Figure 2.

Inhibition of COX-1 and COX-2-dependent prostanoid formation by aspirin in vivo. Aspirin administration (0.1–100 mg/kg, i.v.; 30 min) produced dose-dependent inhibition of serum TXB₂ formation (A) and lung homogenate PGE₂ formation (B) in tissue from WT mice, both responses that are primarily COX-1 dependent. Aspirin also produced dose-dependent inhibition of PGE₂ formation in lung homogenates from COX-1-deficient mice, in which residual prostanoid production (∼0.1% of WT levels) is mediated by COX-2 (C). In all systems, aspirin produced >70% inhibition of COX activity at 100mg/kg. Data are means ± se for tissue from n = 3–5 mice aged 10–12 wk.