EFFECTS OF LONG-TERM PRESSURE OVERLOAD ON REGIONAL MYOCARDIAL GLUCOSE AND FREE FATTY-ACID UPTAKE IN RATS - A QUANTITATIVE AUTORADIOGRAPHIC STUDY
EFFECTS OF LONG-TERM PRESSURE OVERLOAD ON REGIONAL MYOCARDIAL GLUCOSE AND FREE FATTY-ACID UPTAKE IN RATS - A QUANTITATIVE AUTORADIOGRAPHIC STUDY
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DOI：
10.1161/01.cir.81.4.1353
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发表时间：
1990-04-01
期刊：
影响因子：
37.8
通讯作者：
TAKISHIMA, T
中科院分区：
文献类型：
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作者：
KAGAYA, Y;KANNO, Y;TAKISHIMA, T
为了研究长期压力超负荷对局部心肌底物使用的影响，我们使用2-脱氧-D-[U-14 C]葡萄糖（14 C-DG）和β-葡萄糖进行定量放射自显影。甲基[1- 14 C]十七烷酸（14 C-BMHDA）在清醒大鼠与10周的升主动脉缩窄。心重/体重比，腹主动脉缩窄组较假手术组增加27%（P < 0.01）。心肌14 C-DG摄取增加（258 ± 0.01）。63对144 +-。41 nCi/g，p < 0.01，每组n = 6）;然而，14 C-BMHDA提取减少（251 . ±. 69对342 +-。75 nCi/g，p < 0.05，每组n = 7）。在假手术大鼠中，14 C-DG和14 C-BMHDA的摄取在左室前壁和侧壁高于后壁或室间隔。在动脉收缩大鼠，14 C-DG摄取也增加了室间隔，以及在左心室前壁和侧壁，与后壁相比。然而，这四个地区之间的14 C-BMHDA提取没有地区差异。4-[N-甲基-14 C]碘安替比林或肌细胞宽度测定的心肌血流分布显示，无论是在收缩性心肌收缩还是假手术大鼠，四个区域之间均无区域性差异。两组中局部间质纤维化均较小。目前的研究表明，心肌基质摄取改变不均匀，而且这种不均匀性不是因为血流分布，心肌细胞肥大或间质纤维化的区域变化。在其他假手术大鼠中，血管紧张素II诱导的急性压力超负荷的结果，其中心肌14 C-BMHDA提取显著增加（n = 3，p < 0.01），而14 C-DG摄取（n = 3）与正常血压假手术大鼠相比无差异，表明主动脉-缩窄的大鼠不是对左心室压力增加本身的直接反应，而是应该由与长期压力相关的未知因素来解释。超载。
To investigate the effects of long-term pressure overload on regional myocardial substrate use, we performed quantitative autoradiography using 2-deoxy-D-[U-14C]glucose (14C-DG) and .beta.-methyl[1-14C]heptadecanoic acid (14C-BMHDA) in conscious rats with a 10-week ascending aortic constriction. Heart weight/body weight ratio increased by 27% in aortic-constricted rats as compared with sham-operated rats (p < 0.01). Myocardial 14C-DG uptake increased (258 .+-. 63 vs. 144 .+-. 41 nCi/g, p < 0.01, n = 6 for each group); however, 14C-BMHDA extraction decreased (251 .+-. 69 vs. 342 .+-. 75 nCi/g, p < 0.05, n = 7 for each group) in aortic-constricted rats as compared with sham-operated rats. In sham-operated rats, both 14C-DG an 14C-BMHDA uptakes were higher in the left ventricular anterior and lateral walls as compared with the posterior wall or the interventricular septum. In aortic-constricted rats, 14C-DG uptake also increased in the interventricular septum, as well as in the left ventricular anterior and lateral walls, as compared with the posterior wall. There was, however, no regional difference in 14C-BMHDA extraction among these four regions. Myocardial blood flow distribution determined by 4-[N-methyl-14C]iodoantipyrine or myocyte width showed no regional variations among the four regions, either in aortic-constricted or sham-operated rats. Regional interstitial fibrosis was small in either group. The present study suggests that myocardial substrate uptake is altered nonhomogeneously, and that the nonhomogeneity is not because of regional variations in blood flow distribution, myocyte hypertrophy, or interstitial fibrosis. The results of angiotensin II-induced acute pressure overloading in other sham-operated rats, in which a remarkable increase in myocardial 14C-BMHDA extraction (n = 3, p < 0.01) and no difference in 14C-DG uptake (n = 3) as compared with normotensive sham-operated rats were elicited, suggest that the findings in aortic-constricted rats are not direct responses to increased left ventricular pressure itself but rather should be explained by still unknown factors related to prolonged pressure overload.