Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2015 Jun 10;100(6):F541–F552. doi: 10.1136/archdischild-2014-306284

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions

This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 4.0) license, which permits others to distribute, remix, adapt and build upon this work, for commercial use, provided the original work is properly cited. See: http://creativecommons.org/licenses/by/4.0/

PMC Copyright notice

(A) The neuroprotective mechanisms of RIPostC are thought to involve three inter-related pathways induced by remote limb ischaemia. (1) The neuronal pathway involves activation of both local sensory nerves and the autonomic nervous system to mediate protective effects, including the release of humoral factors; (2) the humoral pathway involves endogenous protective factors, including locally acting autocoids and bloodborne humoral factors that travel to the brain and (3) the systemic response includes immune modulation and blood pressure regulation. (B) Within the brain, the three pathways converge to increase cerebral blood flow, ameliorate neuroinflammation and to activate cell survival mechanisms. Direct pro-survival actions within cells are mediated via G-protein-coupled (GPC) receptors and include mitochondrial protection (maintenance of potassium-sensitive ATP channel, prevention of mitochondrial permeability transition pore opening) and transcriptional regulation (both genetic and epigenetic modulation) in the nucleus. (C) Following remote ischaemic stimulus after HI, the effects of these neuroprotective mechanisms are to decrease energy consumption; to increase substrate delivery and offset cerebral secondary energy failure; to protect against cell death and to augment long-term recovery and repair. HI, hypoxia-ischaemia; I/R, ischaemia/reperfusion; RIPostC, remote ischaemic postconditioning.