Myocardial injury associated with hyperinflation of the lung

First paragraph (this article has no abstract)

A recent study [1], conducted in an animal model of acute lung injury, compared a ventilation strategy in which lungs were inflated by brief application of 50 cmH₂O pressure followed by increased positive end-expiratory pressure (recruitment strategy) versus conventional ventilation. The study identified an increased inflammatory reaction in liver sinusoids, and increased serum aspartate aminotransferase (AST) and hyaluronate levels with the recruitment strategy. The authors speculated that deficient oxygen delivery and increased sinusoidal pressures may have caused liver injury. The findings of the study suggest an origin of AST outside the liver because there was no elevation in alanine aminotransferase levels, hepatocellular necrosis, or liver dysfunction. Animals in the group receiving the recruitment strategy required volume support and had temporarily reduced cardiac output. This indicated that the origin of AST elevation was a myocardial injury.