Abstract
The mechanisms underlying the protective effects of remote ischemic preconditioning (RIPC) are not presently clear. Recent studies in experimental models suggest the involvement of the autonomic nervous system (ANS) in cardioprotection. The aim of this study was to investigate the changes in ANS in healthy young volunteers divided into RIPC (n = 22) or SHAM (n = 18) groups. RIPC was induced by 1 cycle of 4 min inflation/5 min deflation followed by 2 cycles of 5 min inflation/5 min deflation of a cuff placed on the upper left limb. The study included analysis of heart rate (HR), blood pressure (BP), heart rate variability (HRV), measurements of microcirculation and porphyrin fluorescence in the limb before and after the RIPC. RIPC caused reactive hyperemia in the limb and reduced blood porphyrin level. A mental load (serial sevens test) and mild motor stress (hyperventilation) were performed on all subjects before and after RIPC or corresponding rest in the SHAM group. Reduction of HR occurred during the experiments in both RIPC and SHAM groups reflecting RIPC-independent adaptation of the subjects to the experimental procedure. However, in contrast to the SHAM group, RIPC altered several of the spectral indices of HRV during the serial sevens test and hyperventilation. This was expressed predominantly as an increase in power of the very low-frequency band of the spectrum, increased values of detrended fluctuation analysis and weakening of correlation between the HRV parameters and HR. In conclusion, RIPC induces changes in the activity of ANS that are linked to stress resistance.
Highlights
The mammalian body can recruit powerful innate mechanisms that are highly effective at protecting tissues and organs against detrimental events including ischemia and reperfusion (I/R) injury
Results of the experiments of remote ischemic preconditioning (RIPC) group are presented in normal font on the white background; results of the experiments of SHAM group are presented in Italic font on the grey background. * Р < 0.05, **P < 0.01, ***P < 0.001 vs. corresponding indices Pre-RIPC. #P < 0.05, ##P < 0.01, ###P < 0.001 vs. corresponding Background
During this test performed after RIPC, heart rate (HR) retained a significant correlation only with high frequency (HF), and Very low frequency 100 (VLF100) lost correlation with all the parameters except VLF50
Summary
The mammalian body can recruit powerful innate mechanisms that are highly effective at protecting tissues and organs against detrimental events including ischemia and reperfusion (I/R) injury. Experiments on animals showed that the heart can be protected against I/R injury by applying several short cycles of ischemia and reperfusion to a tissue or organ that is remote from the heart (Gaspar et al, 2018). The mechanisms responsible for the RIPC-induced protection have not been fully addressed (Pickard et al, 2015). Understanding these mechanisms is critical in the search for mediators that will enable us to achieve optimal protection. Reports have indicated the involvement of humoral, neural and systemic
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