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1 Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana, USA; Indian Center for Vascular Biology and Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA
2 Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana, USA
3 Department of Urology, Indiana University School of Medicine, Indianapolis, Indiana, USA
4 Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana, USA; Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana, USA; Indian Center for Vascular Biology and Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA
* To whom correspondence should be addressed. E-mail: dmeldrum{at}iupui.edu.
The myocardium generates inflammatory mediators during ischemia-reperfusion (I/R),
and these mediators contribute to cardiac functional depression and apoptosis. The great majority
of this data has 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, activation of the p38
mitogen-activated protein kinase (MAPK) signaling pathway following 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-
, IL-1
, and IL-6 (RT-PCR, ELISA); IL-1 and IL-10 mRNA (RT-PCR);
and activation of p38 MAPK (Western blot). All indices of post-ischemic myocardial function
(left ventricular developed pressure, left ventricular end diastolic pressure, +dP/dt and -dP/dt)
were significantly improved in the females compared to the males. Compared to males, females
had decreased myocardial TNF-, IL-1 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.
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