Neumann T, Vollmer A, Schaffner T, Hess O M, Heusch G
Department of Pathophysiology, Center of Internal Medicine, University of Essen, FRG.
J Mol Cell Cardiol. 1999 Jan;31(1):179-92. doi: 10.1006/jmcc.1998.0853.
Heart failure is characterized not only by systolic, but also by diastolic dysfunction. The present study tested whether or not diastolic dysfunction is associated with changes in tissue properties and collagen network structure. Heart failure was induced in seven chronically instrumented, conscious dogs by rapid left ventricular pacing (2 50 min(-1)). After 2-5 [mean: 4+/-1 (S.D.)] weeks pacing, heart failure was apparent from clinical symptoms (ascites, cachexia, edema, exercise intolerance) and hemodynamic parameters (significant increases of heart rate and left ventricular end-diastolic pressure and decreases of left ventricular maximal pressure, dP/dtmax and systolic wall thickening). The left ventricle was dilated, as indicated by a decrease of end-diastolic wall thickness (6.3+/-2.0 v 7.2+/-2.1 mm; P<0.05; sonomicrometry). The left ventricular end-diastolic pressure-strain relation (strain: relative change of end-diastolic wall thickness) was obtained during alterations of loading conditions by inferior caval vein and descending thoracic aortic occlusion. The slope of this relation increased from 85+/-20 to 428+/-188 in heart failure, indicating an increase of left ventricular stiffness. Collagen was stained with picrosirius red and analyzed using polarized light microscopy. In heart failure, the collagen volume fraction remained unchanged (1.9+/-1.2 v 2.3+/-1.3%; N.S.), while the nonuniformity of collagen orientation, as reflected by its standard deviation, was increased (11.1+/-1.8 v 6.1+/-0.4 o; P<0.05). The nonuniformity of collagen fiber orientation correlated with left ventricular stiffness [r=0.75].
心力衰竭不仅以收缩功能障碍为特征，还以舒张功能障碍为特征。本研究测试了舒张功能障碍是否与组织特性和胶原网络结构的变化相关。通过快速左心室起搏（250次/分钟）在7只长期植入仪器的清醒犬中诱发心力衰竭。起搏2 - 5周（平均：4±1（标准差））后，从临床症状（腹水、恶病质、水肿、运动不耐受）和血流动力学参数（心率、左心室舒张末期压力显著增加，左心室最大压力、dP/dtmax和收缩期室壁增厚降低）可以明显看出心力衰竭。如舒张末期室壁厚度降低所示（6.3±2.0对7.2±2.1毫米；P<0.05；超声心动图），左心室扩张。通过下腔静脉和降主动脉闭塞改变负荷条件时，获得左心室舒张末期压力 - 应变关系（应变：舒张末期室壁厚度的相对变化）。心力衰竭时，该关系的斜率从85±20增加到428±188，表明左心室僵硬度增加。用苦味酸天狼星红对胶原进行染色，并使用偏振光显微镜进行分析。在心力衰竭中，胶原体积分数保持不变（1.9±1.2对2.3±1.3%；无显著性差异），而胶原取向的不均匀性（以其标准差反映）增加（11.1±1.8对6.1±0.4度；P<0.05）。胶原纤维取向的不均匀性与左心室僵硬度相关[r = 0.75]。
