STRUCTURAL BASIS FOR CHANGES IN LEFT-VENTRICULAR FUNCTION AND GEOMETRY BECAUSE OF CHRONIC MITRAL REGURGITATION AND AFTER CORRECTION OF VOLUME OVERLOAD
STRUCTURAL BASIS FOR CHANGES IN LEFT-VENTRICULAR FUNCTION AND GEOMETRY BECAUSE OF CHRONIC MITRAL REGURGITATION AND AFTER CORRECTION OF VOLUME OVERLOAD
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DOI：
10.1016/s0022-5223(19)33992-3
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发表时间：
1993-12-01
影响因子：
6
通讯作者：
CARABELLO, BA
中科院分区：
文献类型：
--
作者：
SPINALE, FG;ISHIHRA, K;CARABELLO, BA
对三组犬进行左心室功能和肌细胞结构检查：（1）腱索断裂导致二尖瓣关闭不全3个月（n = 7）； (2) 慢性二尖瓣反流，随后进行二尖瓣置换术和 3 个月的恢复期 (n = 7)，以及 (3) 假手术对照 (n = 8)。测量左心室收缩末期硬度常数（K(ess)）作为左心室收缩功能的指标，并通过电影导管插入术获得应力-应变关系。使用计算机辅助形态测定法检查分离的肌细胞结构和组成，并使用脱氧核糖核酸荧光计算核面积。与对照值相比，慢性二尖瓣反流的左心室收缩功能显着下降（K(ess)，2.1 +/- 0.1 对比 3.6 +/- 0.2；p < 0.05），并通过二尖瓣置换术恢复到对照值（3.8 +/- 0.2）。与对照组相比，二尖瓣反流组和二尖瓣置换组的左心室质量均显着增加（分别为 121 +/- 10、120 +/- 5 与 95 +/- 9 gm；p < 0.05）。肌细胞长度随二尖瓣反流增加超出对照值（194 +/- 4 对比 218 +/- 8 mum；p < 0.05），并在二尖瓣置换术后增加超过二尖瓣反流值（231 +/- 7 mum；p < 0.05）。二尖瓣反流时的肌细胞体积略有增加，超出了对照值（33.5 +/- 0.7 对比 37.6 +/- 1.3 mum3；p = 0.15），二尖瓣置换术后心肌细胞体积显着增加（40.1 +/- 1.2 mum3；p < 0.05）。与对照值相比，二尖瓣反流时肌细胞肌原纤维体积显着下降（14.8 +/- 1.5 对比 22.2 +/- 0.7 muM3；p < 0.05），并且显着增加，超过二尖瓣返流和二尖瓣置换术的对照值（27.1 +/- 1.1 muM3；p < 0.05）。二尖瓣反流的肌细胞核面积与对照值相比保持不变（1430 +/- 122 对比 1163 +/- 89 mum2），但随着二尖瓣置换术显着增加（2209 +/- 250 mum2；p < 0.05）。总之，慢性二尖瓣关闭不全的左心室收缩功能障碍伴随着肌细胞长度的增加和肌原纤维含量的减少。相反，二尖瓣置换术导致的左心室肥厚和左心室泵功能的改善是由于肌细胞体积增加和收缩蛋白含量增加所致。
Left ventricular function and myocyte structure were examined in three groups of dogs: (1) 3 months of mitral regurgitation caused by chordal rupture (n = 7); (2) chronic mitral regurgitation followed by mitral valve replacement and a 3-month recovery period (n = 7), and (3) sham controls (n = 8). The left ventricular end-systolic stiffness constant (K(ess)) was measured as an index of left ventricular contractile function with stress-strain relationships obtained by cinecatheterization. Isolated myocyte structure and composition were examined with computer-assisted morphometry and nuclear area computed with deoxyribonucleic acid fluorescence. Left ventricular contractile function was significantly depressed with chronic mitral regurgitation compared with control values (K(ess), 2.1 +/- 0.1 versus 3.6 +/- 0.2; p < 0.05) and returned to control values with mitral valve replacement (3.8 +/- 0.2). Left ventricular mass significantly increased in both the mitral regurgitation and mitral valve replacement groups compared with control values (121 +/- 10, 120 +/- 5 versus 95 +/- 9 gm, respectively; p < 0.05). Myocyte length increased with mitral regurgitation beyond control values (194 +/- 4 versus 218 +/- 8 mum; p < 0.05) and increased beyond mitral regurgitation values after mitral valve replacement (231 +/- 7 mum; p < 0.05). Myocyte volume with mitral regurgitation increased slightly beyond control values (33.5 +/- 0.7 versus 37.6 +/- 1.3 mum3; p = 0.15) and significantly increased with mitral valve replacement (40.1 +/- 1.2 mum3; p < 0.05). Myocyte myofibril volume significantly declined with mitral regurgitation compared with control values (14.8 +/- 1.5 versus 22.2 +/- 0.7 mum3; p < 0.05) and significantly increased beyond both mitral regurgitation and control values with mitral valve replacement (27.1 +/- 1.1 muM3; p < 0.05). Myocyte nuclear area with mitral regurgitation remained unchanged from control values (1430 +/- 122 versus 1163 +/- 89 mum2) but increased significantly with mitral valve replacement (2209 +/- 250 mum2; p < 0.05). In summary, the left ventricular contractile dysfunction with chronic mitral regurgitation is accompanied by increased myocyte length and reduced myofibril content. In contrast, the left ventricular hypertrophy and improved left ventricular pump function with mitral valve replacement were due to increased myocyte volume and increased contractile protein content.