Deliberation, Unjust Exclusion, and the Rhetorical Turn

Theories of deliberative democracy have faced the charge of leading to the unjust exclusion of voices from public deliberation. The recent rhetorical turn in deliberative theory aims to respond to this charge. I distinguish between two variants of this response: the supplementing approach and the systemic approach. On the supplementing approach, rhetorical modes of political speech may legitimately supplement the deliberative process, for the sake of those excluded from the latter. On the systemic approach, rhetorical modes of political speech are legitimate within public deliberation, just so long as they result in net benefits to the deliberative system. I argue that neither of these two approaches adequately meets the unjust exclusion charge. Whereas the supplementing approach does not go far enough to incorporate rhetorical speech into public deliberation, the systemic approach goes too far by legitimizing forms of rhetoric that risk only exacerbating the problem of unjust exclusion. More constructively, I draw on Aristotle’s conception of rhetoric, as an art (technē) that is a counterpart to dialectic, to argue for a constitutive approach to rhetoric. I show how this approach provides a more expansive notion of deliberation that remains normatively orientated

Endogenous Adenosine Selectively Modulates Oxidant Stress via the A1 Receptor in Ischemic Hearts

We tested the impact of A1 adenosine receptor (AR) deletion on injury and oxidant damage in mouse hearts subjected to 25-min ischemia/45-min reperfusion (I/R). Wild-type hearts recovered ∼50% of contractile function and released 8.2 ± 0.7 IU/g of lactate dehydrogenase (LDH). A1AR deletion worsened dysfunction and LDH efflux (15.2 ± 2.6 IU/g). Tissue cholesterol and native cholesteryl esters were unchanged, whereas cholesteryl ester–derived lipid hydroperoxides and hydroxides (CE-O(O)H; a marker of lipid oxidation) increased threefold, and α-tocopherylquinone [α-TQ; oxidation product of α-tocopherol (α-TOH)] increased sixfold. Elevations in α-TQ were augmented by two- to threefold by A1AR deletion, whereas CE-O(O)H was unaltered. A1AR deletion also decreased glutathione redox status ([GSH]/[GSSG + GSH]) and enhanced expression of the antioxidant response element heme oxygenase-1 (HO-1) during I/R: fourfold elevations in HO-1 mRNA and activity were doubled by A1AR deletion. Broad-spectrum AR agonism (10 μM 2-chloroadenosine; 2-CAD) countered effects of A1AR deletion on oxidant damage, HO-1, and tissue injury, indicating that additional ARs (A2A, A2B, and/or A3) can mediate similar actions. These data reveal that local adenosine engages A1ARs during I/R to limit oxidant damage and enhance outcome selectively. Control of α-TOH/α-TQ levels may contribute to A1AR-dependent cardioprotection. Antioxid. Redox Signal. 11, 2641–2650