Mitochondrial preference for short chain fatty acid oxidation during coronary artery constriction
Mitochondrial preference for short chain fatty acid oxidation during coronary artery constriction
复制标题
DOI：
10.1161/hc0302.102594
复制
发表时间：
2002-01-22
期刊：
影响因子：
37.8
通讯作者：
Vatner, SF
中科院分区：
文献类型：
--
作者：
Lewandowski, ED;Kudej, RK;Vatner, SF
背景-低灌流心肌中减少的脂肪酸氧化被认为是由于线粒体氧化受损所致。这项研究提出了另一种机制，即氧化能力超过了长链脂肪酸(LCFA)的调节进入。方法与结果：在非缺血对照组(n=4)和左前降支(LAD)血流减少5h后(n=7)，左冠状动脉前降支(LAD)分别注入短链脂肪酸[2-C-13]丁酸盐(4 mmoL/L)和葡萄糖(10 mmoL/L)40min。左前降支收缩时，左室壁厚度下降45%+/-8%(P
Background-Reduced fatty acid oxidation in hypoperfused myocardium is believed to result from impaired oxidation in mitochondria. This study suggests another mechanism, that oxidative capacity exceeds regulated entry of long chain fatty acid (LCFA). The ability of myocardium to oxidize fatty acids and metabolize glucose during stenosis was examined in open chest, anesthetized pigs.Methods and Results-The left anterior descending (LAD) coronary artery was infused for 40 minutes (5 mL/min LAD) with [2-C-13] butyrate (4 mmol/L), a short chain fatty acid (SCFA), plus [2-C-13] glucose (10 mmol/L) in either nonischemic controls (n=4) or at the end of 5 hours of LAD flow reduction (40%, n=7). With LAD constriction, left ventricular wall thickening fell 45+/-8% (P