Fig 6.
Different inhibitory effects of opioid receptor antagonists on remifentanil-induced cardioprotection in normal and failing hearts. (a) Inhibition percentage of remifentanil reduced infarct size/area at risk by μ-opioid receptor antagonist CTOP, δ-receptor antagonist NTD or κ-receptor antagonist BNI in isolated normal (left lane) and failing (right lane) hearts (n=6). (b) Inhibition percentage of remifentanil reduced LDH activities (at 5 min of reperfusion) by μ-opioid receptor antagonist CTOP, δ-receptor antagonist NTD, or κ-receptor antagonist BNI in isolated normal (left lane) and failing (right lane) hearts (n=6). The inhibition percentage was calculated according to the formula: % Inhibitionantagonist=[1−(Valuecontrol−Valueantagonist)/(Valuecontrol−ValueRemi)] ×100%. **P<0.01, *P<0.05, one-way anova followed by Tukey's test. (c) Cartoons of a working hypothesis suggesting a dynamic regulation of cardiac μ-opioid receptor expression and the therapeutic potential of these receptors in failing hearts via an ERK/GSK-3β pathway. anova, analysis of variance; CTOP, D-Pen-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2; NTD, naltrindole hydrochloride; BNI, nor-binaltorphimine dihydrochloride; Remi, Remifentanil; ERK, extracellular signal-regulated kinase; GSK3ß, glycogen synthase kinase; I/R, ischaemia-reperfusion; LDH, lactate dehydrogenase; P, phosphorylation.