Abstract
Infection, trauma, and surgery induce a catabolic state characterized by hypermetabolism. This catabolic state usually resolves spontaneously after minor insults to the organism such as elective surgery. However, in sepsis, multiple trauma, and major surgery hypermetabolism may persist and organ failure develop. The sequential failure of lungs, liver, and kidneys has been recognized for many years as a potential sequela of ruptured aneurysm, acute pancreatitis, septic shock, and surgical complications, as well as burns and other trauma. Acute lung injury is the earliest and most frequent organ complication in prolonged catabolic states. Injurious agents such as endotoxin and fibrin split products have been suggested as mediators of acute lung injury. In experimental studies it has been found that a large number of agents may cause lung injury. The bulk of these studies have focused on damage to the pulmonary vascular endothelium. Less attention has been paid to the metabolic function of the lungs with respect to energy utilization as well as specific metabolic functions. This review is concerned with: (1) metabolic changes in the lungs with respect to injurious agents released in sepsis, and following multiple trauma and major surgery; (2) interorgan metabolism in catabolic states with respect to the lungs.
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References
Hedenstierna G (1988) Mechanisms of postoperative pulmonary complications. Acta Chir Scand Suppl 550:152–158
McIntyre RC, Harken AH, Fullerton DA (1994) Mechanisms of pulmonary vascular control in normal and injured lungs. Surgery 115:273–275
Crapo JD, Barry BE, Foscue AA et al. (1980) Structural and biochemical changes in rat lungs occurring during exposures to lethal and adaptive doses of oxygen. Am Rev Respir Dis 122:123–143
Fisher AB (1976) Oxygen and energy utilization. In: Crystal RG (ed) The biochemical basis of pulmonary function. Marcel Dekker, New York, pp 75–104
Felts JM (1964) Biochemistry of the lung. Health Phys 10:973–979
Tierney DF, Levy SE (1976) Glucose metabolism. In: Crystal RG (ed) The biochemical basis of pulmonary function. Marcel Dekker, New York, pp 105–125
Ardawi MS (1991) Metabolism of glucose, glutamine, long chain fatty acids and ketone bodies by lungs of the rat. Biochimie 73(5):557–562
Date H, Matsumura A, Manchester JK et al. (1993) Evaluation of lung metabolism during successful twenty-four-hour canine lung preservation. J Thorac Cardiovasc Surg 101:1037–1043
Kerr JS, Fisher AB, Kleingeller A (1981) Transport of glucose analogues in rat lung. Am J Physiol 241:E191–E195
Wiener CM, Sylvester JT (1993) Effects of insulin, glucose analogues, and pyruvate on vascular responses to anoxia in isolated ferret lungs. J Appl Physiol 74(5):2426–2431
Rounds SS, McMarty, Reeves JT (1981) Glucose metabolism accelerates the decline of hypoxic vasoconstriction in rat lungs. Respir Physiol 44:239–249
Hinshaw DB, Benger JM (1990) Protective effect of glutamine on endothelial cell ATP in oxidant injury. J Surg Res 49:222–227
Bassett DJP, Fisher AB (1976) Pentose cycle activity of the isolated perfused rat lung. Am J Physiol 231:1527–1532
Holm BA, Matalon S (1989) Role of pulmonary surfactant in the development and treatment of adult respiratory distress syndrome. Anesth Analg 69:805–818
Arias-Diaz J, Vara E, Garcia C, Gomez M, Balibrea IL (1993) Tumor necrosis factor-α inhibits synthesis or surfactant by isolated human type II pneumocytes. Eur J Surg 159:541–549
Plumley DA, Austgen TR, Salloum RM et al. (1990) Role of the lungs in maintaining amino acid homeostasis. JPEN 14:569–573
Plumley DA, Souba WW, Hantamaki RD et al. (1990) Accelerated lung amino acid release in hyperdynamic septic surgical patients. Arch Surg 125:57–61
Herskowitz K, Plumley DA, Martin TD et al. (1991) Lung glutamine flux following open heart surgery. J Surg Res 51:82–86
Auslym TR, Chen MK, Salloum RM, Souba WW (1991) Glutamine metabolism by the endotoxin-injured lung. J Trauma 31:1068–1075
Herskowitz K, Bode BP, Block ER, Souba WW (1991) Characterization of L-glutamine transport by pulmonary artery endothelial cells. Am J Physiol 260:L241–L246
Leighton B, Curi R, Hussein A, Newsholme EM (1987) Maximum activities of some key enzymes of glycolysis, glutaminolysis, Krebs cycle and fatty acid utilization in bovine pulmonary endothelial cells. FEBS Letts 225:93–96
Sallek M, Ardawi M (1990) Glutamine-synthesizing activity in lungs of fed, starved, acidotic, diabetic, injured and septic rats. Biochem J 270:829–832
Sarantos P, Howard D, Souba WW (1993) Dexamethasone regulates glutamine synthetase expression in rat lung. Metabolism 42:795–800
Scott Lind D, Copeland EM, Souba WW (1993) Endotoxin stimulates arginine transport in pulmonary artery endothelial cells. Surgery 114:199–205
Ryan US, Ryan JW (1977) Correlations between the fine structure of the alveolar-capillary unit and its metabolic activities. In: Bakkle YS, Vane JR (eds) Metabolic functions of the lung. Marcel Dekker, New York, pp 197–232
Ryan US (1982) Structural bases for metabolic activity. Ann Rev Physiol 44:223–239
Ryan JW, Ryan US (1977) Pulmonary endothelial cells. Federation Proceedings 36:2683–2691
Fanberg BL (1988) Relationship of the pulmonary vascular endothelium to altered pulmonary vascular resistance. Chest 93:101S–105S
Ryan US (1987) Endothelial cell activation responses. In: Ryan US (ed) Pulmonary endothelium in health and disease. Marcel Dekker, New York, pp 3–33
Block ER (1992) Pulmonary endothelial cell pathobiology: Implications for acute lung injury. Am J Med Sci 304:136–144
Persson MG, Wiklund NP, Gustafsson LE (1993) Nitric oxide — more than a vasodilator. Läkartidningen 90:1365–1371
Crutchley DJ (1987) Hemostatic properties of the pulmonary endothelium. In: Ryan US (ed) Endothelium in health and disease. Marcel Dekker, New York, pp 237–273
Esmar CT, Owen W (1981) Identification of an endothelial cell co-actor for thrombin-catalyzed activation of protein C. Proc Natl Acad Sci USA 78:2249–2252
Nawroth PP, Handley DA, Esmar CT, Stern DM (1986) Interleukin-1 induces endothelial cell procoagulant while suppressing cell-surface anticoagulant activity. Proc Natl Acad Sci USA 83:3460–3464
Weitzberg E (1993) Circulatory responses to endothelin-1 and nitric oxide. Acta Physiol Scand 148(S611):5–13
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© 1996 Springer-Verlag Berlin Heidelberg
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Kjæve, J. (1996). The Lungs and the Catabolic State. In: Revhaug, A. (eds) Acute Catabolic State. Update in Intensive Care and Emergency Medicine, vol 21. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-48801-6_13
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DOI: https://doi.org/10.1007/978-3-642-48801-6_13
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-642-48803-0
Online ISBN: 978-3-642-48801-6
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