Glower D D, Schaper J, Kabas J S, Hoffmeister H M, Schaper W, Spratt J A, Davis J W, Rankin J S
Circ Res. 1987 Jun;60(6):850-60. doi: 10.1161/01.res.60.6.850.
Although prolonged functional abnormalities after transient myocardial ischemia have been well described, the interrelationship between postischemic systolic and diastolic alterations remains controversial. Therefore, 24 chronically instrumented conscious dogs were studied with left ventricular and pleural micromanometers, ultrasonic dimension transducers in the left anterior descending (LAD) coronary distribution, and vena caval and coronary artery occluders. The LAD was occluded for 15 minutes and reperfused for 24 hours while vena caval occlusions were performed at intervals to measure myocardial segment length at 0 mm Hg transmural diastolic left ventricular pressure (L0). Coronary occlusion produced an immediate fall in systolic function as assessed by ejection shortening and stroke work and also induced a 16 +/- 4% increase in L0, which was termed diastolic creep. Throughout reperfusion, reversal of diastolic abnormalities correlated strongly with recovery of segmental shortening and stroke work (p less than 0.001). Correlation between systolic dysfunction and diastolic creep was also observed during alteration of inotropic state by dopamine, during initial reperfusion hyperfunction, and during pharmacologic manipulation of afterload. In 5 additional dog hearts fixed in diastole by rapid glutaraldehyde infusion after coronary occlusion, myocardial creep measured by the segment length transducers paralleled sarcomere elongation measured by electron microscopy. Thus, the direct correlation between diastolic creep and systolic dysfunction throughout reperfusion and during hemodynamic alterations suggests that diastolic properties of postischemic myocardium may not be entirely passive and that systolic and diastolic dysfunction induced by ischemia may have a common basis at the cellular level.
尽管短暂性心肌缺血后长期的功能异常已得到充分描述,但缺血后收缩期和舒张期改变之间的相互关系仍存在争议。因此,对24只长期植入仪器的清醒犬进行了研究,使用左心室和胸膜微压计、左前降支(LAD)冠状动脉分布区域的超声尺寸换能器以及腔静脉和冠状动脉阻塞器。LAD阻塞15分钟,再灌注24小时,同时间隔进行腔静脉阻塞,以测量在0 mmHg跨壁舒张期左心室压力(L0)时的心肌节段长度。冠状动脉阻塞导致射血缩短和搏功评估的收缩功能立即下降,还引起L0增加16±4%,这被称为舒张期蠕动。在整个再灌注过程中,舒张期异常的逆转与节段缩短和搏功的恢复密切相关(p<0.001)。在多巴胺改变心肌收缩力状态期间、初始再灌注功能亢进期间以及后负荷的药物操作期间,也观察到收缩功能障碍与舒张期蠕动之间的相关性。在冠状动脉阻塞后通过快速注入戊二醛使另外5只犬心在舒张期固定,通过节段长度换能器测量的心肌蠕动与通过电子显微镜测量的肌节伸长平行。因此,在整个再灌注过程和血流动力学改变期间舒张期蠕动与收缩功能障碍之间的直接相关性表明,缺血后心肌的舒张特性可能并非完全被动,并且缺血诱导的收缩期和舒张期功能障碍可能在细胞水平上有共同的基础。