s-145 and Coronary-Disease

s-145 has been researched along with Coronary-Disease* in 1 studies

Other Studies

1 other study(ies) available for s-145 and Coronary-Disease

Article	Year
Cardioprotective actions of the specific thromboxane receptor antagonist (+)-S145Na following coronary occlusion and reperfusion in the rat. Research communications in chemical pathology and pharmacology, 1990, Volume: 70, Issue:2 We studied the effects of a novel thromboxane receptor antagonist (+)-S145Na, on the loss of myocardial creatine kinase activity in the rat myocardium after 10 minutes of coronary artery ligation, followed by 24 hours of reperfusion. (+)-S145Na (500 micrograms/kg), or its vehicle, was administered 10 minutes after occlusion (just prior to reperfusion) intravenously. Myocardial creatine kinase activity was significantly reduced in the ischemic areas of hearts obtained from rats receiving vehicle when compared to sham operated control rats. This loss in creatine kinase activity was significantly attenuated in hearts obtained from rats receiving (+)-S145Na. These findings further support the important role of thromboxane A2 in the pathogenesis of reperfusion injury following myocardial ischemia, and that (+)-S145Na may be a useful agent in the treatment of myocardial reperfusion injury. Topics: Animals; Bridged Bicyclo Compounds; Coronary Disease; Creatine Kinase; Fatty Acids, Monounsaturated; Heart; Male; Myocardial Reperfusion Injury; Myocardium; Rats; Rats, Inbred Strains; Receptors, Prostaglandin; Receptors, Thromboxane; Thromboxane A2	1990

Article

Year

Cardioprotective actions of the specific thromboxane receptor antagonist (+)-S145Na following coronary occlusion and reperfusion in the rat.

Research communications in chemical pathology and pharmacology, 1990, Volume: 70, Issue:2

We studied the effects of a novel thromboxane receptor antagonist (+)-S145Na, on the loss of myocardial creatine kinase activity in the rat myocardium after 10 minutes of coronary artery ligation, followed by 24 hours of reperfusion. (+)-S145Na (500 micrograms/kg), or its vehicle, was administered 10 minutes after occlusion (just prior to reperfusion) intravenously. Myocardial creatine kinase activity was significantly reduced in the ischemic areas of hearts obtained from rats receiving vehicle when compared to sham operated control rats. This loss in creatine kinase activity was significantly attenuated in hearts obtained from rats receiving (+)-S145Na. These findings further support the important role of thromboxane A2 in the pathogenesis of reperfusion injury following myocardial ischemia, and that (+)-S145Na may be a useful agent in the treatment of myocardial reperfusion injury.

Topics: Animals; Bridged Bicyclo Compounds; Coronary Disease; Creatine Kinase; Fatty Acids, Monounsaturated; Heart; Male; Myocardial Reperfusion Injury; Myocardium; Rats; Rats, Inbred Strains; Receptors, Prostaglandin; Receptors, Thromboxane; Thromboxane A2

1990