[Eicosanoids as mediators in ARDS].
Eicosanoids partly develop from the metabolism of arachidonic acid through the cyclooxygenase or the lipoxygenase pathway. Lipoxygenase products are the leukotrienes (LTA4, LTB4, LTC4, LTD4, LTE4) and the 5-hydroxyeicosatetraenoic acid (5-HETE). Cyclooxygenase products are the prostanoids (prostaglandins [PG] D2, E2, F2, I2 and thromboxane A2). The other part of the eicosanoids develops from the metabolism of two other fatty acids over the same pathways; 8,11,14-eicosatrienoic acid leads to the prostaglandins D1, E1, F1, I1 and the leukotrienes A3, B3, C3, D3, E3. From 5,8,11,14,17-eicosapentaenoic acid result the prostaglandins D3, E3, F3, I3 and the leukotrienes A5, B5, C5, D5, E5. The pathophysiological changes in ARDS are mainly due to an imbalance of opposing effects of mediators. In this regard eicosanoids play an important role which has not yet been clearly determined. Bronchoconstriction and pulmonary hypertension are increased by thromboxane A2 and leukotrienes, whereas they are reduced by PGI2. Pulmonary edema is enlarged by leukotriene, especially, LTB4, whereas PGI2 has a protective effect. The aggregation of platelets is mediated through thromboxane A2, PGF2 and LTB4; PGE1 and PGI2 counteract these reactions. LTB4, in addition to 5-HETE, leads to the activation of inflammatory cells. Drug induced eicosanoid imbalances can be used for therapeutic interventions.
Loick
H M
HM
Klinik und Poliklinik für Anästhesiologie, Westfälische Wilhelms-Universität Münster.
Theissen
J L
JL
D000818:Animals; D015232:Dinoprostone / Q000627:therapeutic use; D015777:Eicosanoids / Q000096:biosynthesis / Q000502:physiology* / Q000627:therapeutic use; D011464:Epoprostenol / Q000627:therapeutic use; D006801:Humans; D012128:Respiratory Distress Syndrome / Q000188:drug therapy / Q000503:physiopathology*
D015777:Eicosanoids; D011464:Epoprostenol; D015232:Dinoprostone
Die Eicosanoide als Mediatoren beim ARDS.