1792.3 Postconditioning
Postconditioning consists in rapid intermittent interruptions of blood flow in the
early reperfusion applied just after the prolonged ischemic insult (Zhao et al. 2003 ).
While preconditioning is applied before an ischemic insult, the postconditioning
(PostC) is applied at the end of ischemia: these differences are fundamental for the
clinical application of these cardioprotective maneuvers.
The first observation of PostC as protective against infarct size was made by the
Vinten-Johansen group’s in 2003 (Zhao et al. 2003 ). The authors demonstrated that
this cardioprotective protocol reduced myocardial inflammation, Ca+2 overload, oxi-
dative stress, infarct size and apoptotic cell death. In this study PostC preserved
endothelial function and the injured tissue produced less edema. Several endogenous
pro-survival signaling pathways are activated during PostC, and their activation is
fundamental for the protection of the heart against lethal myocardial reperfusion
injury (Penna et al. 2006a, b; Tsang et al. 2004 ; Zhao et al. 2003 ; Yang et al. 2004 ).
The protection of the heart at the time of reperfusion has been previously inves-
tigated using several pharmacological approaches (e.g. Ca+2 channel blockers, anti-
inflammatory agents, anti-oxidant therapy, and so forth with mixed outcomes).
Actually, the cardioprotective reperfusion was first suggested in the late 1990s when
it was discovery that several growth factors and drugs are capable of reducing myo-
cardial infarct size if administered at the onset of coronary artery reopening (Penna
et al. 2008 ). However, only when Zhao et al. ( 2003 ) reported the paradoxical obser-
vation that several brief coronary occlusions after an infarcting coronary occlusion
significantly reduced infarct size in vivo model, the interest of researchers to this
phase of reperfusion greatly increased. This cardioprotective approach with brief
ischemia applied at the beginning of reperfusion was called postconditioning and it
has been demonstrated in different animal models (see review Iliodromitis et al.
2009 ; Penna et al. 2008 ; Skyschally et al. 2009 ). The signaling pathways leading to
protection resulted similar to those already demonstrated for preconditioning and
for many pharmacologic agents that protect when infused at reperfusion.
In clinical practice, PostC is a promising adjunctive technique to reperfusion
since it can improve post-infarction outcome and limit left ventricle dilatation and
maladaptive remodeling. Whether postconditioning can attenuate acute contractile
dysfunction is a matter of controversy.
With no doubt postconditioning is appealing for clinician as it can be under their
control. However, ischemic PostC cannot be applied to all patients with acute myo-
cardial infarction and this makes pharmacological PostC an intriguing, but unmet,
clinical objective. For example, ischemic PostC cannot be applied in case of throm-
bolytic intervention, rather than angioplasty. It is, thus necessary to deeply study the
procedure and the mechanisms of protection.
As said, the molecular pathways responsible of PostC are similar to those of IP
protection; in fact, also in PostC there is the activation of RISK and SAFE (Fig. 2 ).
However, the mechanisms of cardioprotection involved in PostC are not exactly the
Cardioprotection and Chromogranin A-Derived Peptides