We studied the role of the δ, µ, and к opioid receptor (OR)
subtypes in the cardioprotective effect of chronic continuous
normobaric hypoxia (CNH) in the model of acuteanoxia/
reoxygenation of isolated cardiomyocytes. Adaptation of rats to
CNH was performed by their exposure to atmosphere containing
12 % of O2 for 21 days. Anoxia/reoxygenation of cardiomyocytes
isolated from normoxic control rats caused the death of 51 % of
cells and lactate dehydrogenase (LDH) release. Adaptation of rats
to CNH resulted in the anoxia/reoxygenation-induced
cardiomyocyte death of only 38 %, and reduced the LDH release.
Pre-incubation of the cells with either the non-selective OR
blocker naloxone (300 nM/l), the δ OR antagonist TIPP(ψ)
(30 nM/l), the selective δ2 OR antagonist naltriben (1 nM/l) or the
μ OR antagonist CTAP (100 nM/l) for 25 minutes before anoxia
abolished the reduction of cell death and LDH release afforded by
CNH. The antagonist of δ1 OR BNTX (1 nM/l) or the κ OR
antagonist nor-binaltorphimine (3 nM/l) did not influence the
cytoprotective effects of CNH. Taken together, the cytoprotective
effect of CNH is associated with the activation of the δ2 and μ OR
localized on cardiomyocytes.
Remote ischemic preconditioning (RIPC) is a novel strategy of protection against ischemia-reperfusion (IR) injury in the heart (and/or other organs) by brief episodes of non-lethal IR in a distant organ/tissue. Importantly, RIPC can be induced noninvasively by limitation of blood flow in the extremity implying the applicability of this method in clinical situations. RIPC (and its delayed phase) is a form of relatively short-term adaptation to ischemia, similar to ischemic PC, and likely they both share triggering mechanisms, whereas mediators and end-effectors may differ. It is hypothesized that communication between the signals triggered in the remote organs and protection in the target organ may be mediated through substances released from the preconditioned organ and transported via the circulation (humoral pathways), by neural pathways and/or via systemic anti-inflammatory and antiapoptotic response to short ischemic bouts. Identification of molecules involved in RIPC cascades may have therapeutic and diagnostic implications in the management of myocardial ischemia. Elucidation of the mechanisms of endogenous cardioprotection triggered in the remote organ could lead to the development of diverse pharmacological RIPC mimetics. In the present article, the authors provide a short overview of RIPC-induced protection, proposed underlying mechanisms and factors modulating RIPC as a promising cardioprotective strategy., T. Ravingerova, V. Farkasova, L. Griecsova, S. Carnicka, M. Murarikova, E. Barlaka, F. Kolar, M. Bartekova, L. Lonek, J. Slezak, A. Lazou., and Obsahuje bibliografii