| Literature DB >> 17056704 |
Shuhei Ota1, Kyota Nakamura, Takuya Yazawa, Yosuke Kawaguchi, Yasuko Baba, Ritsuko Kitaoka, Naoto Morimura, Takahisa Goto, Yoshitsugu Yamada, Kiyoyasu Kurahashi.
Abstract
Ischemia-reperfusion not only damages the affected organ but also leads to remote organ injuries. Hepatic inflow interruption usually occurs during hepatic surgery. To investigate the influence of liver ischemia-reperfusion on lung injury and to determine the contribution of tidal volume settings on liver ischemia-reperfusion-induced lung injury, we studied anesthetized and mechanically ventilated rats in which the hepatic inflow was transiently interrupted twice for 15 min. Two tidal volumes, 6 ml/kg as a low tidal volume (IR-LT) and 24 ml/kg as a high tidal volume (IR-HT), were assessed after liver ischemia-reperfusion, as well as after a sham operation, 6 ml/kg (NC-LT) and 24 ml/kg (NC-HT). Both the IR-HT and IR-LT groups had a gradual decline in the systemic blood pressure and a significant increase in plasma TNF-alpha concentrations. Of the four groups, only the IR-HT group developed lung injury, as assessed by an increase in the lung wet-to-dry weight ratio, the presence of significant histopathological changes, such as perivascular edema and intravascular leukocyte aggregation, and an increase in the bronchoalveolar lavage fluid TNF-alpha concentration. Furthermore, only in the IR-HT group was airway pressure increased significantly during the 6-h reperfusion period. These findings suggest that liver ischemia-reperfusion caused systemic inflammation and that lung injury is triggered when high tidal volume ventilation follows liver ischemia-reperfusion.Entities:
Mesh:
Substances:
Year: 2006 PMID: 17056704 DOI: 10.1152/ajplung.00151.2006
Source DB: PubMed Journal: Am J Physiol Lung Cell Mol Physiol ISSN: 1040-0605 Impact factor: 5.464