Pressure overload surgery does not induce cardiac fibrosis in the American alligator
Pressure overload surgery does not induce cardiac fibrosis in the American alligator
复制标题
压力超负荷手术不会诱发美洲鳄心脏纤维化
DOI：
10.1096/fasebj.25.1_supplement.858.12
复制
发表时间：
2011
期刊：
影响因子：
--
通讯作者：
James Hicks
中科院分区：
文献类型：
--
作者：
Colin Campbell;T. Owerkowicz;J. Eme;J. Blank;James Hicks
在鳄鱼的双主动脉弓系统中，右主动脉从左心室出现，左主动脉（LAo）从右心室出来。LAo允许潜在的肺分流（R-L分流）。LAo的手术消融已被用于测试鳄鱼R-L分流的功能意义。在早期的研究中，左心耳消融导致更大（+65%）的心室质量，更高的DNA含量和双倍的峰值收缩压，但肥大的确切性质尚未描述。我们比较了接受LAo消融术或假手术的幼年短吻鳄的心室横截面。动物要么久坐不动，要么每隔一天锻炼一次。Masson三色染色的组织学评估显示正常心肌生长，具有最小（<2%）的纤维化组织积聚，并且治疗组之间没有显著差异（n=5）。生理性（肌肉）肥大是对定期运动的预期反应，而病理性（纤维化）肥大见于面临慢性压力超负荷的哺乳动物（例如，主动脉束带）。我们的研究结果表明，短吻鳄能够令人印象深刻的心脏可塑性，而不会遭受病理性纤维化的心肌。这种现象与蟒蛇餐后心脏肥大的程度相似。爬行动物心肌生长能力背后的分子机制仍有待阐明。由NSF IOB 00445680资助。
In the dual aortic arch system of crocodilians, the right aorta emerges from the left ventricle, and the left aorta (LAo) exits the right ventricle. The LAo allows for potential pulmonary bypass (R‐L shunt). Surgical ablation of the LAo has been used to test the functional significance of R‐L shunting in alligators. In earlier studies, LAo ablation caused greater (+65%) ventricular mass, higher DNA content and doubled peak systolic pressures, but the exact nature of hypertrophy has not been described. We compared ventricular cross‐sections from juvenile alligators who had undergone LAo ablation or sham surgery. Animals were either sedentary or exercised every other day. Histologic assessment with Masson's trichrome stain showed normal myocardial growth, with minimal (<2%) fibrotic tissue accumulation, and no significant difference between treatment groups (n=5). Physiologic (muscular) hypertrophy is an expected response to regular exercise, and pathologic (fibrotic) hypertrophy is seen in mammals faced with chronic pressure overload (e.g., aortic banding). Our results suggest alligators are capable of impressive cardiac plasticity, without suffering pathologic fibrosis in the myocardium. This phenomenon parallels the magnitude of post‐prandial cardiac hypertrophy in pythons. Molecular mechanisms behind myocardial growth capacity in reptiles remain to be elucidated. Funded by NSF IOB 00445680.