Lung injury measurement

There are a number of biological markers measured in plasma or in bronchoalveolar lavage fluid that can be used for the detection of acute lung injury (21). To determine the extent of lung injury which occurs in septic rabbits we measured three proteins in BAL fluid collected from rabbits. 

At this time the evidence that hyperoxic-induced lung injury was due to excessive oxygen free radical production was still largely indirect. The next major event which specifically addressed this question was the important experiments of Crapo and colleagues in the early 1980 s [10]. These studies conducted with lung tissue were similar to those performed earlier in liver [11] and heart [12]. Crapo and co-workers found that superoxide production, measured as CN-insensitive respiration, was increased in lung slices when exposed to 100% O2 rather than air [10]. This work was extended to the measurement of O2 production in submitochondrial particles [13]. Clearly then exposure of tissues to elevated concentrations of O2 leads to ROS production, the extent of which, in association with local antioxidant defences, will determine the redox balance of the tissue. 

Investigation of those overexposed to screening smokes should include, at least, chest radiograph, pulmonary function tests, arterial oxygen tension measurement, blood clinical chemistry, sputum culture, ophthalmic examination with slit-lamp biomicroscopy, and possibly measurement of intraocular pressure. If available, CT scan may be used to assess the severity of lung injury (Hsu et al., 2005). With some smokes, notably white phosphorus, there may be skin contamination with severe irritation and penetrating bums the management of white phosphoms skin burns is discussed in detail in Section VI.A.2. 

A recent report by Parsons et a/." presented evidence for simultaneous elevation of complement fragments and measurable levels of endotoxin in plasma from patients with ARDS. Because complement activation by toxins and by other mechanisms" is thought to cause neutrophil and platelet activation" and subsequent generation of toxic oxygen species and eico-sanoids various strategies known to activate intravascular complement have been used to examine the role of eicosanoids in lung injury . To... 

Pugin et al. (75) compared IL-8, matrix metalloproteinases (MMP-2 and MMP-9), and procollagen peptide III in the pulmonary edema fluid of patients with ARDS or hydrostatic edema. IL-8, MMP-9, and PCPIII were all elevated in the ARDS edema fluid as compared with the hydrostatic edema fluids. The outcomes of the patients were not reported. Interestingly, the clinical severity of illness scores were similar in the patients with ARDS and cardiogenic edema, so the edema fluid measurements were better than clinical criteria at identifying the patients with severe lung injury. 

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