title: Thromboxane A2-receptor blockade and prostacyclin in porcine Escherichia coli shock.
abstract: Septic shock was induced by intravenous infusion of live Escherichia coli in pigs to investigate the influences on central hemodynamic, coagulation, and fibrinolytic reactions by a thromboxane A2 (TxA2)-receptor blocker (BM 13.177; n = 6) and a prostacyclin analogue (iloprost or ZK 36,374; n = 7). The early pulmonary vasoconstriction following E coli infusion was attenuated, but not abolished, by BM 13.177. Only minor effects were seen after pretreatment with iloprost. Neither drug had any major effect on the coagulation and fibrinolytic activation. These results confirm that TxA2 is an important, but not the only, mediator of early pulmonary vascular response in porcine septicemia and that neither TxA2 nor prostacyclin is of major importance for the hemostatic reactions in this shock model.
authors: Department of Surgery, Lund University, Malmö, Sweden.
authors: E
authors: E
authors: Svartholm
authors: D
authors: D
authors: Bergqvist
authors: U
authors: U
authors: Hedner
authors: J
authors: J
authors: Ljungberg
authors: U
authors: U
authors: Haglund
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D011464:Epoprostenol / Q000494:pharmacology*; D004927:Escherichia coli Infections / Q000503:physiopathology*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006487:Hemostasis / Q000187:drug effects; D016285:Iloprost; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects; D011652:Pulmonary Circulation / Q000187:drug effects; D011982:Receptors, Prostaglandin / Q000037:antagonists & inhibitors*; D017482:Receptors, Thromboxane; D012772:Shock, Septic / Q000139:chemically induced / Q000503:physiopathology*; D013449:Sulfonamides / Q000494:pharmacology*; D014655:Vascular Resistance
chemical_list: D011982:Receptors, Prostaglandin; D017482:Receptors, Thromboxane; D013449:Sulfonamides; C040624:sulotroban; D011464:Epoprostenol; D016285:Iloprost