par Leeman, Marc 
Référence Bailliere's Clinical Anaesthesiology, 10, 1, page (215-230)
Publication Publié, 1996
Référence Bailliere's Clinical Anaesthesiology, 10, 1, page (215-230)
Publication Publié, 1996
Article révisé par les pairs
| Résumé : | In most cases of pulmonary hypertension, the pulmonary circulation retains its ability to dilate or to contract further, because of the release of vasoconstrictor as well as vasodilator mediators. The vascular endothelium synthesizes vasoconstrictor and vasodilator mediators, thereby playing a major role in the control of pulmonary vascular tone. Whether endogenous NO is involved in the maintenance of the normally low basal pulmonary vascular tone remains unsettled. However, many studies indicate that NO is released during hypoxia and lung injury, and counteracts the increase in Ppa. Many data suggest that endogenous ETs could mediate pulmonary hypertension. ET receptor antagonists may prove valuable therapy for lung diseases associated with pulmonary hypertension. Inhaled NO selectively reduces Ppa in various pulmonary hypertensive states and improves gas exchange in many patients with acute lung injury. Inhaled NO may therefore play a role in the treatment of pulmonary hypertension and/or lung injury. However, its long-term toxicity is not yet defined, and its clinical value needs to be evaluated in controlled trials. Complex interactions exist between the pulmonary circulation, the RV and the LV in health and disease. A better understanding of these interactions could promote valuable therapeutic strategies for RV pressure overload. |
