Remote ischemic preconditioning (IPC) is a procedure during which brief periods of ischemia protect distant organ from ischemia-reperfusion injury. Appling IPC on an upper arm, this phenomenon has been demonstrated in several studies. Skeletal muscle tissue oxygenation at rest (StO2) and StO2 deoxygenation rate during vascular occlusion can be measured using near infrared spectroscopy (NIRS). We aimed to investigate the effects of remote upper arm IPC on StO2 and flow-mediated dilatation (FMD) in healthy male volunteers. In a randomized controlled crossover trial, resting StO2, StO2 deoxygenation rate, and FMD were measured on testing arm at baseline and after 60 minutes. After basal measurements IPC protocol on a contralateral arm was performed. StO2 deoxygenation rate was significantly lower after remote, the IPC cycles in comparison to deoxygenation rate at baseline ( versus %, ). Comparison of deoxygenation rates showed a significant difference between the IPC and the control protocol ( , ). No differences were observed in FMD before and after remote IPC and in the control protocol. In healthy young adults, remote IPC reduces StO2 deoxygenation rate but has no significant impact on FMD. NIRS technique offers a novel approach to asses skeletal muscle adaptation in response to remote ischemic stimuli. 1. Introduction Ischemia-reperfusion injury is a systemic event resulting in damage to local and remote organs. Restoration of blood supply to an organ after a critical period of ischemia causes additional tissue damage and organ dysfunction leading to significant morbidity and mortality. It has been described in a number of clinical settings: acute coronary occlusion, cardiopulmonary bypass procedures, organ transplants, and shock [1–3]. Remote ischemic preconditioning (IPC) is a procedure where brief periods of ischemia in one tissue prior to sustained ischemia reduce ischemia-reperfusion injury in another remote tissue [4, 5]. After early experiments in animals [6], both in vitro and in vivo studies suggested the significance of this protective effect in humans, particularly in the setting of myocardial ischemia [7–10]. However, there is still no agreement about standardized IPC protocol. The precise mechanisms involved in IPC are not yet established. A possible pathway involves the generation of nitric oxide and an effect on endothelial function [5, 8]. Molecular mechanism is not completely understood, but probably involves the released humoral mediators from ischemic tissue, including adenosine, bradykinin, and opioids, which react with the cell
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