REGENERATION OF MYOCARDIAL PHOSPHOCREATINE IN PIGS DESPITE CONTINUED MODERATE ISCHEMIA
REGENERATION OF MYOCARDIAL PHOSPHOCREATINE IN PIGS DESPITE CONTINUED MODERATE ISCHEMIA
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DOI：
10.1161/01.res.67.6.1481
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发表时间：
1990-12-01
影响因子：
20.1
通讯作者：
BRISTOW, JD
中科院分区：
文献类型：
--
作者：
PANTELY, GA;MALONE, SA;BRISTOW, JD
评估1小时牛奶和冠状动脉血流量适度降低对心肌高能磷酸盐水平的影响。30只麻醉猪置入左前降动脉和静脉导管，晶体测量瞬时壁厚，以及充满液体的封堵器。用微球测量心肌血流量，并进行一系列心肌活检。在10头猪中，冠状动脉总血流量降低了22%，心内膜下与心外膜下的流量比从1.11降至0.54，壁厚从33%降至15%。心内膜下血流下降48%。缺血1小时内冠状动脉血流量和增厚不变。磷酸肌酸(.mu。mol/g wet wt)在缺血5分钟时从7.6降至3.8（与对照组相比p < 0.005），并在缺血60分钟时恢复正常（7.9）（p = NS）。心内膜下ATP (.mu。Mol /g wet wt)在缺血60分钟时从4.3缓慢下降，稳定在2.1（与对照组相比p < 0.001）。在另外7头猪中发现了类似的磷酸肌酸再生，冠状动脉血流经壁减少43%，心内膜下血流减少66%。在两个不同的对照组（n = 13头猪）中，ATP和磷酸肌酸均无显著变化。尽管持续缺血和低ATP水平，但磷酸肌酸的再生与缺血期间心肌需氧量或耗氧量或区域功能的变化无关。这可能反映了1)缺血心肌的能量需求成功下调以维持细胞活力，或2)细胞主要或通过磷酸肌酸产生ATP能力的代谢异常。
The effects of 1 hour of milk and moderate reductions in coronary blood flow in myocardial high-energy phosphate levels were evaluated. Thirty anesthetized pigs were instrumented with left anterior descending arterial and venous catheters, crystals for instantaneous wall thickness, and a fluid-filled occluder. Measurement of myocardial blood flow was performed with microspheres, and a series of myocardial biopsies also was performed. In 10 pigs, overall coronary blood flow was lowered by 22%, with a fall in subendocardial-to-subepicardial flow ratio from 1.11 to 0.54 an in wall thickening from 33% to 15%. Subendocardial flow fell 48%. Coronary blood flow and thickening were constant during 1 hour of ischemia. Phosphocreatine (.mu.mol/g wet wt) in the subendocardical third of the ischemic zone fell from 7.6 to 3.8 at 5 minutes of ischemia (p < 0.005 verus control) and returned to normal (7.9) at 60 minutes (p = NS), despite ongoing ishemia. Subendocardial ATP (.mu.mol/g wet wt) fell slowly from 4.3 and leveled off at 2.1 at 60 minutes of ischemia (p < 0.001 versus control). Similar regeneration of phosphocreatine was found in seven additional pigs, with a 43% transmural reduction in coronary blood flow and a 66% reduction in subendocardial flow. No significant changes in ATP and phosphocreatine were noted in two different control groups (n = 13 pigs). The regeneration of phosphocreatine despite ongoing ischemia and low ATP levels was not related to changes in myocardial oxygen demand or consumption, or in regional function during the period of ischemia. This may reflect 1) a successful downregulation of the energy needs of the ischemic myocardium to maintain cell viability, or 2) a metabolic abnormality in the ability of the cells to produce ATP primarily or by use of phosphocreatine.