Momomura S, Ingwall J S, Parker J A, Sahagian P, Ferguson J J, Grossman W
Circ Res. 1985 Dec;57(6):822-35. doi: 10.1161/01.res.57.6.822.
Myocardial ischemia due to increased oxygen demand (pacing tachycardia plus critical coronary stenoses) alters diastolic distensibility and relaxation more than ischemia of comparable duration due to coronary occlusion. To investigate the relationship between myocardial diastolic function and metabolism, we compared myocardial high energy phosphate content, tissue pH, and regional blood flow for these two types of ischemia in anesthetized open-chest dogs. Myocardial biopsies were done with a high-speed air-turbine biopsy drill, permitting rapid (less than 1-second) freezing of tissue samples from both nonischemic and ischemic areas, while myocardial pH was measured with a hydrogen ion-selective polymer membrane implanted in the subendocardium. After 3 minutes of pacing tachycardia in dogs with critical coronary stenoses (demand-type ischemia, n = 14), regional systolic function (% segment shortening by ultrasonic crystals) was mildly depressed (from 19 +/- 2% control to 13 +/- 2% post-pacing, P less than 0.01), while left ventricular diastolic pressure-segment length relations shifted upward, indicating decreased distensibility of the ischemic myocardial segment. Associated with these changes in function, subendocardial adenosine triphosphate decreased (from 31.3 +/- 1.5 to 27.9 +/- 1.0 nmol/mg protein, P less than 0.01), as did creatine phosphate (53.8 +/- 2.1 to 39.6 +/- 2.5 nmol/mg protein, P less than 0.01), while myocardial pH declined slightly (delta pH = -0.14 +/- 0.02, P less than 0.01). In contrast, at 3 minutes of coronary artery occlusion (primary ischemia, n = 14), regional segment shortening was replaced by systolic bulging (% shortening decreased from 17 +/- 2% to -2 +/- 1% during occlusion, P less than 0.01), while left ventricular pressure-segment length relations were not shifted upward, and there was no decrease in diastolic distensibility of the ischemic segment. With coronary artery occlusion, subendocardial adenosine triphosphate declined slightly (33.2 +/- 0.5 to 29.2 +/- 2.0 nmol/mg, P less than 0.05), while creatine phosphate decreased substantially (51.1 +/- 2.3 to 7.8 +/- 1.4 nmol/mg protein, P less than 0.01). Myocardial pH fell strikingly (delta pH = -0.33 +/- 0.03, P less than 0.01), and the decline was 236% of that seen with demand-type ischemia. Regional myocardial blood flow (microsphere technique) showed a decreased endocardial:epicardial (endo:epi) ratio (1.04 +/- 0.04 control vs. 0.40 +/- 0.05 during pacing, P less than 0.01) and absolute subendocardial flow (1.02 +/- 0.47 to 0.47 +/- 0.05 ml/min per g, P less than 0.01) with demand-type ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)
因氧需求增加(起搏性心动过速加严重冠状动脉狭窄)导致的心肌缺血,相较于同等时长的冠状动脉闭塞性缺血,对舒张期扩张性和舒张功能的影响更大。为研究心肌舒张功能与代谢之间的关系,我们在麻醉开胸犬中比较了这两种类型缺血时的心肌高能磷酸含量、组织pH值及局部血流。采用高速气涡轮活检钻进行心肌活检,可使非缺血区和缺血区的组织样本快速(不到1秒)冷冻,同时通过植入心内膜下的氢离子选择性聚合物膜测量心肌pH值。在患有严重冠状动脉狭窄的犬中进行3分钟起搏性心动过速(需求型缺血,n = 14)后,局部收缩功能(超声晶体测量的节段缩短百分比)轻度降低(从对照时的19±2%降至起搏后的13±2%,P<0.01),而左心室舒张压 - 节段长度关系向上移位,表明缺血心肌节段的扩张性降低。与这些功能变化相关的是,心内膜下三磷酸腺苷减少(从31.3±1.5降至27.9±1.0 nmol/mg蛋白,P<0.01),磷酸肌酸也减少(从53.8±2.1降至39.6±2.5 nmol/mg蛋白,P<0.01),而心肌pH值略有下降(ΔpH = -0.14±0.02,P<0.01)。相比之下,在冠状动脉闭塞3分钟时(原发性缺血,n = 14),局部节段缩短被收缩期膨出取代(闭塞期间缩短百分比从17±2%降至 -2±1%,P<0.01),而左心室压力 - 节段长度关系未向上移位,缺血节段的舒张期扩张性也未降低。冠状动脉闭塞时,心内膜下三磷酸腺苷略有下降(从33.2±0.5降至29.2±2.0 nmol/mg,P<0.05),而磷酸肌酸大幅减少(从51.1±2.3降至7.8±1.4 nmol/mg蛋白,P<0.01)。心肌pH值显著下降(ΔpH = -0.33±0.03,P<0.01),下降幅度是需求型缺血时的236%。局部心肌血流(微球技术)显示,需求型缺血时心内膜:心外膜(endo:epi)比值降低(对照时为1.04±0.04,起搏时为0.40±0.05,P<0.01),心内膜下绝对血流降低(从1.02±0.47降至0.47±0.05 ml/min per g,P<0.01)。(摘要截取自400字)