The interaction of mediator systems in the regulation of pulmonary vascular tone

Acute lung injury continues to be a severe complication of critically ill p atients despite advances in intensive care medicine. Systemic inflammatory reactions following severe trauma lead to increased pulmonary arterial pres sure and capillary leakage by the modulation of mediator expression in the lung. Pulmonary perfusion pressure is regulated by a balance of vasoconstri ctive mediators on the one hand and vasodilators on the other hand. Endothe lin-1 (ET-1) and thromboxane A2 (TXA(2)) are the predominant vasoconstricto rs in the pulmonary circulation whereas nitric oxide (NO) and prostacyclin (PGI(2)) are the main vasodilators. Furthermore, platelet activating factor (PAF), neuropeptides, angiotensin, purines, histamine, serotonine, and kin ines have an influence in pulmonary vascular tone.