Increased XXXX in exhaled gas as an early marker of lung inflammation in a model of @entity295 .

@entity1 @entity295 @entity1505 @entity651 @entity842 @entity35
@entity842 (NO) has been implicated in the pathologic vasodilation of @entity295 . Because NO can be measured in the exhaled gas of animals and @entity1 , we hypothesized that increases in exhaled NO would occur in a septic model. Using a blinded design, 10 male @entity35 (300 to 400 g) were anesthetized, paralyzed, tracheotomized, and randomized (5/group) to receive an intravenous injection of either lipopolysaccharide (LPS) (Salmonella typhosa, 20 mg/kg) or placebo (equal volume of saline). Thereafter, exhaled gas was collected and measurements of NO concentration were made using chemiluminescence every 20 min for 300 min during ventilation (RR 40 breaths/min, VT 3 ml; PEEP 0, FIO2 0.21). Another group of 10 animals (5 LPS; 5 control) were treated in the same fashion and then killed at 240 min and an arterial blood sample obtained for blood gas and @entity1505 determinations. Pressure volume (PV) curves were constructed and lungs removed, preserved, and submitted for histologic evaluation. LPS-treated @entity35 had lower mean arterial pressures than the control group, p < 0.0001. No significant differences in static lung compliance and PV curves were found in the two groups. @entity1505 levels were greater in the LPS group (1.40 +/- 0.24 ng/ml) versus control group (0.09 +/- 0.04 ng/ml), p < 0.001. By contrast to the control group, exhaled NO concentration rose in all LPS-treated @entity35 at approximately 100 min and at about 160 min reached a plateau that was 6 times greater than control levels (p < 0.0001). There was greater interstitial, airspace, and @entity651 in the LPS group (p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
