In a prospective study, the systemic inflammatory consequences of surgery-induced lung tissue injury were evaluated using biochemical markers. The aim was to examine whether this type of injury produces a specific pattern of prostanoid plasma levels (prostacyclin, thromboxane, PGE2, PGF2 alpha, and PGM). We, therefore, compared 18 patients (group 1) who underwent thoracotomy without injury to the lung with 26 patients (group 2) that had a resection of pulmonary tissue due to benign diseases. Group 2 patients clearly revealed increased plasma levels of C-reactive protein as well as of the granulocyte-specific PMN-elastase. In particular, there was a pronounced release of prostacyclin and its antagonist thromboxane A2 following lung tissue resection. In contrast to group 1 patients, lung tissue damage resulted in immediately elevated plasma levels of PGF2 alpha and PGE2. When, however, taking into account the time course of PGM, the stable cleavage product of PGF2 alpha, there was no hint of an altered pulmonary metabolic capacity. Presumably, this pattern of elevated prostanoid levels in group 2 is the result of the surgical damage to the lung tissue. Therefore, it can be suggested to be specific for that type of injury. Thus, the release of prostanoids following surgery-induced lung tissue damage may indicate the importance of these mediators, particularly in thoracic injuries associated with lung damage since those may lead to post-traumatic pulmonary dysfunction. These substances may also be useful in evaluating both the severity and the extent of lung tissue damage following major trauma.