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Effects of flurbiprofen on myocardial cell damage in acute myocardial ischemia.

Fluribiprofen, a non steroidal anti-inflammatory agent, was studied in anesthetized cats subjected to acute myocardial ischemia. Flurbiprofen was given at 0.25, 1 or 4 mg/kg bolus intravenously at 0.5 hours and again at 2.5 hours. Assessment of ischemic myocardial preservation was appraised by measurement of S-T segment elevation, and plasma and cardiac tissue creatine phosphokinase (CK) specific activity. Plasma thromboxane B2 (TB2) concentrations measured by specific radioimmunoassay for TB2, and arachidonic-induced platelet aggregation were also assessed. All three doses of flurbiprofen prevented both the increase to plasma TB2 concentrations occuring in MI (p less than 0.05) at 2, 3 and 4 hours) and platelet aggregation induced by arachidonic acid. However, flurbiprofen at either 0.25 or 4 mg/kg failed to prevent the increase in the S-T segment, the increase in plasma CK activity and failed to maintain myocardial CK values in the ischemic region. At 1 mg/kg, flurbiprofen returned S-T segment to normal values and preserved myocardial CK activities but only slightly prevented the increase in plasma CK activity. These data suggest that the low and high dose of flurbiprofen showed no protection during acute myocardial ischemia, while the intermediate dose was effective. The reason for the narrow range of myocardial preservation is not clear.