乳清酸对急性心肌梗塞非梗塞区心肌线粒体的有益作用

Beneficial Effect of Orotic Acid on Mitochondria of Noninfarcted Myocardium after Acute Myocardial Infarction

结扎大鼠冠状动脉前降支造成急性心肌梗塞（ＡＭＩ），分成乳清酸治疗组（ＡＭＩＯＡ），生理盐水治疗组（ＡＭＩＮＳ）和假手术组（ＳＯＮＳ）。观察非梗塞区心肌线粒体功能、结构及心肌纤维的改变。在ＡＭＩ后２４，７２ｈ，ＡＭＩＮＳ组Ｒ３，ＲＣＲ，ＯＰＲ有意义降低，ＡＭＩＯＡ组则明显增加（Ｐ＜０．０１），且与ＳＯＮＳ组相似（Ｐ＞０．０５）。ＡＭＩＮＳ组非梗塞区心肌超微结构，特别是边缘区表现为线粒体基质减少，外膜崩解，嵴模糊；肌纤维Ⅰ带增宽，Ｚ线突出，扭曲或断裂，收缩带形成。在ＡＭＩＯＡ组上述结构基本正常。结果提示：乳清酸保护了非梗塞区心肌功能和结构。其可能机制是乳清酸增加蛋白质和磷脂的合成，修复了线粒体结构。

Acute myocardial infarction was produced in rats through ligating the left anterior descending coronary artery. These rats were divided into three groups: orotic acid-treated group(AMIOA), 0.9% sodium chloride solution-treated group(AMINS) and sham-operation group(SONS). The function of mitochondria, ultrastructure of mitochondria and myofibril in noninfarcted myocardium area had been observed. On 24 th, 72 nd hour after AMI, R3, P/O, RCR and OPR significantly decreased in AMINS group., while markly increased in AMIOA group(P<0.01) which was similar to that in SONS group. Ultrastructure of noninfarcted myocardium especially border area in AMINS showed that: matrix of mitochondria reduced, outer membrane ruptured, cristae disorganized with much damage, I band enlarged, Z line stood out, zigzaged or discontinued,contraction band formed, while these chnages in AMIOA group were mainly normal. These results indicate that orotic acid improved function and structure of noninfarcted myocardium. The possible mechanism is that orotic acid may increase biosynthesis of protien and phospholipid, and repair structure of mitochondria.