Hypoxemia is a common manifestation of various disorders and generates pressure overload to the heart. Here we analyzed the expression of lipocalin-type prostaglandin D synthase (L-PGDS) in the heart of C57BL/6 mice kept Under normobaric hypoxia (10% O-2) that generates hemodynamic stress. Northern and Western blot analyses revealed that the expression levels of L-PGDS mRNA and protein wet e significantly increased (>twofold) after 14 days of hypoxia, compared to the mice kept under normoxia. immunohistochemical analysis indicated that L-PGDS was increased in the myocardium of auricles and ventricles and the Pulmonary venous myocardium at 28 days of hypoxia. Moreover, Using C57BL/6 mice lacking heme oxygenase-2 (HO-2(-/-)) a model of chronic hypoxemia, we showed that the expression level of L-PGDS protein was twofold higher in the heart than that of wild-type mouse. L-PGDS expression is induced in the myocardium Under hypoxemia, which may reflect the adaptation to the hemodynamic stress, (c) 2009 Elsevier Inc. All rights reserved.