SYSTEMIC RELEASE OF PROSTANOIDS AFTER SURGERY-INDUCED LUNG-TISSUE INJURY

In a prospective study, the systemic inflammatory consequences of surg ery-induced lung tissue injury were evaluated using biochemical marker s. The aim was to examine whether this type of injury produces a speci fic pattern of prostanoid plasma levels (prostacyclin, thromboxane, PG E(2), PGF(2 alpha), and PGM). We, therefore, compared 18 patients (gro up 1)who underwent thoracotomy without injury to the lung with 26 pati ents (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-elastas e. In particular, there was a pronounced release of prostacyclin and i ts antagonist thromboxane A(2) following lung tissue resection. In con trast to group 1 patients, lung tissue damage resulted in immediately elevated plasma levels of PGF(2 alpha) and PGE(2). When, however, taki ng into account the timecourse of PGM, the stable cleavage product of PGF(2 alpha), there was no hint of an altered pulmonary metabolic capa city. 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 ma y indicate the importance of these mediators, particularly in thoracic injuries associated with lung damage since those may lead to post-tra umatic pulmonary dysfunction. These substances may also be useful in e valuating both the severity and the extent of lung tissue damage follo wing major trauma.