New Insights into Cardioprotection by Ischemic Preconditioning and Other Forms of Stress^a

Abstract

Ischemic preconditioning has not only received wide attention in heart research, but has also been a topic of extensive studies involving other organs. In several of these studies, it has been shown that in spite of differences in the endpoints used to assess protection, the same mediators as in myocardial ischemic preconditioning may be involved. However, several of the putative mediators do not require ischemia to become activated. This has guided us and others to investigate whether the myocardium can also be protected by brief ischemia in other organs and whether other non-pharmacological forms of stress, which do not produce ischemia but are capable of activating these potential mediators, are also cardioprotective.

Determinants of Delayed Preconditioning Against Myocardial Stunning in Chronically Instrumented Pigs

“…This would be analogous to the previous demonstration that an ischemic stimulus that can provide PC against infarction following a subsequent 40-minute coronary occlusion, but offered no benefit when the occlusion was extended to 3 hours duration[17]. This finding was interpreted as showing that PC merely delayed rather than prevented myocyte necrosis[17][6]. The present investigation suggests that a similar situation may occur with delayed PC against stunning, in which a PC stimulus can improve the deficit-of-function following a relatively modest ischemic episode (repetitive brief occlusions), but a more severe episode (single prolonged occlusion) is afforded no protection.…”

Transient NMDA Receptor Inactivation Provides Long-Term Protection to Cultured Cortical Neurons from a Variety of Death Signals

“…As such, the 30 min MK-801 exposure used in the present study constitutes a "sublethal" stress that is consistent with conventional thinking related to preconditioning mechanisms. As with other preconditioning paradigms (Ferdinandy et al, 1998;de Zeeuw et al, 1999), this imposed stress can stimulate compensatory survival mechanisms that protects neurons from lethal insults at later times. However, to the best of our knowledge, no reported preconditioning agent or condition exhibits such longlasting protection against such a diverse group of neurotoxic agents as does MK-801.…”

Myocardial protection by remote preconditioning: the role of nuclear factor kappa-B p105 and inducible nitric oxide synthase

“…A preconditioning-like myocardial protection can be evoked by systemic stimuli such as lipopolysaccharide, hypoxia, hyperoxia, and nitric oxide [1][2][3]. It has also become evident that short episodes of ischemia and reperfusion of other organs such as mesenterium, kidney, or hind limbs will protect the heart (remote preconditioning) [1,4].…”