BMS 180448

01/01/1996 - "BMS-180448 ameliorates morphological evidence of ischemia/reperfusion myocardial damage in the isolated rat heart model, in agreement with physiological and biochemical parameters."
05/01/2007 - "In isolated rat hearts subjected to 30-min global ischemia followed by 30-min reperfusion, BMS-180448 (1, 3 and 10 microM) significantly increased reperfusion left ventricular developed pressure (LVDP) and 30-min reperfusion double product (heart rate x LVDP) in a concentration-dependent manner, while decreasing left ventricular end-diastolic pressure (LVEDP) throughout reperfusion period in a concentration-dependent manner. "
01/01/1997 - "BMS-180448 also significantly enhanced the functional reserve after the 25-min period of global ischemia. "
02/01/1996 - "BMS-180448 was given as a total dose of 4.2, 1.4 or 0.5 mg/kg over 30 min, starting 15 min before ischemia. "
04/01/1997 - "Drug administered at the midpoint of ischemia reduced infarct size approximately 44%, whereas delaying BMS-180448 infusion until the 5th min of reperfusion reduced, but still provided a significant (17%) level of salvage. "

07/01/1997 - "Moreover, the cerebral vasodilator effect of K(ATP) openers, which has been thought responsible for the occurrence of headache in clinical trials, has been found lacking in BMS-180448; this difference may represent a clear advantage in the pharmacologic profile of the agent."

01/01/1996 - "Cardioprotective effects of BMS-180448 following ischemia/reperfusion consisted of a reduced rate of contracture formation, reduced LDH release, and enhanced recovery of contractile function during reperfusion (P < 0.05). "
11/01/1995 - "Cromakalim and BMS-180448 both further significantly increased time to contracture in both normothermic and hypothermic arrested hearts; this was accompanied by enhanced recovery of reperfusion contractile function and reduced cumulative LDH release. "
11/01/1995 - "In isolated ischemic guinea pig hearts, cromakalim and BMS-180448 had similar cardioprotective potencies (EC25 of 3.2 and 3.3 microM, respectively, for increasing time to the onset of contracture). "
01/01/1995 - "In globally ischemic rat hearts, BMS-180448 was cardioprotective (EC25 for increasing time to contracture = 2.5 microM), with potency equal to that of cromakalim (EC25 = 4.9 microM) despite being significantly less potent as a peripheral smooth muscle relaxant (methoxamine-constricted rat aorta). "
12/27/1995 - "Measurements of ischemic damage made in isolated perfused rat hearts demonstrated that cromakalim and BMS-180448 were equipotent as cardioprotective agents; time to contracture was increased with an EC25 value of 4.8 and 4.7 microM, respectively, and lactate dehydrogenase levels were significantly reduced compared to those in the presence of vehicle. "

04/01/1997 - "Preocclusion administration of BMS-180448 was associated with a 35% reduction in infarct damage from that recorded in vehicle-treated control ferrets. "
04/01/1997 - "Drug administered at the midpoint of ischemia reduced infarct size approximately 44%, whereas delaying BMS-180448 infusion until the 5th min of reperfusion reduced, but still provided a significant (17%) level of salvage. "
01/01/1995 - "In anesthetized dogs subjected to 90-min coronary occlusion/reperfusion, BMS-180448 reduced infarct size (IS) by 50% without hemodynamic effects. "
11/01/1996 - "In the absence of PC, activation of ATP-sensitive potassium channels with the cardiac-selective agonist BMS-180448 significantly (p < 0.01) reduced infarct size from 66% to 37% of the risk zone. "

01/01/1995 - "BMS-180448 provides the opportunity to explore the cardioprotective actions of this class of agents without the possible complications (hypotension, coronary steal) that may be caused by the currently available KATP openers."
12/27/1995 - "Based on the reduced cardiac electrophysiologic and vascular effects of BMS-180448, we suggest that BMS-180448 should provide cardioprotective efficacy similar to cromakalim with reduced risk of hypotension or arrhythmias."
02/01/1996 - "Both compounds increased HR. Effects of BMS-180448 occurred at doses higher than those of cromakalim, but at doses slightly lower than those needed to cause hypotension (ED(HR)/ED(MABP) ratio of 0.18 for BMS-180448). "