Low invasive therapy with gratnilotyte colony stimulating factor in patients with coronary artery dicease

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1) In patients with acute myocardial infarction, subcutaneous treatment with G-CSF at a dose of 2-5 mg/kg significantly improved ejection fraction at 1 months after myocardial infarction assacsed by left ventriculogram (Suzuki K, et. al. Circ J 2006)2) Rabbits underwent 30 min of coronary occlusion followed by 48 hours of reperfusion Pravastatin (1 or 5mg/kg) or saline was intravenously administered 10 min before ischemia. Pravastatin (5mg/kg) was also administered 10 min before reperfusion. L-NAME (10mg/kg), chelerythrine (5mg/kg) or 5-HD (5mg/kg) was i.v. administered 10 min before pravastatin injection. The infarct size was determined. The myocardial interstitial levels of 2, 5-DHBA and NOx, and the intensity of myocardial dihydroethidium staining were obtained. Pre-ischemic treatment with pravastatin reduced the infarct size (34±5% and 24±4%, 1 and 5mg/kg, respectively) but not pre-reperfusion treatment (42.1±3.7%) compared with the control (45±3%). This effect was blocked by L-NAME (42.6±4%), chelerythrine (50.9±3%) and 5-HD (52.7±2%), respectively. Pre-ischemic treatment with pravastatin increased myocardial NOx levels and attenuated the 2,5-DHBA levels and the intensity of dihydroethidium staining during reperfusion. Chelerythrine abolished the increase in NOx levels by pravastatin. Pre-ischemic treatment with pravastatin reduces the myocardial infarct size via protein kinase C-dependent nitric oxide production, decreasing hydroxyl radicals and superoxide, and opening the mitochondrial KATP channels.