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核苷单磷酸和三磷酸以及磷酸烯醇丙酮酸对在正常体温下遭受心脏停搏的大鼠心脏的相互关联作用。

Interrelated effects of nucleoside mono- and triphosphates and phosphoenolpyruvate on rat hearts subjected to cardioplegic arrest at normothermia.

作者信息

Thelin S, Hultman J, Ronquist G, Hansson H E

出版信息

Scand J Thorac Cardiovasc Surg. 1987;21(1):33-8. doi: 10.3109/14017438709116916.

DOI:10.3109/14017438709116916
PMID:3035709
Abstract

Supplementation with phosphoenolpyruvate (PEP) and ATP was previously found to enhance the protective effect of potassium cardioplegia on rat hearts subjected to extensive ischemic trauma (30 min at 37 degrees C) in the paracorporeal rat heart model. In the present experiments, the ischemia time was reduced to 20 min (37 degrees C). Ventricular work after ischemia was best in control rats with potassium cardioplegia only. Supplementing the cardioplegic solution with PEP and ATP (group I) resulted in significantly reduced postischemic ventricular work and increased efflux of the creatine kinase isoenzyme MB (CK-MB). The same result was obtained when adenosine monophosphate (AMP) was added to the supplementation (group II). When guanosine monophosphate (GMP) was added instead of AMP (group III), the negative effects of PEP and ATP in the cardioplegic solution were partly abolished. Plain potassium cardioplegia, without additives, nevertheless gave the best results. There were no significant intergroup differences in the myocardial content of adenine nucleotides. The results contrasted with those in the previous study of more protracted ischemic trauma (30 min at 37 degrees C) and possible explanations are discussed.

摘要

先前发现在体外大鼠心脏模型中,补充磷酸烯醇丙酮酸(PEP)和三磷酸腺苷(ATP)可增强钾停搏液对遭受广泛缺血损伤(37℃下30分钟)的大鼠心脏的保护作用。在本实验中,缺血时间缩短至20分钟(37℃)。仅使用钾停搏液的对照大鼠缺血后的心室功能最佳。在停搏液中补充PEP和ATP(I组)导致缺血后心室功能显著降低,肌酸激酶同工酶MB(CK-MB)流出增加。在补充物中添加单磷酸腺苷(AMP)时也得到了相同的结果(II组)。当添加鸟苷单磷酸(GMP)代替AMP时(III组),停搏液中PEP和ATP的负面影响部分被消除。然而,无添加剂的单纯钾停搏液效果最佳。各组间腺嘌呤核苷酸的心肌含量无显著差异。这些结果与先前关于更长时间缺血损伤(37℃下30分钟)的研究结果形成对比,并对可能的解释进行了讨论。

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