J Korean Soc Emerg Med.
1998 Dec;9(4):496-504.
Deferoxamine Pretreatment Reduces Infarct Size of Acute Myocardial Infarction in a Rabbit Model
Abstract
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BACKGROUND: Reperfusion of ischemic myocardium has been postulated to result in a specific oxygen radical mediated tissue injury. Iron may liberate during ischemia and we hypothesized that administration of the iron chelator, deferoxamine during ischemia would result in improved recovery after postischemic reperfusion.
PURPOSE: To test whether iron-catalyzed processes contribute to myocardial necrosis during ischemia and reperfusion, deferoxamine was administered to block iron catalyzed hydroxyl radical formation in rabbits.
METHODS
Eleven rabbits were divided into two groups: control group (n=5) and deferoxamine pretreatment group (n=6). the left circumflex coronay artery was ligated for 30 minutes and reperfused for 180 minutes. Area at risk (AR) was measured by non-stained area with ethylene blue injection into left atrium after left circumflex coronary artery ligation. Infarct size was measured by weighing after tripheyltetrazolium chloride staining. Heart rate was measured using electrocardiographic recording and systemic blood pressure was monitored by pressure transducer connected to the catheter in the left ventricle.
RESULTS
1. There was no significant difference of heart rate and blood pressure in deferoxamine pretreatment group compared with control group. 2. There was significant decrease of serum iron concentration after continuous infusion of deferoxamine compared with serum iron concentration before ligation of coronary artery (P<0.05). 3. There was no significant difference of area at risk between control and deferoxamine pretreatment group. 4. Area at necrosis to area at risk was significantly reduced in deferoxamine pretreatment group compared with control group (P<0.05) The results suggest that deferoxamine infusion prior to coronary artery occlusion has a significant benefit in reducing infarct size in this model.
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