Abstract
A moderate pulmonary hypertension is a hallmark of experimental, as well as clinical, acute lung injury. Pulmonary hypertension in acute lung injury, appears to be caused primarily by a partially reversible increase in extra-alveolar vascular closing pressure, the latter being modulated by vasodilating products of the cyclooxygenase pathway of arachidonic acid metabolism, as well as by an endogenous release of nitric oxide. Gas exchange in acute lung injury is improved by increased pulmonary vascular tone. However it is also improved by inhaled nitric oxide, which increases perfusion to the better aerated lung areas. Whether pharmacological interventions aimed at the prevention of right ventricular failure in acute lung injury improve right ventriculo-vascular coupling sufficiently to exert a favourable influence on outcome, remains to be shown.
