Orthopedic trauma‐induced pulmonary dysfunction in obese Zucker rats

Obese patients with orthopedic trauma are at increased risk of pulmonary dysfunction and mortality. There is evidence that orthopedic trauma increases prostaglandin E 2 (PGE 2 ), which has been reported to cause pulmonary dysfunction and edema. We hypothesize that increased PGE 2 production is responsible for the orthopedic trauma‐induced pulmonary dysfunction in obesity. Orthopedic trauma was induced in 11–13 wk old lean (LZ) and obese Zucker rats (OZ) by soft tissue injury and local injection of bone components in both hindlimbs. OZ exhibited a significantly larger increase in circulating levels of PGE 2 as compared with LZ after orthopedic trauma ( Figure 1). Additionally, trauma treatment resulted in a decreased VO 2 in OZ (8.97 ± 0.29 to 7.75 ± 0.12 ml/min, n=5) with no effect in LZ. Pulmonary vascular resistances in an isolated lung preparation from non‐trauma LZ and OZ were determined before and 30 minutes after infusion of PGE 2 (10 −7 M). PGE 2 treatment in the isolated lungs resulted in an increase in pulmonary resistances in the LZ and OZ (0.41 ± 0.02 to 0.66 ± 0.12, n = 5 and 0.42 ± 0.04 to 0.96 ± 0.24 mmHg/ml/min, n =5, respectively). These results suggest that the increased PGE 2 levels in response to orthopedic trauma may contribute to the pulmonary dysfunction in the OZ.