Journal of applied physiology
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When the abdomen in quadriplegic subjects is given a passive mechanical support, the expansion of the lower rib cage during inspiration is greater and the inward displacement of the upper rib cage is smaller. These changes have traditionally been attributed to an increase in the appositional force of the diaphragm, but the mechanisms have not been assessed. ⋯ Application of the abdominal plate caused a marked increase in the inspiratory cranial and outward displacement of rib 10 and a decrease in the inspiratory caudal displacement of rib 5. Analysis of the results showed, however, that 1) the insertional and appositional forces contributed nearly equally to the increased inspiratory displacement of rib 10 and 2) the decrease in the expiratory displacement of rib 5 was the result of both the greater displacement of the lower ribs and the decrease in pleural pressure.
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Mechanical ventilation is a crucial component of the supportive care provided to patients with acute respiratory distress syndrome. Current practice stipulates the use of a low tidal volume (VT) of 6 ml/kg ideal body weight, the presumptive notion being that this limits overdistension of the tissues and thus reduces volutrauma. We have recently found, however, that airway pressure release ventilation (APRV) is efficacious at preventing ventilator-induced lung injury, yet APRV has a very different mechanical breath profile compared with conventional low-VT ventilation. ⋯ Our predictions indicate that APRV is more effective at recruiting the lung than low-VT ventilation, but without causing more overdistension of the tissues. On the other hand, low-VT ventilation generally produces less intratidal recruitment than APRV. Predictions such as these may be useful for deciding on the relative benefits of different ventilation modes and thus may serve as a means for determining how to ventilate a given lung in the least injurious fashion.
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Prolonged mechanical ventilation (MV) leads to rapid diaphragmatic atrophy and contractile dysfunction, which is collectively termed "ventilator-induced diaphragm dysfunction" (VIDD). Interestingly, endurance exercise training prior to MV has been shown to protect against VIDD. Further, recent evidence reveals that sedentary animals selectively bred to possess a high aerobic capacity possess a similar skeletal muscle phenotype to muscles from endurance trained animals. ⋯ In conclusion, these data demonstrate that possession of a high intrinsic aerobic capacity alone does not afford protection against VIDD. Importantly, these results suggest that endurance exercise training differentially alters the diaphragm phenotype to resist VIDD. Interestingly, levels of heat shock protein 72 did not differ between strains, thus potentially representing an important area of difference between animals with intrinsically high aerobic capacity and exercise-trained animals.
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Inhaled nitric oxide (INO) improves ventilation-perfusion matching and alleviates pulmonary hypertension in patients with acute respiratory distress syndrome. However, outcome has not yet been shown to improve, and nonresponse is common. A better understanding of the mechanisms by which INO acts may guide in improving treatment with INO in patients with severe respiratory failure. ⋯ We conclude that INO in short-term experiments, in addition to causing selective pulmonary vasodilation in ventilated lung regions, increases the ET-A/ET-B mRNA expression ratio in lung tissue. This might augment the vasoconstriction in atelectatic lung regions, enhancing the redistribution of pulmonary blood flow to ventilated lung regions which are reached by INO. Such vasoconstriction may be an important additional factor explaining the effect of INO.