Fig. 2. Infarct size analysis. Remote preconditioning (RPC) and U-50,488H (10 mg/kg intravenous) greatly reduced the infarct size induced by ischemia–reperfusion (I/R), an effect that was abolished by nor-binaltorphimine (nor-BNI, 10 mg/kg intravenous), a specific κ-opioid receptor antagonist, and atractyloside (Atr, 5 mg/kg intravenous), a mitochondrial permeability transition pore activator. Naltrindole (5 mg/kg intravenous), a δ-opioid receptor antagonist, did not attenuate the effect of RPC. Administration of dynorphin (24 ng/kg intravenous), the endogenous κ-opioid receptor agonist, induced effects similar to those of U-50,488H and RPC. Infarct size is expressed as percentage of risk zone. Values are mean ± SD. n values are indicated on the columns. **P < 0.01 versus I/R. ## P < 0.01 versus RPC. δδ P < 0.01 versus U-50,488H.