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Protection of the heart by ischaemic preconditioning: mechanisms and possibilities for pharmacological exploitation

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      The term preconditioning first significantly entered the medical lexicon in 1986 when Murry et al. [1] demonstrated that a prior modest ischemic stress significantly reduced cardiac damage from a subsequent highly damaging ischemic stress using the dog model. These findings were substantially replicated and then generalized to other organs and animal models, other inducing agents, and endpoints [2,3]. Amidst the rapid and robust expansion of this concept the term preconditioning became widely accepted and used with various modifiers such as ischemic preconditioning, hypoxic preconditioning and remote preconditioning, adding appropriate specificity to diverse inducing experimental protocols.

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      Such therapeutic profiles make them “new interesting modern tools” to be recommended for the treatment of cardiovascular diseases. Considering the data presented and discussed in this review and from the current state of knowledge regarding the efficacy of some kinin agonists demonstrated in experimental animal (Couture & Girolami, 2004; Heitsch, 2003; Madeddu et al., 2007; Manolis et al., 2010; Marceau & Regoli, 2004; Parratt, 1994; Rodi et al., 2005; Sharma & Thani, 2004; Tonduangu et al., 2004; Yao et al., 2007) and in clinical studies (Leesar et al., 1999; Matsumoto et al., 2001; Minai et al., 2001; Prasad et al., 1999; Pretorius et al., 2003; Wang et al., 2009; Wei et al., 2004), both B1R and B2R agonists, either the naturally occurring agonists BK, Lys-BK and Lys-desArg9BK, their stabilized peptide analogues resistant to degradation (Amblard et al., 1999; Bélanger et al., 2009; Côté et al., 2009; Dendorfer et al., 1999; Taraseviciene-Stewart et al., 2005; Vavrek et al., 1992) or the non-peptides agonists (e.g. FR190997 (Asano et al., 1998; Gobeil et al., 1999)), may find therapeutical applications in the following conditions: Preconditioning in cardiac surgery, postconditioning after myocardial infarct.

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      Ischemic preconditioning (IP) is a powerful innate mechanism to protect against ischemic reperfusion (IR) injury. IP is an early stress response that occurs during repeated episodes of brief and moderate vascular occlusion and reperfusion and can render the ischemic organ more tolerant to a subsequent ischemic insult.1–3 Since its first description by Murry et al.4 (1986) in the heart, IP has been shown to reduce the extent of myocardial infarct size as well as the damage to skeletal muscle, brain or hepatic tissue induced by subsequent exposure to severe ischemia in a variety of species.5–7

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    1

    J. R. Parratt is Professor of Cardiovascular Pharmacology at the University of Strathclyde, Glasgow, UK G1 1XW

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