Treatment of acute myocardial ischaemia with a selective antagonist of thromboxane receptors (BM 13.177).
In order to elucidate the role of endogenous thromboxane A2 in myocardial ischaemia, cats were subjected to 5 h of permanent occlusion of the left anterior descending coronary artery (LAD) and treated with the thromboxane receptor antagonist BM 13.177 (5 mg kg-1 h-1, i.v.). In comparison with vehicle-treated LAD-occluded cats, BM 13.177 significantly attenuated the loss of creatine phosphokinase-specific activity from the ischaemic myocardium and antagonized the ischaemia-induced rise in the ST-segment of the electrocardiogram. BM 13.177 at the dose used did not reduce plasma thromboxane levels or ischaemia-induced platelet aggregate formation but considerably antagonized thromboxane-dependent platelet secretion ex vivo. The study demonstrates some beneficial effects of selective blockade of thromboxane receptors on biochemical and electrophysiological parameters of acute myocardial ischaemia.
D000255:Adenosine Triphosphate / Q000097:blood; D000818:Animals; D001792:Blood Platelets / Q000378:metabolism; D002415:Cats; D003327:Coronary Disease / Q000188:drug therapy*; D003402:Creatine Kinase / Q000378:metabolism; D004562:Electrocardiography; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D009206:Myocardium / Q000201:enzymology; D011956:Receptors, Cell Surface / Q000187:drug effects*; D011982:Receptors, Prostaglandin / Q000187:drug effects*; D017482:Receptors, Thromboxane; D013449:Sulfonamides / Q000627:therapeutic use*; D013928:Thromboxane A2 / Q000096:biosynthesis; D013997:Time Factors
D005343:Fibrinolytic Agents; D011956:Receptors, Cell Surface; D011982:Receptors, Prostaglandin; D017482:Receptors, Thromboxane; D013449:Sulfonamides; D013928:Thromboxane A2; C040624:sulotroban; D000255:Adenosine Triphosphate; D003402:Creatine Kinase