Salvage of Ischaemic myocardium by tenoxicam during acute myocardial infarction in the anaesthetized cats

ABSTRACT

Recently, antiinflammatory agents have been claimed to reduce infarct size in a number of models of coronary artery occlusion. In this work, the ability of the new antiinflammatory drug tenoxicam to limit infarct size [I.S.] was assessed in cats, 5 hours after ligation of the left anterior descending coronary artery. The drug was given intravenously 10 mns before ligation. In the ligated non-treated group, the S-T segment was raised significantly from isoelectric to reach 5 +/- 0.4 mm at the end of the experiment. Serum MB-CK level increased significantly from a pre-occlusion level of 162 +/- 13 U/L to reach 813.3 +/- 19.8 U/L 5 hours later. The I.S. measured by planimetry in serial cardiac sections and stained by hematoxylin basic fuchsin picric acid stain, was found to measure 32.2% of the heart. One cat died ventricular fibrillation. In the treated non-ligated group, no positive data were observed except significant bradycardia. In the group treated with the smaller dose of tenoxicam [0.25 mg/kg] and ligated, the heart rate was significantly reduced, there was significant decrease in S-T segment elevation [1.5 +/- 0.2 mm]. Significant reduction of serum MB-CK level [340 +/- 13 U/L] and of infarct size [11.9%] occurred. Ventricular fibrillation and death did not occur. Doubling the dose of tenoxicam proved to have a more marked cardio-protective action. The bradycardia was more, there was significant decrease in S-T segment elevation [1 + 0.2 mm]. The reduction in serum MB-CK level [207.6 +/- 12 U/L] and I.S. [7.1%] was more marked. No deaths occurred. In conclusion, tenoxicam in a dose of 0.25 and 0.5 mg/kg could protect the heart against extension of infarct size. Several mechanisms for this effect of the drug has been discussed