IMPAIRED THICKENING OF NONISCHEMIC MYOCARDIUM DURING ACUTE REGIONAL ISCHEMIA IN THE DOG
IMPAIRED THICKENING OF NONISCHEMIC MYOCARDIUM DURING ACUTE REGIONAL ISCHEMIA IN THE DOG
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DOI：
10.1161/01.cir.71.5.1048
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发表时间：
1985-01-01
期刊：
影响因子：
37.8
通讯作者：
WEISS, JL
中科院分区：
文献类型：
--
作者：
LIMA, JAC;BECKER, LC;WEISS, JL
为研究局部缺血后非缺血心肌的局部功能，在18只麻醉开胸犬上建立了冠状动脉回旋支分级狭窄模型。二维超声心动图视图在每个闭塞程度的横截面上获得，该横截面由缝到左心室心外膜的2至3个金属珠标记。在左心室周围16个等距点处测量收缩期增厚百分比，并与微球确定的局部心肌血流量相关。基线增厚平均为44.9 ±。百分之六点四在透壁缺血期间，收缩期增厚百分比下降至-16.1 . ±-。在缺血区域中为4.0%，并且在邻近的非缺血区域中也降低（至2.4 ± 4.0%）。在最接近缺血区域[邻近1]的节段中为2.4%，在最接近缺血区域[邻近1]的节段中为15.5 ±-。3.9在更远的节段中[相邻2]），但在缺血区域的正对面节段中（远端区域）无变化。在内膜下缺血期间，收缩期增厚的百分比仅在缺血区和邻近区域下降（1.4 ± 0.05）。5.2%和24.9 ±。5.0%）。在透壁缺血期间，对7只犬静脉注射0.21至0.42 mg/min双嘧达莫，导致非缺血区血流增加3至5倍，缺血区血流无变化;任何区域的功能均未改变。在透壁缺血期间，对5只犬静脉注射普萘洛尔0.1 mg/kg，以抑制远端区域的收缩力。收缩期增厚百分比在远程下降（从50.0 .+-。7.7%至34.6 .+-。5.6%），但在相邻的1个增加（从-0.25 . ±. 3.7%至15.2 .+-。3.9%）和相邻2例（17.4 ±. 2.8%至33.4 .+-。3.9%），缺血区无变化。在透壁缺血期间，紧邻缺血区域的非缺血心肌的收缩期增厚百分比显著受损，而在距离缺血边界相对较远的区域受损程度较低。因此，功能障碍高估了冠状动脉完全闭塞后局部缺血的程度。在内膜下缺血期间，缺血区域的功能停止，非缺血心肌的功能损害仅限于紧邻区域。邻近区域的功能障碍不是由局部氧需求增加或盗血现象相关的相对缺血引起的。继发于收缩期间左心室形状变化的邻近缺血区域的非缺血心肌的机械束缚可能导致透壁缺血期间邻近区域的收缩期增厚受损。
To study the regional function of nonischemic myocardium after the onset of regional ischemia, graded circumflex coronary arterial stenosis was induced in 18 open-chest anesthetized dogs. Two-dimensional echocardiographic views were obtained at each degree of occlusion in a cross-sectional plane marked by 2 to 3 metal beads sewn to the left ventricular epicardium. Percent systolic thickening was measured at 16 equally spaced points around the left ventricle and correlated with microsphere-determined regional myocardial blood flow. Baseline thickening averaged 44.9 .+-. 6.4%. During transmural ischemia percent systolic thickening decreased to -16.1 .+-. 4.0% in the ischemic region and also decreased in adjacent nonischemic regions (to 2.4 .+-. 2.4% in segments closest to the ischemic region [adjacent 1] and to 15.5 .+-. 3.9 in segments further away [adjacent 2]), but was unchanged in segments directly opposite the ischemic region (remote region). During subendocardial ischemia, percent systolic thickening fell only in the ischemic and adjacent 1 regions (1.4 .+-. 5.2% and 24.9 .+-. 5.0%, respectively). Dipyridamole, 0.21 to 0.42 mg/min i.v. given to 7 dogs during transmural ischemia, caused a 3- to 5-fold increase in flow to the nonischemic and no change in flow to the ischemic region; function was not altered in any region. Propranolol, 0.1 mg/kg i.v. was given to 5 dogs during transmural ischemia to depress contractility in the remote region. Percent systolic thickening fell in the remote (from 50.0 .+-. 7.7% to 34.6 .+-. 5.6%), but increased in adjacent 1 (from -0.25 .+-. 3.7% to 15.2 .+-. 3.9%) and in adjacent 2 (from 17.4 .+-. 2.8% to 33.4 .+-. 3.9%) regions and remained unchanged in the ischemic region. During transmural ischemia percent systolic thickening is markedly impaired in nonischemic myocardium immediately adjacent to the ischemic region and is impaired to a lesser degree in regions located relatively far from the ischemic border. Dysfunction therefore overestimates the extent of regional ischemia after total coronary occlusion. During subendocardial ischemia function ceases in the ischemic region and functional impairment of nonischemic myocardium is restricted to immediately adjacent regions. Dysfunction of adjacent regions is not caused by relative ischemia related to increased local O2 demands or to a steal phenomenon. Mechanical tethering of nonischemic myocardium adjacent to ischemic regions, secondary to changes in left ventricular shape during contraction, may contribute to the impairment of systolic thickening in adjacent regions during transmural ischemia.