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缺血后收缩功能障碍与细胞内游离[Mg2+]升高无关:一项对离体大鼠和兔心脏的31P-NMR研究。

Post-ischemic contractile dysfunction does not correlate with an elevated intracellular free [Mg2+]: a 31P-NMR study on isolated rat and rabbit hearts.

作者信息

Schreur J H, de Beer R, Van Echteld C J, Ruigrok T J

机构信息

Interuniversity Cardiology Institute of The Netherlands, Department of Cardiology, University Hospital, Utrecht.

出版信息

J Mol Cell Cardiol. 1993 Sep;25(9):1015-24. doi: 10.1006/jmcc.1993.1114.

Abstract

The aim of this study was to investigate whether intracellular free Mg2+ (Mgr), which increases during myocardial ischemia due to hydrolysis of ATP, remained elevated during reperfusion after a relatively short period of ischemia and thereby could account for temporary post-ischemic contractile dysfunction, often referred to as stunning. 31P-magnetic resonance (31P-NMR) spectroscopy was used to follow creatine phosphate, adenosine triphosphate, intracellular inorganic phosphate, intracellular pH and Mgr simultaneously with left ventricular developed pressure (LVDP) and coronary flow in isolated rat and rabbit hearts, which were perfused (37 degrees C) according to Langndorff. LVDP was measured in an isovolumic way by means of an intraventricular latex balloon. Rat hearts (300 beats/min) were made globally ischemic for 15 min and rabbit hearts (180 beats/min) for 15 or 20 min. All hearts were reperfused for 60 min. Control hearts were perfused for 75 min without being made ischemic. During ischemia Mgr (mmol/l) increased from 0.76 +/- 0.20 to 4.34 +2- 1.99 in the rat hearts, and from 0.72 +/- 0.22 to 2.18 +/- 1.06 (15 min) and 2.35 +/- 1.26 (20 min) in the rabbit hearts. During reperfusion Mgr in the three groups returned to the level of the control hearts within 7.5 min, and LVDP within 25 min. At the end of the reperfusion period ATP content amounted to 56 +/- 17% (rat hearts), 66 +/- 10% (rabbit hearts; 15 min ischemia group) and 61 +/- 7% (rabbit hearts; 20 min ischemia group) of the pre-ischemic levels. The results confirm that in vitro stunning is a short-lived phenomenon and indicate that an increased Mgr is not involved in this temporary mechanical dysfunction.

摘要

本研究的目的是调查细胞内游离镁离子(Mgr),其在心肌缺血期间因ATP水解而增加,在相对短暂的缺血期后的再灌注期间是否仍保持升高,从而能否解释缺血后暂时的收缩功能障碍,即通常所说的心肌顿抑。采用31P磁共振(31P-NMR)波谱法,在离体大鼠和兔心脏中,同时监测磷酸肌酸、三磷酸腺苷、细胞内无机磷酸盐、细胞内pH值和Mgr,以及左心室舒张末压(LVDP)和冠状动脉血流量,这些心脏按照Langndorff法在37℃下进行灌注。LVDP通过心室内乳胶球囊以等容方式测量。大鼠心脏(300次/分钟)进行全心缺血15分钟,兔心脏(180次/分钟)进行缺血15或20分钟。所有心脏均再灌注60分钟。对照心脏灌注75分钟未进行缺血处理。在缺血期间,大鼠心脏中的Mgr(mmol/L)从0.76±0.20增加到4.34±1.99,兔心脏中从0.72±0.22增加到2.18±1.06(15分钟)和2.35±1.26(20分钟)。在再灌注期间,三组中的Mgr在7.5分钟内恢复到对照心脏水平,LVDP在25分钟内恢复。在再灌注期结束时,ATP含量分别为缺血前水平的56±17%(大鼠心脏)、66±10%(兔心脏;缺血15分钟组)和61±7%(兔心脏;缺血20分钟组)。结果证实,体外心肌顿抑是一种短暂现象,并表明Mgr升高与这种暂时的机械功能障碍无关。

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