Key result
Rat myocardial ischemia-reperfusion reduces tissue FABP ~66% and raises plasma levels correlating with ischemia area.
p-value: p=<0.005
Loss of FABP during ischemia and reperfusion in rats suggests its leakage may contribute to myocardial damage.
FABP leakage may exacerbate ischemic injury in rats; hypothesis-generating for biomarker or therapeutic roles, requiring human validation.
Fatty acids and their metabolites have been implicated as a cause of myocardial damage during ischemia. Fatty acid binding protein (FABP), an abundant low molecular weight protein present in the cytosol of myocytes, has been postulated to be a key fatty acid carrier protein in the myocardium. Postulating that loss of FABP during ischemia could cause an increase in unbound intracellular fatty acids contributing to myocardial damage, we measured plasma FABP levels during 60 min of myocardial ischemia followed by 60 min of reperfusion in the rat. Peak levels were seen 15 min after reperfusion. Plasma levels were higher with larger areas of myocardial ischemia (1720 +/- 528 ng/ml vs. 216 +/- 76 ng/ml with smaller areas, P less than 0.02). Tissue levels after 60 min of ischemia and 60 min of reperfusion were decreased by over 50%, (1.0 +/- 0.3 mg FABP/g wet wt compared with 2.9 +/- 0.4 mg FABP/g wet wt in normal myocardium, P less than 0.005). The data is consistent with the proposal that loss of FABP contributes to the myocardial damage associated with ischemia and reperfusion. Additional studies are needed to determine the exact role of FABP in the regulation of fatty acid metabolism in the heart.
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Anne A. Knowlton (1989) studied Myocardial ischemia and reperfusion. Myocardial ischemia and reperfusion vs. Normal myocardium / smaller areas of ischemia was evaluated on Plasma and tissue FABP levels (p=<0.005). Myocardial ischemia and reperfusion in rats led to significantly decreased tissue FABP levels (1.0 vs 2.9 mg/g, P<0.005) and increased plasma FABP levels that correlated with the area of ischemia.
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