Recovery of regional contractile function and oxidative metabolism in stunned myocardium induced by 1-hour circumflex coronary artery stenosis in chronically instrumented dogs.

Recovery of regional contractile function and oxidative metabolism in stunned myocardium induced by 1-hour circumflex coronary artery stenosis in chronically instrumented dogs.
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长期仪器狗 1 小时回旋冠状动脉狭窄引起的心肌顿挫的局部收缩功能和氧化代谢的恢复。

DOI:
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发表时间:
1993
影响因子:
20.1
通讯作者:
J. Melin
J. Melin
中科院分区:
医学1区
文献类型:
--
作者:
G. Heyndrickx;W. Wijns;D. Vogelaers;Y. Degrieck;A. Bol;G. Vandeplassche;J. Melin

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采用正电子发射断层扫描(PET)技术,对冠脉严重狭窄1小时所致顿抑心肌局部机械功能及整体氧化和脂肪酸代谢的变化进行了评价。27只犬,长期测量正常和缺血区的左心室压力和局部心肌壁增厚,造成1小时的心肌缺血,这是由于冠状动脉左回旋支分级狭窄造成的,导致最小的残余血流。缺血区冠状动脉狭窄1小时平均跨壁心肌流量降至0.34±0.04ml/min/g(正常区心肌流量0.96+/-0.10ml/min/g)。缺血区的收缩期壁增厚几乎完全消失(-97+/-4%)。再灌流时,收缩期壁增厚立即恢复,但仍处于抑制状态。随着时间的推移,逐渐恢复。24小时后收缩期室壁增厚仍受到抑制(-20+/-6%,p<0.01)。术后1周,管壁增厚已完全恢复,与对照组无明显差异。此外,在所有狗的尸检中,壁厚测量的部位都没有坏死。在进行正电子发射计算机断层扫描研究时,4只接受心肌活检的狗的电子显微镜检查没有发现异常。使用[1-11C]醋酸酯示踪剂(在再灌注后6小时、1周和2周进行)和[1-11C]棕榈酸示踪剂(在再灌注后6小时、12小时、24小时、1周和2周进行)进行动态PET研究,可以计算在随访期间不同时间不同感兴趣区域的局部组织时间-活动曲线。尽管完全再灌流,但在缺血的后段,观察到异常的[1-11C]乙酸酯和[1-11C]棕榈酸动力学,早期11C清除曲线成分的斜率显著降低。重复的正电子发射计算机断层扫描显示整体氧化代谢和脂肪酸代谢逐渐正常化,这与机械功能恢复的时间进程平行。因此,冠脉狭窄1小时后再灌流引起的心肌缺血与长时间的缺血后机械和代谢功能障碍有关。这种短暂的氧输送减少导致了脂肪酸β氧化的长期损害,以及尽管完全复氧,整体氧化代谢的降低。功能和代谢恢复的时间进程相似。
Stunned myocardium produced by 1 hour of critical coronary artery stenosis was evaluated for alteration in regional mechanical function and overall oxidative and fatty acid metabolism by positron emission tomography (PET) in chronically instrumented dogs. Twenty-seven dogs, chronically instrumented for measurements of left ventricular pressure and regional myocardial wall thickening in normal and ischemic zones, were subjected to a 1-hour period of myocardial ischemia produced by graded left circumflex coronary artery stenosis, resulting in minimal residual flow. Mean transmural myocardial flow during 1-hour coronary stenosis decreased to 0.34 +/- 0.04 ml/min per gram in the ischemic zones (normal zone transmural flow, 0.96 +/- 0.10 ml/min per gram). Systolic wall thickening in the ischemic zone was almost completely abolished (-97 +/- 4%). On reperfusion, systolic wall thickening immediately resumed but remained depressed. Progressive recovery was noted with time. At 24 hours, systolic wall thickening was still depressed (-20 +/- 6%, p < 0.01). At 1 week, wall thickening had completely recovered and was no longer significantly different from the control condition. In addition, the absence of necrosis at the site of wall thickness measurements was confirmed at autopsy in all dogs. No abnormalities were found by electron microscopy in four dogs undergoing myocardial biopsies at the time of PET studies. Dynamic PET studies using [1-11C]acetate tracer (performed at 6 hours, 1 week, and 2 weeks after reperfusion) and [1-11C]palmitic acid tracer (performed at 6 hours, 12 hours, 24 hours, 1 week, and 2 weeks after reperfusion) allowed the computation of regional tissue time-activity curves in different regions of interest at different times during follow-up. Despite full reperfusion, abnormal [1-11C]acetate and [1-11C]palmitic acid kinetics were observed in the posterior segments, previously subjected to ischemia, as evidenced by a significant decrease in the slope of the early 11C clearance curve component. Repeat PET studies revealed progressive normalization of overall oxidative metabolism and fatty acid metabolism, which paralleled the time course of recovery of mechanical function. Thus, myocardial ischemia, produced by 1-hour coronary artery stenosis, followed by full reperfusion is associated with a prolonged period of postischemic mechanical and metabolic dysfunction. This transient reduction in oxygen delivery induced a prolonged impairment in fatty acid beta-oxidation as well as a reduction in overall oxidative metabolism despite full reoxygenation. A similar time course for recovery of function and metabolism was observed.
在有意识的狒狒中,短期冠状动脉闭塞后,肌酸激酶的释放与心肌坏死无关。
DOI: 10.1016/s0735-1097(85)80216-3
发表时间: 1985
影响因子: 24
作者:
Heyndrickx,GR;Amano,J;Kenna,T;Fallon,JT;Patrick,TA;Manders,WT;Rogers,GG;Rosendorff,C;Vatner,SF
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DOI: 10.1152/ajpheart.1991.261.6.h2058
发表时间: 1991
期刊: The American journal of physiology
影响因子: --
作者:
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通讯作者: Schelbert,HR
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DOI: 10.1161/01.cir.79.1.134
发表时间: 1989
期刊: Circulation
影响因子: 37.8
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DOI: 10.1016/s0022-2828(87)80593-x
发表时间: 1987
影响因子: 5
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DOI: 10.1161/01.res.67.6.1481
发表时间: 1990-12-01
影响因子: 20.1
作者:
PANTELY, GA;MALONE, SA;BRISTOW, JD
通讯作者: BRISTOW, JD