Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion.
Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion.
复制标题
长期冠状动脉狭窄产生的持续局部功能障碍：再灌注后逐渐恢复。
DOI：
10.1161/01.cir.68.1.170
复制
发表时间：
1983
期刊：
影响因子：
37.8
通讯作者：
RossJr,J
中科院分区：
文献类型：
--
作者：
Matsuzaki,M;Gallagher,KP;Kemper,WS;White,F;RossJr,J
研究人员对 10 只清醒的狗进行长期非透壁性缺血研究，并研究了再灌注的早期和晚期影响。使用液压封堵器产生 5 小时的部分回旋冠状动脉狭窄，然后在 20 分钟内逐渐释放，测量左心室压力、局部心肌功能（通过声测法测量收缩壁增厚）、冠状动脉血流速度（脉冲多普勒）和心肌血流量（微球）。在冠状动脉狭窄期间，经常调整封堵器，以将收缩期壁增厚减少至对照的 50% 至 75%（平均对照的 62.6%）。部分冠状动脉狭窄 4 小时时，心肌内层缺血区域的心肌血流量减少（心内膜下，从对照时的 0.81 +/- 0.18 到 0.36 +/- 0.08 SD，p 小于 0.01；中壁，从 0.77 +/- 0.20 到 0.46 +/- 0.07 ml/min/g，p小于 0.01），伴有心内膜下电图 ST 段显着抬高（0.83 +/- 0.96 至 4.58 +/- 4.10 mV；p 小于 0.05），左心室 dP/dt 降低（3503 +/- 462 至 2991 +/- 339 mm Hg/sec；p 小于 0.01）。部分冠状动脉狭窄完全解除后几分钟内，ST段恢复控制，内层心肌血流量增加（心内膜下，1.37 +/- 0.39，p小于0.01；中壁，0.97 +/- 0.28，p小于0.05），但收缩期壁增厚和左心室dP/dt显着降低，并保持在24、48和48之间。 72小时时心肌血流正常。到第 7 天，收缩期壁增厚和左心室 dP/dt 已恢复到控制（分别为控制的 94.1 +/- 7.0%，3353 +/- 605 mm Hg/sec；NS）。缺血引起的组织学变化仅占缺血壁晶体间组织的2.7%（平均），但不含晶体的后乳头肌缺血性损伤占31.9%。因此，5小时非透壁缺血减轻的局部心肌功能障碍持续至少3天，左心室游离壁仅有轻微损伤，但后乳头肌有相当大的梗塞。然后，游离壁的区域和整体收缩功能在 1 周内完全恢复。
Prolonged nontransmural ischemia was produced and the early and late effects of reperfusion were studied in 10 conscious dogs instrumented over the long term. Five hours of partial circumflex coronary artery stenosis was produced with a hydraulic occluder, followed by gradual release over 20 min, with measurements of left ventricular pressure, regional myocardial function (systolic wall thickening by sonomicrometry), coronary blood flow velocity (pulsed Doppler), and myocardial blood flow (microspheres). During coronary stenosis the occluder was adjusted frequently to maintain a reduction of systolic wall thickening to 50% to 75% of control (average 62.6% of control). Myocardial blood flow in the ischemic area at 4 hr of partial coronary stenosis was reduced in the inner layers of the myocardium (subendocardium, from 0.81 +/- 0.18 at control to 0.36 +/- 0.08 SD, p less than .01; midwall, from 0.77 +/- 0.20 to 0.46 +/- 0.07 ml/min/g, p less than .01), accompanied by significant ST segment elevation on the subendocardial electrogram (0.83 +/- 0.96 to 4.58 +/- 4.10 mV; p less than .05) and decreased left ventricular dP/dt (3503 +/- 462 to 2991 +/- 339 mm Hg/sec; p less than .01). Within a few minutes after complete release of partial coronary stenosis, ST segments returned to control and myocardial blood flow of the inner layers was increased (subendocardium, 1.37 +/- 0.39, p less than .01; midwall, 0.97 +/- 0.28, p less than .05), but systolic wall thickening and left ventricular dP/dt were significantly depressed and remained reduced at 24, 48, and 72 hr when myocardial blood flow was normal. By seven days, systolic wall thickening and left ventricular dP/dt had returned to control (94.1 +/- 7.0% of control, 3353 +/- 605 mm Hg/sec, respectively; NS). Histologic changes caused by ischemia constituted only 2.7% (average) of the tissue between the crystals in the ischemic wall, but ischemic damage in the posterior papillary muscle, which did not contain crystals, was 31.9%. Thus, regional myocardial dysfunction reduced by nontransmural ischemia for 5 hr persisted for at least 3 days, with only slight damage to the left ventricular free wall but considerable infarction of the posterior papillary muscle. Full recovery of regional and global contractile function of the free wall then occurred within a period of 1 week.