Korean J Physiol Pharmacol.  2017 Mar;21(2):145-152. 10.4196/kjpp.2017.21.2.145.

Neurogenic pathways in remote ischemic preconditioning induced cardioprotection: Evidences and possible mechanisms

Affiliations
  • 1Department of Pharmaceutical Sciences and Drug Research, Punjabi University Patiala, Patiala 147002, India. amteshwarjaggi@yahoo.co.in

Abstract

Remote ischemic preconditioning (RIPC) is an intrinsic phenomenon whereby 3~4 consecutive ischemia-reperfusion cycles to a remote tissue (noncardiac) increases the tolerance of the myocardium to sustained ischemiareperfusion induced injury. Remote ischemic preconditioning induces the local release of chemical mediators which activate the sensory nerve endings to convey signals to the brain. The latter consequently stimulates the efferent nerve endings innervating the myocardium to induce cardioprotection. Indeed, RIPC-induced cardioprotective effects are reliant on the presence of intact neuronal pathways, which has been confirmed using nerve resection of nerves including femoral nerve, vagus nerve, and sciatic nerve. The involvement of neurogenic signaling has been further substantiated using various pharmacological modulators including hexamethonium and trimetaphan. The present review focuses on the potential involvement of neurogenic pathways in mediating remote ischemic preconditioning-induced cardioprotection.

Keyword

Cardioprotection; Femoral nerve; Neurogenic; Remote preconditioning; Sciatic nerve

MeSH Terms

Brain
Femoral Nerve
Hexamethonium
Ischemic Preconditioning*
Myocardium
Negotiating
Nerve Endings
Neurons
Sciatic Nerve
Sensory Receptor Cells
Trimethaphan
Vagus Nerve
Hexamethonium
Trimethaphan

Figure

  • Fig. 1 Mesenteric artery occlusion and intramesentric infusion of adenosine leads to enhanced local release of adenosine which stimulates sensory nerves fibers and relays the signals to the nerve fibers terminating on the myocardium to provide cardioprotection.

  • Fig. 2 RIPC activates neurogenic pathways including stimulation of vagus nerves which in turn prevents the loss of CX43 gap junction proteins to provide cardioprotective effects.Secondly, RIPC stimulus enhances opioid release and activates myocardial opioid receptors to induce cardioprotection. Furthermore, RIPC also increases CGRP release and activates sensory C nerve fibers to induce cardioprotection.


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