RESUMO
An analysis of the literature data performed by the authors shows that the main contenders for the role of the end effector of ischemic preconditioning of the heart are: (1) MPT pore (2) nexuses (3) cytoskeleton. Thus, almost all of the known intracellular molecular cascades eventually converge on MPT pore, on the components of the cytoskeleton and nexuses.
Assuntos
Precondicionamento Isquêmico Miocárdico , Traumatismo por Reperfusão Miocárdica/metabolismo , Miócitos Cardíacos/metabolismo , Animais , Citoesqueleto/metabolismo , Humanos , Canais KATP/metabolismo , Proteínas de Transporte da Membrana Mitocondrial/metabolismo , Poro de Transição de Permeabilidade Mitocondrial , Traumatismo por Reperfusão Miocárdica/terapiaRESUMO
It was investigated the role of δ-, µ- и κ-opioid receptors (ORs) in the development of cytoprotective effect of chronic normobaric hypoxia (CNH) using anoxia/reoxygenation of isolated cardiomyocytes. Adaptation to CNH was achieved by the maintenance of rats for 21 days at atmosphere containing 12% O2. Anoxia/reoxygenation of isolated cardiomyocytes of intact rats evoked a death of 23% cells and enhancement of lactate dehydrogenase (LDH) release from cells. Anoxia/reoxygenation of isolated cardiomyocytes of adapting rats induced a death of only 2.5% cells and LDH release decreased by 25%. Preliminary incubation of cells with the OR blocker naloxone (300 nM) or the δ-OR antagonist TIPP(ψ) (30 nM) or the selective δ2-OR antagonist naltriben (1 nM) or the µ-OR antagonist CTAP (100 nM) 25 min prior to anoxia abolished adaptive enhancement of cell survival and a decrease in LDH release. The blocking of δ1-OR by BNTX (1 nM) or κ-OR by nor-binaltorphimine (3 nM) not affected on the cytoprotection at CNH. Consequently, cardiac cell δ2- and µ-opioid receptors are involved in the cytoprotective effect of chronic normobaric hypoxia.
