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Ann Thorac Surg 2002;73:1910-1911
© 2002 The Society of Thoracic Surgeons

Original article: cardiovascular

Invited commentary

A. Leinsa, J. Cremer, MD, PhDa

a Department of Cardiovascular Surgery, University of Kiel, Arnold-Hellerstr. 7, D-24105 Kiel, Germany

e-mail: aleins@kielheart.uni-kiel.de


   Introduction
 
Cardiac surgery especially with the use of cardiopulmonary bypass (CPB) is associated with significant systemic inflammatory response. One manifestation of systemic inflammatory response with excessive pro-inflammatory cytokine expression is lactic acidosis [1, 2]. Hyperlactatemia is a hallmark of severe circulatory failure or shock and is correlated with outcome in critical illness patients [3]. In these patients, lactic acidosis is mainly related to an elevated lactate production, whereas alterations in lactate utilization due to hypoxic liver damage is negligible [4].

There is evidence for a direct effect of TNF and interleukines (ILs) on lactic acid production and lactic homeostasis. The proinflammatory TNF-{alpha} may directly increase lactic acid production by inhibiting pyrovate . . . [Full Text of this Article]


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Lactic acidosis after cardiac surgery is associated with polymorphisms in tumor necrosis factor and interleukin 10 genes
Thomas Ryan, Joanna Balding, Eilis M. McGovern, John Hinchion, Wendy Livingstone, Zeb Chughtai, and Owen P. Smith
Ann. Thorac. Surg. 2002 73: 1905-1909. [Abstract] [Full Text] [PDF]





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