Knowlton A A, Apstein C S, Saouf R, Brecher P
Cardiovascular Institute, Boston University School of Medicine, MA 02118.
J Mol Cell Cardiol. 1989 Jun;21(6):577-83. doi: 10.1016/0022-2828(89)90823-7.
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.
脂肪酸及其代谢产物被认为是缺血期间心肌损伤的一个原因。脂肪酸结合蛋白（FABP）是一种存在于心肌细胞胞质溶胶中的丰富的低分子量蛋白质，据推测它是心肌中关键的脂肪酸载体蛋白。我们推测，缺血期间FABP的缺失可能会导致细胞内未结合脂肪酸增加，从而导致心肌损伤，于是我们测量了大鼠心肌缺血60分钟后再灌注60分钟期间的血浆FABP水平。再灌注15分钟后出现峰值水平。心肌缺血面积较大时血浆水平更高（大面积为1720±528 ng/ml，小面积为216±76 ng/ml，P<0.02）。缺血60分钟和再灌注60分钟后的组织水平下降了50%以上（1.0±0.3 mg FABP/g湿重，而正常心肌为2.9±0.4 mg FABP/g湿重，P<0.005）。这些数据与FABP的缺失导致与缺血和再灌注相关的心肌损伤这一观点一致。需要进一步的研究来确定FABP在心脏脂肪酸代谢调节中的具体作用。
