A comparison of the anti‐inflammatory and anti‐nociceptive activity of nitroaspirin and aspirin

Nitroaspirin (2.5–50 mg kg −1 , i.p. or 2.5–100 mg kg −1 , p.o.) and aspirin (2.5–100 mg kg −1 , i.p. or p.o.) exhibit anti‐inflammatory activity in the carrageenan‐induced hindpaw oedema model in the rat. When administered i.p., nitroaspirin was a more effective anti‐oedema agent than aspirin particularly in the ‘early’ phase (i.e. up to 60 min) of the response. The ED 50 values for nitroaspirin and aspirin as inhibitors of the ‘late’ phase response (measured at 180 min) were 64.3 μmol kg −1 and >555 μmol kg −1 , respectively. When administered p.o., neither nitroaspirin nor aspirin exhibited significant anti‐inflammatory activity in the ‘early’ phase and were of similar potency in the ‘late’ phase. Thus, at the highest dose used (100 mg kg −1 , 360 min) orally administered nitroaspirin (aspirin in parenthesis) inhibited oedema formation by 46.9±1.6% (47.2±3.8%, both n =6, P <0.05). Nitroaspirin and aspirin (25–200 mg kg −1 , p.o.) caused dose‐related inhibition of the hyperalgesia to mechanical stimulation following intraplantar injection of carrageenan in the rat. ED 50 values were 365 μmol kg −1 and 784 μmol kg −1 , respectively. Neither drug influenced the threshold for mechanical stimulation in the contralateral (i.e. untreated) hindpaw. Nitroaspirin and aspirin (2.5–100 mg kg −1 , p.o.) caused dose‐related inhibition of acetic acid induced abdominal constrictions in the mouse (ED 50 values of 154.7 μmol kg −1 and 242.8 μmol kg −1 , respectively). Nitroaspirin and aspirin (>200 mg kg −1 , p.o.) reduced the ‘late’ phase (but not the ‘early’ phase) of the formalin‐induced hindpaw licking assay in the mouse. Similarly, nitroaspirin and aspirin (>50 mg kg −1 , p.o.) prolonged tail withdrawal latency following application of a noxious heat stimulus in the mouse.British Journal of Pharmacology (2000) 129 , 343–350; doi: 10.1038/sj.bjp.0703064