SM 20550

06/01/2000 - "In perfused hearts exposed to 40 min of global ischemia and 20 min of reperfusion, SM-20550 (10(-8)-10(-7) M) significantly reduced the elevation of left ventricular end-diastolic pressure during reperfusion, improved the postischemic recovery of developed pressure, and prevented coronary perfusion pressure increase after reperfusion. "
04/01/2002 - "The aim of this study was to investigate whether a selective Na+/H+ exchange inhibitor, SM-20550, can modulate the mitochondrial respiratory function and mitochondrial Ca2+ content in isolated rat hearts subjected to 40 min of ischemia and 20 min of reperfusion. "
01/01/2001 - "The aim of this study was to test the protective effect of an Na+/H+ exchange (NHE) inhibitor, SM-20550, on ischemia/reperfusion-induced endothelial dysfunction. "
04/01/2002 - "The mitochondrial Ca2+ content was significantly increased after ischemia/reperfusion but was suppressed by treatment with SM-20550 (10, 100 nM). "
04/01/2002 - "SM-20550 (10, 100 nM) was administered for 5 min prior to ischemia and for 20 min during the reperfusion period. "

01/01/2002 - "Moreover, the combination of 2 min of IPC and 0.03 mg/kg of SM-20550 significantly reduced infarct size by 64%, although neither 0.03 mg/kg SM-20550 nor 2 min of IPC alone reduced infarct size significantly. "
01/01/2002 - "This reduction in infarct size was similar to that produced by 0.1 mg/kg SM-20550 or 5 min of IPC alone. "
01/01/2002 - "The combination of 5 min of IPC and 0.1 mg/kg of SM-20550 significantly reduced infarct size by 78%. "
01/01/2002 - "In contrast, 0.1 mg/kg of SM-20550 significantly reduced infarct size by 62%. "
01/01/2002 - "Treatment with SM-20550 at 0.03 mg/kg had a nonsignificant tendency to reduce infarct size (18%). "

01/01/2000 - "This study was designed to evaluate the effects of an Na+/H+ exchange inhibitor, SM-20550, on ischemia-reperfusion injury in the skeletal muscle. "
06/01/2001 - "The effect of an Na+/H+ exchange inhibitor, SM-20550, on the adhesion, emigration and accumulation of leukocytes was studied in ischemia and reperfusion injury models using rat mesenteric venules or rabbit heart. "
06/01/2000 - "These results suggest that SM-20550 is a potent, highly specific Na+/H+ exchange inhibitor, which exerts a protective effect against myocardial ischemia/reperfusion injury. "
02/01/2001 - "The protective effects of Na+ - H+ exchange inhibitors SM-20550 (SM) and 5-(N-ethyl-N-isopropyl)-amiloride (EIPA) against ischemia-reperfusion injury were investigated in guinea pig Langendorff hearts. "
06/01/2000 - "We investigated the effect of a newly synthesized compound, SM-20550 [N-(aminoiminomethyl)-1,4-dimethyl-1H-indole-2-carboxamide methanesulfonic acid] on Na+/H+ or Na+/Ca2+ exchange activity in rat cardiomyocytes, and on radioligand binding with several channels or receptors in membrane preparations, and ischemia/reperfusion injury in isolated perfused rat hearts. "

04/01/2002 - "These results suggest that SM-20550 improved survival after myocardial infarction, at least due to its antinecrotic effect."
09/15/2000 - "Reduction of myocardial infarct size by SM-20550, a novel Na(+)/H(+) exchange inhibitor, in rabbits."
04/01/2002 - "Effects of SM-20550, a new Na(+)/H(+) exchange inhibitor, on survival and infarct size in rat myocardial infarction."
11/01/2007 - "Effects of SM-20550 against myocardial infarction-induced arrhythmias, late infarct expansion, and left ventricular dysfunction."
04/01/2002 - "The effect of a novel potent Na(+)/H(+) exchange inhibitor, SM-20550 [N-(aminoiminomethyl)-1,4-dimethyl-1H-indole-2-carboxamide methanesulfonic acid], on survival after myocardial infarction was studied. "

06/01/2000 - "These results suggest that SM-20550 is a potent, highly specific Na+/H+ exchange inhibitor, which exerts a protective effect against myocardial ischemia/reperfusion injury. "
01/01/2002 - "The effects of SM-20550 [N-(aminoiminomethyl)-1,4-dimethyl-1H-indole-2-carboxamide methanesulfonic acid], an Na+/H+ exchange inhibitor, on ischemic preconditioning (IPC) were studied in a rabbit model of myocardial ischemia and reperfusion injury. "