Nitric oxide and sepsis.
The ability of NO to control microcirculatory blood flow, maintain vascular integrity, and act as an antiinflammatory mediator appears to be dependent on endothelial-derived NO. The function of excess NO production by iNOS in sepsis and septic shock is unclear but iNOS-derived NO may contribute to systemic hypotension. The use of more specific inhibitors for iNOS will help to define the role of iNOS in sepsis. Modulation of the pulmonary NO-cGMP signal transduction system following LPS treatment results in hyporesponsiveness to inhaled NO and impaired pulmonary vascular response to vasodilators, suggesting potential mechanisms of the pulmonary dysregulation observed in sepsis.
Holzmann
A
A
Klinik fuer Anaesthesiologie, Ruprecht-Karls-Universitaet, Heidelberg, Germany.
D000280:Administration, Inhalation; D000328:Adult; D000818:Animals; D002648:Child; D006801:Humans; D009569:Nitric Oxide / Q000008:administration & dosage / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D011652:Pulmonary Circulation / Q000502:physiology; D018805:Sepsis / Q000503:physiopathology*
D009569:Nitric Oxide; D019001:Nitric Oxide Synthase