Visner M S, Arentzen C E, Parrish D G, Larson E V, O'Connor M J, Crumbley A J, Bache R J, Anderson R W
Circulation. 1985 Mar;71(3):610-9. doi: 10.1161/01.cir.71.3.610.
The alterations in regional diastolic mechanics that occur during regional myocardial ischemia (creep and increased myocardial stiffness) may be the result of interactions between the ischemic and surrounding nonischemic myocardium rather than the direct result of ischemia. Thus similar changes may not occur when the entire left ventricle is ischemic. Thus similar changes may not occur when the entire left ventricle is ischemic. To investigate this proposition, left ventricular diastolic mechanics were studied in seven chronically instrumented conscious dogs during global left ventricular ischemia. The anterior-posterior, septal-free wall, and base-apex axes of the left ventricle were measured with ultrasonic dimension transducers. Left and right ventricular pressures were measured with micromanometers. Myocardial blood flows were measured with left atrial injections of 15 microns radioactive microspheres. Global left ventricular ischemia was induced by hydraulic constriction of the left main coronary artery, which resulted in a 54% decrease in mean left ventricular subendocardial blood flow. Left ventricular volume, midwall circumference, and midwall circumferential stress were calculated from ellipsoidal shell theory. To construct pressure-strain and stress-strain relationships from diastolic data collected during vena caval occlusions, all measured and calculated dimensions were normalized to Lagrangian strains (fractional extension from unstressed dimension). During ischemia, creep (elongation of unstressed dimension) occurred in each of the three left ventricular axes. The mean unstressed dimension of the anterior-posterior axis increased from 5.39 +/- 0.53 to 5.85 +/- 0.50 cm ( p less than or equal to .05); the septal-free wall unstressed dimension increased from 5.11 +/- 0.53 to 5.72 +/- 0.80 cm (p less than or equal to .05); and the base-apex unstressed dimension increased from 7.04 +/- 0.61 to 7.25 +/- 0.65 cm (p less than or equal to .05). The relationship between diastolic midwall circumferential stress and strain shifted upward and to the left with ischemia, indicating that an increase in intrinsic myocardial stiffness had occurred. As a result of these mechanical alterations, there was a decrease in left ventricular chamber compliance that was manifested by a leftward shift of the diastolic pressure-volume strain relationship. Neither systolic bulging nor dysynchronous systolic shortening occurred in any of the three left ventricular spatial axes during ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)
局部心肌缺血期间发生的局部舒张力学改变(蠕动和心肌僵硬度增加)可能是缺血心肌与周围非缺血心肌相互作用的结果,而非缺血的直接结果。因此,当整个左心室缺血时,可能不会出现类似变化。为了研究这一命题,在七只长期植入仪器的清醒犬身上,于左心室整体缺血期间对左心室舒张力学进行了研究。用超声尺寸换能器测量左心室的前后径、室间隔-游离壁径和心底-心尖径。用微测压计测量左、右心室压力。通过向左心房注射15微米放射性微球来测量心肌血流量。通过液压收缩左冠状动脉主干诱导左心室整体缺血,这导致左心室平均心内膜下血流量减少54%。根据椭球壳理论计算左心室容积、中层圆周和中层圆周应力。为了根据腔静脉闭塞期间收集的舒张期数据构建压力-应变和应力-应变关系,将所有测量和计算的尺寸归一化为拉格朗日应变(从未受力尺寸的分数伸长)。缺血期间,左心室的三个轴均出现蠕动(未受力尺寸的伸长)。前后径的平均未受力尺寸从5.39±0.53厘米增加到5.85±0.50厘米(p≤0.05);室间隔-游离壁未受力尺寸从5.11±0.53厘米增加到5.72±0.80厘米(p≤0.05);心底-心尖未受力尺寸从7.04±0.61厘米增加到7.25±0.65厘米(p≤0.05)。缺血时,舒张期中层圆周应力与应变的关系向上向左移动,表明心肌固有僵硬度增加。由于这些力学改变,左心室腔顺应性降低,表现为舒张期压力-容积应变关系向左移位。缺血期间,左心室的三个空间轴均未出现收缩期膨出或不同步收缩期缩短。(摘要截短于400字)