Journal of applied physiology
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The purpose of the study was to determine if repeated exertional heat injuries (EHIs) worsen the inflammatory response. We assessed the impact of a single EHI bout (EHI0) or two separate EHI episodes separated by 1 (EHI1), 3 (EHI3), and 7 (EHI7) days in male C57BL/6J mice (n = 236). To induce EHI, mice underwent a forced running protocol until loss of consciousness or core temperature reached ≥ 42.7°C. ⋯ NEW & NOTEWORTHY Mice undergoing repeated exertional heat injuries, within 1 wk of an initial heat injury, appear to have some protective adaptations. During the second exertional heat injury, mice were able to run longer and sustain higher body temperatures before collapse. Despite this, the mice undergoing a second exertional heat injury were more resilient to the heat as evidenced by attenuated minimum body temperature, higher HPS70 (serum and liver), lower corticosterone, and lower FABP2.
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Tidal volume delivered by mechanical ventilation to a sedated patient is distributed in a nonphysiological pattern, causing atelectasis (underinflation) and overdistension (overinflation). Activation of the diaphragm during controlled mechanical ventilation in these sedated patients may provide a method to reduce atelectasis and alveolar inhomogeneity, protecting the lungs from ventilator-induced lung injury while also protecting the diaphragm by preventing ventilator-induced diaphragm dysfunction. We studied the hypothesis that diaphragm contractions elicited by transvenous phrenic nerve stimulation, delivered in synchrony with volume-control ventilation, would reduce atelectasis and lung inhomogeneity in a healthy, normal lung pig model. ⋯ NEW & NOTEWORTHY Temporary transvenous diaphragm neurostimulation has been shown to mitigate diaphragm atrophy in a preclinical model. This study contributes to this work by demonstrating that diaphragm neurostimulation can also offer lung protection from ventilator injury, providing a potential solution to the dilemma of lung- versus diaphragm-protective ventilation. Our findings show that neurostimulation on every breath preserved [Formula: see text]/[Formula: see text], end-expiratory lung volume, alveolar homogeneity, and required lower pressures than lung-protective ventilation over 50 h in healthy pigs.
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Regional viscoelastic properties of thoracic tissues in acute respiratory distress syndrome (ARDS) and their change with position and positive end-expiratory pressure (PEEP) are unknown. In an experimental porcine ARDS, dorsal and ventral lung (R2,L and E2,L) and chest wall (R2,cw and E2,cw) viscoelastic resistive (R) and elastic (E) parameters were measured at 20, 15, 10, and 5 cmH2O PEEP in supine and prone position. E2 and R2 were obtained by fitting the decay of pressure after end-inspiratory occlusion to the equation: Pviscmax (t) =R2 e-t/τ2, where t is the length of occlusion and τ2 time constant. ⋯ Prone position tended to decrease lung viscoelastic resistive component. PEEP had a significant effect on dorsal lung viscoelastic elastance. Finally, lung viscoelastic resistance correlated with the amount of lung collapse assessed by electrical impedance tomography.
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The purpose of this study was to determine whether the plethysmographic variability index ("PVi") can predict preload responsiveness in patients with nasal high flow (NHF) (≥30 L/min) with any sign of hypoperfusion. "Preload responsiveness" was defined as a ≥10% increase in stroke volume (SV), measured by transthoracic echocardiography, after passive leg raising. SV and PVi were reassessed in preload responders after receiving a 250-mL fluid challenge. Twenty patients were included and 12 patients (60%) were preload responders. ⋯ NEW & NOTEWORTHY This is the first study that analyzes the use of noninvasive plethysmographic variability index (PVi) for preload assessment in patients treated with nasal high flow (NHF). Its results showed that PVi might identify preload responders. Therefore, PVi may be used in the day-to-day clinical decision-making process in critically ill patients treated with NHF, helping to provide adequate resuscitation volume.
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Randomized Controlled Trial
The effect of long-acting dual bronchodilator therapy on exercise tolerance, dynamic hyperinflation, and dead space during constant work rate exercise in COPD.
We investigated whether dual bronchodilator therapy (glycopyrrolate/formoterol fumarate; GFF; Bevespi Aerosphere) would increase exercise tolerance during a high-intensity constant work rate exercise test (CWRET) and the relative contributions of dead space ventilation (VD/VT) and dynamic hyperinflation (change in inspiratory capacity) to exercise limitation in chronic obstructive pulmonary disease (COPD). In all, 48 patients with COPD (62.9 ± 7.6 yrs; 33 male; GOLD spirometry stage 1/2/3/4, n = 2/35/11/0) performed a randomized, double blind, placebo (PL) controlled, two-period crossover, single-center trial. Gas exchange and inspiratory capacity (IC) were assessed during cycle ergometry at 80% incremental exercise peak work rate. ⋯ NEW & NOTEWORTHY This study was a randomized clinical trial (NCT03081156) that collected detailed physiology data to investigate the effect of dual bronchodilator therapy on exercise tolerance in COPD, and additionally to determine the relative contributions of changes in dead space ventilation (VD/VT) and dynamic hyperinflation to alterations in exercise limitation. We utilized a unique noninvasive method to assess VD/VT (transcutaneous carbon dioxide, Tc[Formula: see text]) and found that dual bronchodilators yielded a moderate improvement in exercise tolerance. Importantly, attenuation of dynamic hyperinflation rather than change in dead space ventilation was the most important contributor to exercise tolerance improvement.