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Updated: Jan 24, 2026
Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents
Published on: June 2, 2015
Changes in cerebral autoregulation and blood biomarkers after remote ischemic preconditioning
Zhen-Ni Guo1, Wei-Tong Guo1, Jia Liu1
1From the Stroke Center (Z.-N.G., W.-T.G., H.M., F.-L.Z., H.J., X.S., Y.Y.) and Clinical Trial and Research Center for Stroke (Z.-N.G., P.Z., Y.Y.), Department of Neurology, First Hospital of Jilin University, Changchun; Laboratory for Engineering and Scientific Computing, Institute of Advanced Computing and Digital Engineering (J.L.) and Center for Antibody Drug, Institute of Biomedicine and Biotechnology (J.C.), Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen University Town; Department of Neurology (K.H.), Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China; Department of Neurology, Taipei Medical University-Shaung Ho Hospital (H.-H.H.), and Cerebrovascular Treatment and Research Center (H.-H.H.), College of Medicine, Taipei Medical University, Taiwan; and Institute of Sound and Vibration Research (D.M.S.), University of Southampton, UK.
Objective:
To determine the effect of remote ischemic preconditioning (RIPC) on dynamic cerebral autoregulation (dCA) and various blood biomarkers in healthy adults.
Methods:
A self-controlled interventional study was conducted. Serial measurements of dCA were performed at 7 time points (7, 9, and 11 am; 2, 5, and 8 pm, and 8 am on the next day) without or with RIPC, carried out at 7:20 to 8 am. Venous blood samples were collected at baseline (7 am) and 1 hour after RIPC, and blood biomarkers, including 5 neuroprotective factors and 25 inflammation-related biomarkers, were measured with a quantitative protein chip.
Results:
Fifty participants were enrolled (age 34.54 ± 12.01 years, 22 men). Compared with the results on the day without RIPC, dCA was significantly increased at 6 hours after RIPC, and the increase was sustained for at least 24 hours. After RIPC, 2 neuroprotective factors (glial cell-derived neurotrophic factor and vascular endothelial growth factor-A) and 4 inflammation-related biomarkers (transforming growth factor-β1, leukemia inhibitory factor, matrix metallopeptidase-9, and tissue inhibitor of metalloproteinase-1) were significantly elevated compared with their baseline levels. Conversely, monocyte chemoattractant protein-1 was significantly lower compared with its baseline level.
Conclusions:
RIPC induces a sustained increase of dCA from 6 to at least 24 hours after treatment in healthy adults. In addition, several neuroprotective and inflammation-related blood biomarkers were differentially regulated shortly after RIPC. The increased dCA and altered blood biomarkers may collectively contribute to the beneficial effects of RIPC on cerebrovascular function.
Clinicaltrialsgov Identifier:
NCT02965547.
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