guidelines. Their maximum frequency was obtained by applying discrete pseudo Wigner-Ville distribution, suitable for non-stationary signals, and an objective method to estimate the maximum frequency, the modified geometric method. The effects of the breathing rate and the tidal volume on the spectra of the crackles were also investigated. The role of the high-pass filter cutoff frequency of the acquisition system on the characteristics of the acquired crackles was also assessed in this present study. Higher high-pass filter cutoff frequency allows for higher amplification which modifies the maximum frequency and the 2CD index. It is shown that the crackles acquired according to the CORSA guidelines have higher frequencies and shorter 2CD indexes than those previously reported, highlighting the need for the standardization and detailed report of the acquisition setup when quantifying lung sounds. The results pointed out that the maximum frequency and the 2CD indexes may allow crackles generated by fibrosis to be distinguished from the ones generated by the heart failure and pneumonia. It is not possible, however, by means of these two indexes, to differentiate between pneumonia and heart failure crackles.

Cigarette smoke dissociates inflammation and lung remodeling in OVA-sensitized and challenged mice.

We evaluated the effects of cigarette smoke (CS) on lung inflammation and remodeling in a model of ovalbumin (OVA)-sensitized and OVA-challenged mice. Male BALB/c mice were divided into 4 groups: non-sensitized and air-exposed (control); non-sensitized and exposed to cigarette smoke (CS), sensitized and air-exposed (OVA) (50 µg+OVA 1% 3 times/week for 3 weeks) and sensitized and cigarette smoke exposed mice (OVA+CS). IgE levels were not affected by CS exposure. The increases in total bronchoalveolar fluid cells in the OVA group were attenuated by co-exposure to CS, as were the changes in IL-4, IL-5, and eotaxin levels as well as tissue elastance (p<0.05). In contrast, only the OVA+CS group showed a significant increase in the protein expression of IFN-γ, VEGF, GM-CSF and collagen fiber content (p<0.05). In our study, exposure to cigarette smoke in OVA-challenged mice resulted in an attenuation of pulmonary inflammation but led to an increase in pulmonary remodeling and resulted in the dissociation of airway inflammation from lung remodeling.

Effects of positive end-expiratory pressure in an experimental model of acute myocardial infarct in wistar rats.

UNLABELLED: Our purpose in this study was to access the pulmonary effects of mechanical ventilation with positive end-expiratory pressure (PEEP; 10 cmH2O) or without PEEP (zero PEEP-ZEEP) in a rat model of acute myocardial infarction that resulted in hypotension but not in pulmonary congestion. METHODS: Wistar rats were anesthetized (1.5% isoflurane) and myocardial infarct was induced by ligature of the anterior interventricular coronary artery. Rats with myocardial infarct were compared with sham-operated (Sham) and closed thorax groups. RESULTS AND CONCLUSION: There was a significant decrease in MAP in the acute myocardial infarct group (92.5 +/- 4.2 mmHg) when compared with closed chest group (113.0 +/- 4.4 mmHg). There was no significant difference between acute myocardial infarct and Sham groups in PEEP or ZEEP. Mechanical ventilation for 120 min resulted in a significant increase in respiratory system elastance in the groups ventilated with ZEEP (2.59 +/- 0.17 and 2.32 +/- 0.17 cmH2O.mL, Sham and acute myocardial infarct groups, respectively). This effect of mechanical ventilation was not observed in the presence of PEEP in both groups. There was no significant increase in the amount of perivascular pulmonary edema measured in all groups studied. Mean airspace linear intercept and lung tissue distortion index also did not show statistically significant difference between Sham and acute myocardial infarct groups. We conclude that in this experimental model of acute myocardial infarct (12.4 +/- 4.1% area of necrotic tissue and 26.4 +/- 4.0% area of ischemic tissue), there was a protective pulmonary effect of PEEP.