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Angiotensin II plays a pathophysiologic role in lung inflammation. Elevated levels of inflammatory cytokines are found in the plasma during pulmonary edema caused by endotoxin (LPS). The angiotensin converting enzyme (ACE) inhibitor, perindoprilate, is an effective agent in the prevention of acute lung injury and fibrosis. The aim of the present study was to investigate whether the ACE-inhibition would improve the systemic endotoxin-induced inflammatory response in the lung in an experimental model of lung injury. Sixteen sheep were anesthetized with thiopental, intubated and mechanically ventilated. LPS from E.coli (2 mg.kg-1.h-1) was infused for 24 h. Perindoprilate, 0.4 mg.kg-1.h-1 or placebo was infused during 24 h prior to the infusion of endotoxin. In order to investigate the inflammatory process in the lungs during endotoxemia, 16F-fluorodeoxyglucose (FDG) was injected and the lung radioactivity was followed by photon emission tomography (PET). Plasma markers of inflammation were also measured. There were no differences between the control animals (n = 8) and perindoprilate-treated animals (n = 8) before infusion of endotoxin. The median [range] peak FDG uptake of the lung increased by 86% [49-120%] in the control group (n = 8) while the peak FDG uptake
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