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Basic Res Cardiol. 2018 Jun 1;113(4):25. doi: 10.1007/s00395-018-0684-z.

Neural mechanisms in remote ischaemic conditioning in the heart and brain: mechanistic and translational aspects.

Author information

1
The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.
2
Department of Cardiology, Karolinska University Hospital, 171 76, Stockholm, Sweden.
3
The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, WC1E 6HX, UK. d.yellon@ucl.ac.uk.

Abstract

Remote ischaemic conditioning (RIC) is a promising method of cardioprotection, with numerous clinical studies having demonstrated its ability to reduce myocardial infarct size and improve prognosis. On the other hand, there are several clinical trials, in particular those conducted in the setting of elective cardiac surgery, that have failed to show any benefit of RIC. These contradictory data indicate that there is insufficient understanding of the mechanisms underlying RIC. RIC is now known to signal indiscriminately, protecting not only the heart, but also other organs. In particular, experimental studies have demonstrated that it is able to reduce infarct size in an acute ischaemic stroke model. However, the mechanisms underlying RIC-induced neuroprotection are even less well understood than for cardioprotection. The existence of bidirectional feedback interactions between the heart and the brain suggests that the mechanisms of RIC-induced neuroprotection and cardioprotection should be studied as a whole. This review, therefore, addresses the topic of the neural component of the RIC mechanism.

KEYWORDS:

Cardioprotection; Neuroprotection; Remote ischaemic conditioning

PMID:
29858664
PMCID:
PMC5984640
DOI:
10.1007/s00395-018-0684-z
[Indexed for MEDLINE]
Free PMC Article

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