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[异丙肾上腺素在实验性心肌梗死中诱导ST段抬高但无室壁运动加重及心肌缺血]

[Isoproterenol induces ST-segment elevation without wall motion aggravation and myocardial ischemia in experimental myocardial infarction].

作者信息

Yamamoto T, Katori R

机构信息

First Department of Internal Medicine, Kinki University School of Medicine, Osaka.

出版信息

J Cardiol. 1995 Sep;26(3):167-75.

PMID:7473047
Abstract

The mechanism of exercise-induced ST-segment elevation in previous myocardial infarction was investigated using isoproterenol infusion with atrial pacing to simulate exercise hemodynamics in seven closed chest dogs with myocardial infarction. The myocardial infarction was induced by cellulose embolization of the left anterior descending artery. One week after infarction, 1) isoproterenol 0.3 microgram/min infusion, 2) right atrial pacing alone, and 3) isoproterenol infusion after the injection of propranolol 0.5 mg/kg were performed. The heart rate was kept constant by atrial pacing during the examination. Precordial ST-segment deviation, left ventricular global and regional wall motions, lactate extraction ratio, and regional myocardial blood flow were measured. Isoproterenol induced a significant elevation of the ST-segment, i.e., the sum of ST-segment elevation at chest leads V2, V3 and V4, sigma STV234, increased from 0.32 +/- 0.11 (mean +/- SEM) to 0.82 +/- 0.22 mV (p < 0.01). However, pacing alone and isoproterenol with pretreated propranolol did not. During isoproterenol-induced ST-segment elevation, left ventricular ejection fraction increased (29.2 +/- 3.3 to 39.1 +/- 3.9%, p < 0.01), lactate extraction ratio decreased but within the normal range for lactate metabolism (30.2 +/- 7.0 to 16.7 +/- 4.2%, p < 0.01), and the inner/outer ratio of regional blood flow did not change significantly (0.81 +/- 0.18 to 0.97 +/- 0.13 in the non-infarct border area, NS; 0.37 +/- 0.04 to 0.42 +/- 0.07 in the infarct border area, NS). Isoproterenol enhanced ventricular wall motion in the border and non-infarct areas, but did not induce aggravation in the infarct area.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

利用异丙肾上腺素输注联合心房起搏来模拟运动血流动力学,对7只患有心肌梗死的开胸犬进行研究,以探讨既往心肌梗死患者运动诱发ST段抬高的机制。心肌梗死通过左前降支动脉纤维素栓塞诱导产生。梗死一周后,进行了以下操作:1)输注0.3微克/分钟的异丙肾上腺素;2)单独进行右心房起搏;3)注射0.5毫克/千克普萘洛尔后输注异丙肾上腺素。检查期间通过心房起搏使心率保持恒定。测量胸前导联ST段偏移、左心室整体和局部壁运动、乳酸摄取率以及局部心肌血流量。异丙肾上腺素可使ST段显著抬高,即胸导联V2、V3和V4处ST段抬高总和(σSTV234)从0.32±0.11(平均值±标准误)升高至0.82±0.22毫伏(p<0.01)。然而,单独起搏以及异丙肾上腺素联合预先使用普萘洛尔则不会出现这种情况。在异丙肾上腺素诱发ST段抬高期间,左心室射血分数增加(从29.2±3.3%增至39.1±3.9%,p<0.01),乳酸摄取率降低,但仍在乳酸代谢的正常范围内(从30.2±7.0%降至16.7±4.2%,p<0.01),局部血流的内外比值无显著变化(非梗死边缘区从0.81±0.18变为0.97±0.13,无统计学意义;梗死边缘区从0.37±0.04变为0.42±0.07,无统计学意义)。异丙肾上腺素增强了边缘区和非梗死区的心室壁运动,但未导致梗死区病情加重。(摘要截断于250字)

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