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依诺昔酮对非衰竭和衰竭人心脏制剂中磷酸二酯酶的抑制作用。

Phosphodiesterase inhibition by enoximone in preparations from nonfailing and failing human hearts.

作者信息

Bethke T, Eschenhagen T, Klimkiewicz A, Kohl C, von der Leyen H, Mehl H, Mende U, Meyer W, Neumann J, Rosswag S

机构信息

Abteilung Allgemeine Pharmakologie, Universitäts-Krankenhaus Eppendorf, Universität Hamburg, Fed. Rep. of Germany.

出版信息

Arzneimittelforschung. 1992 Apr;42(4):437-45.

PMID:1386515
Abstract

The effects of enoximone (MDL 17043, Perfan, CAS 77671-31-9) on the activities of the phosphodiesterase (PDE) isoenzymes I-IV and on force of contraction were investigated in ventricular preparations isolated from failing (end-stage myocardial failure, NYHA IV) and non-failing human hearts. In both tissues four PDE isoenzymes (PDE I-IV) with similar properties were separated by DEAE-sepharose chromatography. The effects of enoximone on PDE I-IV activities did not differ between non-failing and failing human hearts. As compared to PDE I (IC50 2100 mumol/l) and II (IC50 2900 mumol/l) enoximone is a selective PDE III (cGMP-inhibited PDE, IC50 5.9 mumol/l) and PDE IV (cGMP-insensitive PDE, IC50 21.1 mumol/l) inhibitor. Milrinone, 3-isobutyl-1-methylxanthine (IBMX) and UD-CG 212 Cl, a derivative of pimobendan, were studied in the failing heart for comparison. Milrinone inhibited PDE I-IV activities similar to enoximone, revealing IC50 values for inhibition of PDE III and IV (1.2 and 3.3 mumol/l) which were about two orders of magnitude lower than that of PDE I and II (173 and 306 mumol/l). UD-CG 212 Cl was the most potent (IC50 0.05 mumol/l) and most selective PDE III inhibitor tested (IC50 for PDE I, II and IV were 175, 181 and 40.8 mumol/l, resp.), whereas IBMX inhibited PDE I-IV nonselectively (IC50 15.3, 26.2, 5.6, 5.8 mumol/l, respectively). In trabeculae carneae from nonfailing and failing human hearts enoximone increased force of contraction only marginally by 18.0 +/- 9.1% (n = 8) and 24.5 +/- 8.7% (n = 9) of the predrug value.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在从晚期心肌衰竭(纽约心脏协会心功能IV级)的衰竭和非衰竭人类心脏分离出的心室标本中,研究了依诺昔酮(MDL 17043,Perfan,化学物质登记号77671 - 31 - 9)对磷酸二酯酶(PDE)同工酶I - IV活性及收缩力的影响。在这两种组织中,通过DEAE - 琼脂糖凝胶色谱法分离出了四种性质相似的PDE同工酶(PDE I - IV)。依诺昔酮对PDE I - IV活性的影响在非衰竭和衰竭人类心脏之间并无差异。与PDE I(半数抑制浓度[IC50]为2100 μmol/L)和II(IC50为2900 μmol/L)相比,依诺昔酮是一种选择性PDE III(cGMP抑制性PDE,IC50为5.9 μmol/L)和PDE IV(cGMP不敏感性PDE,IC50为21.1 μmol/L)抑制剂。为作比较,在衰竭心脏中研究了米力农、3 - 异丁基 - 1 - 甲基黄嘌呤(IBMX)和匹莫苯丹衍生物UD - CG 212 Cl。米力农抑制PDE I - IV活性类似于依诺昔酮,其抑制PDE III和IV的IC50值(分别为1.2和3.3 μmol/L)比PDE I和II(分别为173和306 μmol/L)低约两个数量级。UD - CG 212 Cl是所测试的最有效(IC50为0.05 μmol/L)且最具选择性的PDE III抑制剂(对PDE I、II和IV的IC50分别为175、181和40.8 μmol/L),而IBMX非选择性地抑制PDE I - IV(IC50分别为15.3、26.2、5.6、5.8 μmol/L)。在非衰竭和衰竭人类心脏的心肌小梁中,依诺昔酮仅使收缩力略有增加,分别为给药前值的18.0±9.1%(n = 8)和24.5±8.7%(n = 9)。(摘要截短于250字)

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