|1.||Grover, G J: 3 articles (05/2004 - 06/2001)|
|2.||Yoo, Sung-Eun: 2 articles (05/2007 - 07/2003)|
|3.||Shin, Hwa-Sup: 2 articles (05/2007 - 07/2003)|
|4.||Maslov, L N: 2 articles (05/2004 - 04/2003)|
|5.||Bogomaz, S A: 2 articles (05/2004 - 04/2003)|
|6.||Lishmanov, A Iu: 2 articles (05/2004 - 04/2003)|
|7.||Solenkova, N V: 2 articles (05/2004 - 04/2003)|
|8.||Yi, Kyu-Yang: 1 article (05/2007)|
|9.||Jung, In-Sang: 1 article (05/2007)|
|10.||Lee, Chang-Soo: 1 article (05/2007)|
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. "
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. "
01/01/1997 - "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. "
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. "
|4.||Hypotension (Low Blood Pressure)
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). "
01/01/1995 - "In anesthetized dogs subjected to 90-min coronary occlusion/reperfusion, BMS-180448 reduced infarct size (IS) by 50% without hemodynamic effects. "
04/01/1997 - "In anesthetized ferrets, BMS-180448 (2 mg/kg) or vehicle was infused i.v. during a 40-min interval beginning 1) 10 min before coronary occlusion, 2) at the 45th min of ischemia or 3) at the 5th min of reperfusion. "
|1.||Adenosine Triphosphate (ATP)
|2.||Potassium Channels (Potassium Channel)
|7.||Proteins (Proteins, Gene)
|9.||Nitric Oxide (Nitrogen Monoxide)
|10.||Methoxamine (Methoxamine Hydrochloride)
|1.||Induced Heart Arrest (Cardioplegia)