Lung metabolism and systemic organ function.
In the past decade a variety of metabolic events have been described which occur in the lungs. These processes, such as the clearance of serotonin and norepinephrine, the inactivation of bradykinin and the activation of angiotensin II, and the synthesis of prostaglandins, may have a direct impact on systemic organ function. Under certain circumstances the lungs produce prostaglandins that may lead to severe hemodynamic instability and death. Pressure breathing with hyperinflation is a potent pulmonary metabolic stimulus. This commonly used therapeutic maneuver has been shown to increase fibrinolytic activity. The application of end-expiratory pressure will further enhance the fibrinolytic state by virtue of the pulmonary secretion of plasminogen activator. Positive end-expiratory pressure (PEEP) will also cause a lowering of the cardiac output, which is related at least in part to lung metabolism. Circulating factors are released during PEEP that have a negative inotropic effect. It is reasonable to view respiratory failure not only as a defect in gas exchange but also as a derangement in lung metabolism.
D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D001920:Bradykinin / Q000378:metabolism; D002302:Cardiac Output; D003326:Coronary Circulation; D004285:Dogs; D004727:Endothelium / Q000378:metabolism; D005342:Fibrinolysis; D006801:Humans; D008168:Lung / Q000378:metabolism* / Q000503:physiopathology; D009638:Norepinephrine / Q000378:metabolism; D010477:Perfusion; D011175:Positive-Pressure Respiration; D011453:Prostaglandins / Q000378:metabolism; D011985:Receptors, Serotonin; D012121:Respiration, Artificial
D011453:Prostaglandins; D011985:Receptors, Serotonin; D000804:Angiotensin II; D001920:Bradykinin; D009638:Norepinephrine