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大鼠心脏极化和去极化停搏时的基础代谢能量需求

Basal metabolic energy requirements of polarized and depolarized arrest in rat heart.

作者信息

Sternbergh W C, Brunsting L A, Abd-Elfattah A S, Wechsler A S

机构信息

Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710.

出版信息

Am J Physiol. 1989 Mar;256(3 Pt 2):H846-51. doi: 10.1152/ajpheart.1989.256.3.H846.

Abstract

Basal energy requirements of polarized [tetrodotoxin (TTX), 25 microns] and depolarized [potassium (K), 20 mM] arrested hearts were studied by continuously measuring myocardial oxygen consumption (MVO2) during 60 min of normothermic arrest in isolated Langendorff-perfused rat hearts. TTX, a fast sodium channel blocker, was used to produce polarized arrest because of its specificity and reversibility. MVO2 was significantly lower in the polarized (TTX) group at all time points, a typical difference occurring 30 min after arrest (0.070 +/- 0.005 vs. 0.109 +/- 0.006 ml O2.min-1.g dry wt-1, P less than 0.001). Coronary flow was lower in the polarized group (14.3 +/- 1.4 vs. 28.4 +/- 2.2 ml.min-1.g dry wt-1, P less than 0.001, data at 30 min of arrest), but flow-restricted studies showed basal MVO2 to be independent of variation in coronary flow within this range. Recovery of function was similar in both groups. Ventricular pressure during cardiac arrest was lower in the polarized group (5.5 +/- 1.2 vs. 10.3 +/- 1.3 mmHg, P less than 0.01, data at 30 min of arrest), implying reduced myocardial wall tension and a lower intracellular calcium concentration. These results suggest that polarized arrest can decrease myocardial metabolic demands below that of depolarized arrest. A plausible mechanism is a reduction in myocardial wall tension caused by decreased calcium influx mediated by the Na-Ca exchanger.

摘要

通过在离体Langendorff灌注大鼠心脏常温停搏60分钟期间连续测量心肌耗氧量(MVO2),研究了极化[河豚毒素(TTX),25微米]和去极化[钾(K),20毫摩尔]停搏心脏的基础能量需求。TTX是一种快速钠通道阻滞剂,由于其特异性和可逆性,被用于产生极化停搏。在所有时间点,极化(TTX)组的MVO2均显著较低,停搏后30分钟出现典型差异(0.070±0.005对0.109±0.006毫升O2·分钟-1·克干重-1,P<0.001)。极化组的冠状动脉血流量较低(14.3±1.4对28.4±2.2毫升·分钟-1·克干重-1,P<0.001,停搏30分钟时的数据),但流量限制研究表明,在此范围内基础MVO2与冠状动脉流量变化无关。两组的功能恢复相似。极化组心脏停搏期间的心室压力较低(5.5±1.2对10.3±1.3毫米汞柱,P<0.01,停搏30分钟时的数据),这意味着心肌壁张力降低和细胞内钙浓度降低。这些结果表明,极化停搏可使心肌代谢需求低于去极化停搏。一个合理的机制是由钠-钙交换体介导的钙内流减少导致心肌壁张力降低。

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