Experimental Studies on the Occurrence of Cardiac Hypertrophy in Ischemic Heart and Its Possible Mechanisms

我们评估了反复短暂的冠状动脉闭塞是否会导致遭受可逆性缺血损伤的区域的心肌肥厚。在5只清醒犬上，测量了冠状动脉左回旋支(LCCA)灌注区心内膜下段长度和左心室压力。术后完全恢复，167例(平均)2min闭塞LCCA，持续22d。LCCA区的静息舒张末长度增加了6.6%(p&lt；0.05)。在组织学检查中，与左冠状动脉前降支(LAD)灌注区相比，LCCA区的心肌细胞大小有不成比例的增加(18.2 mU比15.4 mU，p&lt；0.05)。在另外5只犬中，LCCA区和LAD区的心肌细胞大小相似(14.2亩比14.0亩，p=NS)。我们的结论是，反复短暂的缺血发作导致局部心肌肥大局限于缺血区。最大结合…非缺血区与哌唑嗪结合的多部位密度(Bmax)为13.0+-6.5(fmol/mg蛋白)，缺血区为14.6；+-9.5(fmol/mg蛋白)。离解常数(K_D)非缺血区为0.17+-0.13(NM)，缺血区为0.17+-0.17(NM)。这两个参数没有显著差异。非缺血区与缺血区H-二氢别肾上腺素结合的Bmax，72.2&lt；+-+-gt；35.5(fmol/mg蛋白)和K_&lt；D‘&gt；1.00&lt；+--0.25(NM)与缺血区的Bmax：76.8；+-lt；25.8(fmol/mg蛋白)，K_&lt；D：&gt；1.43&lt；+--&gt；0.75(NM)无显著差异。非缺血区与缺血区PN200-100结合的Bmax，250&lt；+-gt；126(fmol/mg蛋白)和K_&lt；D‘&gt；0.24&lt；+-gt；0.03(NM)与缺血区的175&lt；+-gt；19(fmol/mg蛋白)和0.03&lt；+-gt；0.14(NM)也无显著差异。这些结果提示，反复结扎诱导心肌肥厚的机制可能与肾上腺素能α1和β受体及钙通道药物结合受体的数量和质量变化无关。较少

We evaluated whether repeated brief coronary occlusion induces myocardial hypertrophy in the region subjected to reversible ischemic insult. In 5 conscious dogs, a subendocardial segment length in the area perfused by the left circumflex coronary artery (LCCA) was measured along with left ventricular pressure. After complete recovery from surgery, 167 (mean) 2 min LCCA occlusions were repeated for 22 days. The resting end-diastolic segment length in the LCCA area was increased by 6.6% (p<0.05). On histologic examination, there was a disproportionate increase in myocardial cell size in the LCCA area compared with the area perfused by the left anterior descending coronary artery (LAD) (18.2 mu vs. 15.4 mu, p<0.05). In an additional similarly instrumented 5 dogs, myocardial cell size in the LCCA and LAD areas was comparable (14.2mu vs. 14.0mu, p=NS). We conclude that the repeated brief ischemic episodes induced regional myocardial hypertrophy confined to the ischemic area.The maximal bind … More ing site density (Bmax) for [^3] prazosin binding was 13.0<plus-minus>6.5 (fmol/mg protein) (mean <plus-minus>SD) in the nonischemic area and 14.6<plus-minus>9.5 (fmol/mg protein) in the ischemic area. The dissociation constant (K_D) was 0.17<plus-minus>0.13 (nM) in the nonischemic area and 0.17<plus-minus>0.17 (nM) in the ischemic area. Both the parameters were not significantly different. The Bmax, 72.2<plus-minus>35.5 (fmol/mg protein) and the K_<D'> 1.00<plus-minus>0.25 (nM) for H dihydroalloprenolol binding, in the nonischemic area were not significantly different from those (Bmax : 76.8<plus-minus>25.8 (fmol/mg protein), K_<D:> 1.43<plus-minus>0.75 (nM) in the ischemic area, respectively. The Bmax, 250<plus-minus>126 (fmol/mg protein) and the K_<D'> 0.24<plus-minus>0.03 (nM) for [^3H] (+) PN200-100 binding in the nonischemic area were also insignificantly different from 175<plus-minus>19 (fmol/mg protein) and 0.03<plus-minus>0.14 (nM) in the ischemic area, respectively. These results suggest that the mechanism contributing to myocardial hypertrophy induced by repeated occlusion appears to involve no quantitative and qualitative changes of adrenergic alpha1 and beta, and also calcium channel drug binding receptors. Less