Prevention Of Acute Lung Injury Research Articles

A role for the anti-inflammatory properties of tetracyclines in the prevention of acute lung injury.

The etiology of inflammatory disorders involves many cellular, plasmatic and humoral pathways of signaling culminating in the production of enzymatic and free radical mediated tissue damage. Multiple redundant pathways of initiation and elusive temporal expression of initiators pose formidable barriers to effective treatment. Nowhere is this more evident than in the adult respiratory distress syndrome (ARDS), a systemic inflammatory disorder leading to pulmonary failure where, despite significant advances in intensive care management, mortality has improved only 10% over the last decade. Tetracyclines, in addition to their anti-microbial properties, exhibit inhibitory activity toward several initiators of the inflammatory cascade and mediators of tissue damage. In this review we discuss how the broad spectrum anti-inflammatory properties of the tetracyclines make them attractive candidates for use in the prevention of acute lung injury.

Prevention of rabbit acute lung injury by surfactant, inhaled nitric oxide, and pressure support ventilation.

Improvement of pulmonary perfusion and blood oxygenation and prevention of acute lung injury (ALI) may rely on ventilation strategy. We hypothesized that application of a combined surfactant, inhaled nitric oxide (iNO), and pressure support ventilation (PSV) should more effectively protect the lungs from injury. Anesthetized and intubated adult rabbits weighing 2.8 +/- 0.3 kg were allowed to breathe room air while receiving oleic acid intravenously (60 microl/kg). Within 90 min this caused a reduction of Pa(O(2)) from 94 +/- 7 to 48 +/- 3 mm Hg and dynamic lung compliance (Cdyn) from 1.59 +/- 0.22 to 0.85 +/- 0.10 ml/cm H(2)O/kg (both p < 0.01), and increase of intrapulmonary shunting (Q S/Q T) from 9.4 +/- 1.2 to 27 +/- 5% (p < 0.05). PSV was subsequently applied with 3 cm H(2)O of continuous positive airway pressure and FI(O(2)) of 0.3, and the animals were randomly allocated to four groups, receiving: (1) PSV only (Control, n = 10); (2) iNO at 20 ppm (NO, n = 9); (3) surfactant phospholipids at 100 mg/kg (Surf, n = 8); and (4) surfactant at 100 mg/kg and iNO at 20 ppm (SNO, n = 8). PSV level was varied to maintain a tidal volume of 8 to 10 ml/kg for another 12 h or until early animal death. Five animals in the SNO, three each in the NO and Surf group, and one in the Control group survived 12 h (SNO versus Control, p < 0.05). The NO, Surf, and SNO groups had significantly improved mean Pa(O(2)) (> 70 mm Hg, p < 0.05), and reduced Q S/Q T (15, 19, and 17%, respectively, p < 0.05) at 6 and 12 h, but not in the Control group. The SNO group had the highest values of Cdyn at 12 h, alveolar aeration and disaturated phosphatidylcholine-to-total protein ratio in bronchoalveolar lavage fluid, and the lowest wet-to-dry lung weight ratio and lung injury score (p < 0.05). The results indicate that early alleviation of ALI by surfactant, iNO, and PSV is due to synergistic effects, and only PSV in this model had limited effects.

Prevention of acute lung injury using a sulfhydryl agent

Prevention of acute lung injury using a sulfhydryl agent