Direct induction of acute lung and myocardial dysfunction by liver ischemia and reperfusion

Avi A. Weinbroum*, Edith Hochhauser, Valery Rudick, Yoram Kluger, Patrik Sorkine, Ela Karchevsky, Eran Graf, Pnina Boher, Ron Flaishon, Dimitri Fjodorov, David Niv, Bernardo A. Vidne

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Objectives: To investigate whether liver ischemia and reperfusion (IR) directly affect functions of remote organs. Background: Cardiovascular and respiratory dysfunction follows hemorrhage, spinal shock, or trauma as a result of no-flow-reflow phenomena. Hepatic IR induces remote organ damage probably by xanthine oxidase and oxygen species. Materials and Methods: Isolated rat livers, lungs, and hearts were perfused with Krebs-Henseleit solutions. After stabilization, livers were either perfused or made ischemic. Then, livers and hearts or livers and lungs were reperfused in series, and the liver was disconnected and the second organ continued to perfuse with the accumulated effluents. Measurements and Main Results: Ischemic and reperfused liver effluent contained high lactate dehydrogenase and uric acid concentrations compared with controls: xanthine oxidase increased 60 to 100 times. Ischemic and reperfused lung peak inspiratory pressure almost doubled; airway static compliance halved; myocardial contractility decreased to 70% of baseline: wet weight-to-dry weight ratios of lungs and livers increased. Conclusion: Ischemic and reperfused liver can directly induce myocardial and pulmonary dysfunction, presumably by oxidant-induced injury.

Original languageEnglish
Pages (from-to)627-635
Number of pages9
JournalJournal of Trauma and Acute Care Surgery
Issue number4
StatePublished - Oct 1997


  • Inspiratory pressure
  • Ischemia-reperfusion
  • Myocardial contractility
  • Posttrauma
  • Static compliance
  • Xanthine oxidase


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