Introduction: When alveoli collapse the traction forces exerted on their walls by adjacent expanded units may increase and concentrate. These forces may promote its re-expansion at the expense of potentially injurious stresses at the interface between the collapsed and the expanded units. We developed an experimental model to test the hypothesis that a local non-lobar atelectasis can act as a stress concentrator, contributing to inflammation and structural alveolar injury in the surrounding healthy lung tissue during mechanical ventilation. Methods: A total of 35 rats were anesthetized, paralyzed and mechanically ventilated. Atelectasis was induced by bronchial blocking: after five minutes of stabilization and pre-oxygenation with F_IO₂ = 1.0, a silicon cylinder blocker was wedged in the terminal bronchial tree. Afterwards, the animals were randomized between two groups: 1) Tidal volume (V_T) = 10 ml/kg and positive end-expiratory pressure (PEEP) = 3 cmH₂O (V_T10/PEEP3); and 2) V_T = 20 ml/kg and PEEP = 0 cmH₂O (V_T20/zero end-expiratory pressure (ZEEP)). The animals were then ventilated during 180 minutes. Three series of experiments were performed: histological (n = 12); tissue cytokines (n = 12); and micro-computed tomography (microCT; n = 2). An additional six, non-ventilated, healthy animals were used as controls. Results: Atelectasis was successfully induced in the basal region of the lung of 26 out of 29 animals. The microCT of two animals revealed that the volume of the atelectasis was 0.12 and 0.21 cm³. There were more alveolar disruption and neutrophilic infiltration in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. Edema was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in the V_T20/ZEEP than V_T10/PEEP3 group. The volume-to-surface ratio was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. We did not find statistical difference in tissue interleukin-1β and cytokine-induced neutrophil chemoattractant-1 between regions. Conclusions: The present findings suggest that a local non-lobar atelectasis acts as a stress concentrator, generating structural alveolar injury and inflammation in the surrounding lung tissue.

To assess the effect of atelectasis during mechanical ventilation on the periatelectatic and normal lung regions in a model of atelectasis in rats with acute lung injury induced by lipopolysaccharide. Twenty-four rats were randomized into the following four groups, each with 6 animals: the Saline-Control Group, Lipopolysaccharide Control Group, Saline-Atelectasis Group, and Lipopolysaccharide Atelectasis Group. Acute lung injury was induced by intraperitoneal injection of lipopolysaccharide. After 24 hours, atelectasis was induced by bronchial blocking. The animals underwent mechanical ventilation for two hours with protective parameters, and respiratory mechanics were monitored during this period. Thereafter, histologic analyses of two regions of interest, periatelectatic areas and the normally-aerated lung contralateral to the atelectatic areas, were performed. The lung injury score was significantly higher in the Lipopolysaccharide Control Group (0.41 ± 0.13) than in the Saline Control Group (0.15 ± 0.51), p < 0.05. Periatelectatic regions showed higher lung injury scores than normally-aerated regions in both the Saline-Atelectasis (0.44 ± 0.06 x 0.27 ± 0.74 p < 0.05) and Lipopolysaccharide Atelectasis (0.56 ± 0.09 x 0.35 ± 0.04 p < 0.05) Groups. The lung injury score in the periatelectatic regions was higher in the Lipopolysaccharide Atelectasis Group (0.56 ± 0.09) than in the periatelectatic region of the Saline-Atelectasis Group (0.44 ± 0.06), p < 0.05. Atelectasis may cause injury to the surrounding tissue after a period of mechanical ventilation with protective parameters. Its effect was more significant in previously injured lungs.

Background: Post-COVID-19 syndrome (PCS) is associated with persistent pulmonary, autonomic, and hemodynamic impairments. However, the acute effects of spinal manipulation on these systems in adults with PCS remain unclear. Purpose: To investigate the acute effects of combined cervical and thoracic spinal manipulation on pulmonary function, heart rate variability, and blood pressure in adults with PCS. Methods: This exploratory, hypothesis-generating study included 10 adults with PCS randomized to three sequences of spinal manipulation, sham manipulation, and control using a Latin-square crossover design with one-week washouts. Spirometry (FVC, FEV1, and FEV1/FVC) was assessed immediately after each intervention. Blood pressure and heart rate variability indices (RMSSD, SDNN, pNN50, LF, HF, and LF/HF ratio) were recorded at rest and 15, 30, 45, and 60 minutes post-intervention. Friedman/Wilcoxon tests and baseline-corrected sensitivity analyses were performed. Results: No significant differences were observed among conditions for FVC, FEV1, FEV1/FVC (all p>0.70), or the area under the curve of blood pressure, RMSSD, pNN50, HF, and LF/HF ratio (all p>0.27). Differences in SDNN and LF did not survive Bonferroni-corrected comparisons and disappeared after baseline correction, indicating between-session baseline variability rather than intervention effects. Conclusion: A single session of combined cervical and thoracic spinal manipulation did not produce consistent acute improvements in pulmonary function, blood pressure, or heart rate variability in adults with PCS. These physiological variables should not be considered primary indicators of response to an isolated manipulation session.