This chapter details vascular-based therapies for lung injury and associated acute respiratory failure. Physiological processes contributing to the disrup- tion of pulmonary vascular regulation in lung injury are also described (Chapter 8 gives additional details on mechanisms and mediators important in pulmonary vascular dysfunction). During acute injury, the overall bal- ance of vasoconstriction and vasodilation in the lungs is shifted towards vasoconstriction, leading to ventilation=perfusion (VA=Q) mismatching, increased pulmonary vascular resistance (PVR), and pulmonary hyperten- sion (PH). These factors, along with associated decreases in cardiac output, compromise gas exchange and reduce systemic oxygen delivery. This chap- ter discusses pharmacologic therapies targeting various aspects of injury- associated pulmonary vascular pathophysiology. Particular coverage is devoted to the clinical use of short-acting inhaled vasodilators normally synthesized by the vascular endothelium: nitric oxide (NO) and prostacyclin (PGI2). Therapies utilizing phosphodiesterase (PDE) inhibitors or other agents that work in concert with NO and PGI2 are also covered. In addition, the use of selective vasoconstrictors, anticoagulants, and growth factors in the treatment of pulmonary vascular dysfunction is also noted. An important emphasis of discussion is that continuing mechanistic basic research is crucial for improving understanding about regulatory pathways and processes involved in vascular pathology in lung injury to facilitate future therapeutic development.
|Original language||English (US)|
|Title of host publication||Lung Injury|
|Subtitle of host publication||Mechanisms, Pathophysiology, and Therapy|
|Number of pages||42|
|State||Published - Jan 1 2005|
ASJC Scopus subject areas