gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

The Role of the p38 and p42/p44 MAP kinases in Remote Preconditioning Versus Ischemic Preconditioning

Meeting Abstract (Hypertonie 2004)

  • M. Heidbreder - Universitätsklinikum Schleswig-Holstein, Lübeck (Lübeck, D)
  • A. Naumann - Universitätsklinikum Schleswig-Holstein, Lübeck (Lübeck, D)
  • K. Tempel - Universitätsklinikum Schleswig-Holstein, Lübeck (Lübeck, D)
  • A. Dendorfer - Universitätsklinikum Schleswig-Holstein, Lübeck (Lübeck, D)
  • P. Dominiak - Universitätsklinikum Schleswig-Holstein, Lübeck (Lübeck, D)

Hypertonie 2004. 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Hannover, 24.-27.11.2004. Düsseldorf, Köln: German Medical Science; 2005. Doc04hochP22

The electronic version of this article is the complete one and can be found online at:

Published: August 10, 2005

© 2005 Heidbreder et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Brief episodes of myocardial ischemia protect the heart against a subsequent, sustained ischemic insult - a phenomenon termed as 'Ischemic Preconditioning' (IPC). A similar phenomenon occurs after brief phases of ischemia and reperfusion in remote organs ('Remote Preconditioning', RPC). We investigated the myocardial signal cascade of RPC with regard to the mitogen-activated protein (MAP) kinases p38 and p42/p44 which are important mediators of 'classical' IPC.

Anesthetized male rats were randomized either to RPC (15 min occlusion of the mesenteric artery), IPC (15 min occlusion of the left coronary artery) or 30 min waiting period (controls). After 15 min of reperfusion, organs were prepared for MAP kinases analyses, or myocardial infarction was induced by 30 min of coronary artery occlusion followed by 150 min reperfusion. Infarct size was determined by TTC staining. Activated MAP kinases were quantified in myocardial and small intestinal tissues by immunoblotting.

RPC significantly reduced the myocardial infarction size (control 61.3 ± 1.17 vs. 32.0 ± 6.63 RPC). In the small intestine, RPC activated both, p42 and p44 MAP kinases whereas p38 remained unaffected. In the heart, RPC was not sufficient to activate any of the surveyed MAP kinases whereas IPC increased the phosphorylated forms of p42/p44.

We conclude that activation of p42/44 MAP kinases is restricted to the ischemic area in either heart or intestine, and is not transferred to remote organs. Consequently, activation of p42/p44 is not mandatory for myocardial protection by RPC.