Babu V. Naidu

TL;DR: Tumor necrosis factor alpha and interleukin 1beta help regulate the development of lung ischemia-reperfusion injury and appear to promote injury by altering expression of proinflammatory and anti-inflammatory cytokines and influencing tissue neutrophil recruitment.

TL;DR: The potential to pretreat recipients of lung transplantation with statins to ameliorate reperfusion injury is promising and the protective effects of simvastatin are likely mediated by modulation of endothelial nitric oxide synthase.

TL;DR: It is likely that the alveolar macrophage is the key early source of multiple proinflammatory mediators that orchestrate lung ischemia-reperfusion injury and is protective against injury, supporting its central role in oxidant stress-induced cytokine and chemokine release and the subsequent development of lung injury.

TL;DR: Cyclosporine and tacrolimus treatment before reperfusion was protective against lung ischemia-reperfusion injury in rats, and the decreased expression of cytokine messenger RNA indicates that both cyclosporines and tacrosporine may exert their protective effects at the pretranscriptional level.

TL;DR: The deleterious effects of lung ischemia-reperfusion injury are in part mediated by the formation of peroxynitrite, as enhanced decomposition of this species is protective in this model.