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Am J Physiol Endocrinol Metab 288: E321-E326, 2005. First published September 14, 2004; doi:10.1152/ajpendo.00278.2004
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Sex differences in the myocardial inflammatory response to ischemia-reperfusion injury

Meijing Wang,1,2 Lauren Baker,1,2 Ben M. Tsai,1 Kirstan K. Meldrum,3 and Daniel R. Meldrum1,2,4

Departments of 4Cellular and Integrative Physiology, 1Surgery, and 3Urology, and the 2Indiana Center for Vascular Biology and Medicine, Indiana University School of Medicine, Indianapolis, Indiana

Submitted 23 June 2004 ; accepted in final form 10 September 2004

The myocardium generates inflammatory mediators during ischemia-reperfusion (I/R), and these mediators contribute to cardiac functional depression and apoptosis. The great majority of these data have been derived from male animals and humans. Sex has a profound effect over many inflammatory responses; however, it is unknown whether sex affects the cardiac inflammatory response to acute myocardial I/R. We hypothesized the existence of inherent sex differences in myocardial function, expression of inflammatory cytokines, and activation of the p38 mitogen-activated protein kinase (MAPK) signaling pathway after I/R. Isolated rat hearts from age-matched adult males and females were perfused (Langendorff), and myocardial contractile function was continuously recorded. After I/R, myocardium was assessed for expression of TNF-{alpha}, IL-1{beta}, and IL-6 (RT-PCR, ELISA); IL-1{alpha} and IL-10 mRNA (RT-PCR); and activation of p38 MAPK (Western blot). All indexes of postischemic myocardial function [left ventricular developed pressure, left ventricular end-diastolic pressure, and maximal positive (+dP/dt) and negative (–dP/dt) values of the first derivative of pressure] were significantly improved in females compared with males. Compared with males, females had decreased myocardial TNF-{alpha}, IL-1{beta}, and IL-6 (mRNA, protein) and decreased activation of p38 MAPK pathway. These data demonstrate that hearts from age-matched adult females are relatively protected against I/R injury, possibly due to a diminished inflammatory response.

myocardial infarction; tumor necrosis factor; signal transduction


Address for reprint requests and other correspondence: D. R. Meldrum, 545 Barnhill Dr., Emerson Hall 215, Indianapolis, IN 46202 (E-mail: dmeldrum{at}iupui.edu)




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