Non-Ischemic Remote Cardioprotective Phenomena

Abstract

Ischemic preconditioning (IPC) is a powerful cardioprotective phenomenon that occurs in several species. IPC means that transient ischemic makes the cardioprotection in the subsequent period of ischemic thus it limits the scope of myocardial infarction. The reports of recent years have obtained the conclusion that this cardioprotection can be also induced by the non-ischemic preconditioning such as metabolic stimulation of myocardial cells and distention of the left ventricle. From the physiological point of view, the protective effect of non-ischemic preconditioning is associated with the higher proportion of myocardial cell metabolism. Remote ischemic preconditioning (RIC) is a therapeutic measure for cardioprotection against the deleterious effect of acute ischemia-reperfusion injury (IRI). And, it’s beneficial effects are also seen in other organs (lung, liver, kidney, brain) and tissues (skeletal muscle). Although the mechanism of RIC has not yet been completely determined, there are several probable hypotheses supporting the cardioprotection induced by RIC, which include the neuronal pathway, humoral pathway, and systemic response. Recently, some researchers have provided experimental evidence for the cardioprotection under non-ischemic trauma at a site from the heart produced by a transverse abdominal incision. This study demonstrated that protection could be elicited by non-ischemic stimulus which they term “remote preconditioning of trauma (RPCT)”. Because of remote preconditioning of trauma, which is produced by an abdominal incision only through the skin, so it means that it’s non-ischemic. Although remote ischemiac stimulus has been shown to elicit cardioprotection against IRI, there are not many reports about the remote non-ischemic stimulus and its mechanism. In this article, we provide a review of cardioprotection, the potential mechanism of RPCT as well as its clinical prospects.