O2- and pneumonia-induced lung injury. I. Pathological and morphometric studies

Abstract

The physiological, morphological, and morphometric findings of several lung injury models in baboons have been compared in the following six study groups: 1) initial injury with oleic acid followed by ventilation with 100% O2, 2) ventilation with 100% O2, 3) ventilation with 80% O2, 4) ventilation with 80% O2 followed by inoculation of Pseudomonas aeruginosa, 5) ventilation with 40% O2, and 6) normal nonventilated room-air-breathing animals. The animals were maintained for 11 days in an intensive care unit. Light microscopically, animals ventilated with 40 and 80% O2 showed mild lung injury, consisting mostly of an increase in alveolar macrophages in peribronchiolar sites and focal alveolar wall widening. The 100% O2-oleic acid, 100% O2, and 80% O2-Pseudomonas-treated baboons showed mixed exudative-reparative diffuse alveolar lesions. Ultrastructurally, the type II cells of these three groups had significantly altered morphology with aberrations of lamellar body configurations. Morphometric findings showed increases in type II and interstitial cells and decreases in type I and endothelial cells in these injured animals. A striking finding was that the physiological, morphological, and morphometric changes of an 80% O2-Pseudomonas insult was as injurious as 100% O2. This synergistic effect of hyperoxia and infection very likely reflects the most frequent evolution of adult respiratory distress syndrome in patients in intensive care units.

Antioxidants improve antibacterial function in hyperoxia-exposed macrophages

“…An increased bacterial burden and dissemination of the infection was also noted at the time of autopsy in the mice exposed to hyperoxia [4]. Other studies have demonstrated that an otherwise sub-lethal bacterial load of PA resulted in increased mortality in hyperoxia-exposed hamsters and a synergistic response is also supported by morphometric studies in a baboon model of BPD [5]. Crouse and colleagues demonstrated that hyperoxia caused a persistence of ureaplasma colonization, potentiates the inflammatory response and increases mortality associated with an otherwise benign infection [6].…”

“…Bacterial adherence leading to colonization is the first step in the process of invasive pulmonary infection, with phagocytosis by alveolar macrophages critically important in preventing invasive pulmonary infection. Several studies have suggested that hyperoxia impairs pulmonary immunity and increases the risk of invasive pulmonary infection in newborn animal models and preterm infants (2)(3)(4)(5)(6). In fact, the STOP-ROP study suggested that preterm infants receiving higher inspired oxygen concentrations had an increased incidence of pneumonia and BPD, although the study was not designed to specifically examine this outcome [2].…”

Assessment of pulmonary oxygen toxicity: Relevance to professional diving; a review

“…In addition, ventilated patients are at risk of developing ventilator-associated pneumonia (Altemeier and Sinclair, 2007). A combination of hyperoxia and bacterial lung infection leads to deteriorating effects with respect to pulmonary oxygen toxicity (Coalson et al, 1989). Furthermore, it is still subject of debate whether hyperoxia in septic subjects has a protective or a deteriorating effect on the immunity (Baleeiro et al, 2003;Hauser et al, 2009;Hou et al, 2009).…”

The Thioredoxin Reductase-1 Inhibitor Aurothioglucose Attenuates Lung Injury and Improves Survival in a Murine Model of Acute Respiratory Distress Syndrome

“…In acute lung injury (ALI) models, bacterial or acid-induced lung injury is further exacerbated by hyperoxic exposure (1,6,21,22,27). Thus, the present studies utilized an adult murine ARDS model which combines inflammatory and hyperoxic exposures to test the hypothesis that ATG treatment attenuates lung inflammation and injury, increases pulmonary GSH levels, and improves survival.…”