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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Bradykinin metabolism in rat hearts with left-ventricular hypertrophy following myocardial infarction.
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Bradykinin metabolism in rat hearts with left-ventricular hypertrophy following myocardial infarction.

机译：心肌梗塞后大鼠左室肥厚的缓激肽代谢。

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摘要

The aim of the present study was to assess the contribution of angiotensin I converting enzyme (ACE)and neutral endopeptidase (NEP) in the coronary degradation of bradykinin (BK) after left-ventricular hypertrophy following myocardial infarction (MI) in rats. Myocardial infarction was induced by left descendant coronary artery ligation, and the contribution of ACE and NEP in the degradation of exogenous BK after a single passage through the coronary bed was assessed at 2, 5, and 36 days post-MI. BK degradation rate (V(max)/Km) was found to be significantly lower in hearts at 36 days (3.30 +/- 0.28 min(-1)) compared with 2 days (4.39 +/- 0.32 min(-1)) for noninfarcted hearts, but this reduction was just above the statistical level of significance for post-MI hearts. In infarcted hearts, V(max)/Km was increased significantly 5 days post-MI (4.91 +/- 0.28 min(-1)) compared with the 2 and 36 day-groups (3.43 +/- 0.20 and 2.78 +/- 0.16 min(-1), respectively). The difference between noninfarcted and MI was significant only 2 days post-MI. Treatment with the vasopeptidase inhibitor, omapatrilat, showed that the relative contribution of ACE and NEP combined increased over time in infarcted hearts and became significantly higher 36 versus 2 days post-MI. Finally, the treatment with an ACE inhibitor (enalaprilat) and a NEP inhibitor (retrothiorphan) in the 36-day infarcted and noninfarcted hearts showed that the relative contribution of ACE in infarcted hearts was comparable with that of noninfarcted hearts, whereas the relative contribution of NEP was increased significantly in infarcted hearts. In conclusion, experimental MI in rats induces complex changes in the metabolism of exogenous BK. The changes resulted in an increased relative contribution of NEP 36 days after infarction.
机译：本研究的目的是评估大鼠心肌梗死（MI）后左室肥大后血管紧张素I转化酶（ACE）和中性内肽酶（NEP）在缓激肽（BK）冠状动脉降解中的作用。左后冠状动脉结扎可诱发心肌梗塞，在心肌梗死后第2、5和36天评估ACE和NEP对单次通过冠状动脉床后外源性BK降解的贡献。发现第36天（3.30 +/- 0.28 min（-1））的心脏BK降解率（V（max）/ Km）显着低于2天（4.39 +/- 0.32 min（-1））对于非梗死性心脏，这一降低仅略高于心梗后心脏的统计学显着性水平。与2和36天组（3.43 +/- 0.20和2.78 +/-）相比，梗死后心脏梗死后5天的V（max）/ Km显着增加（4.91 +/- 0.28 min（-1））。 0.16 min（-1））。非梗塞和心肌梗死之间的差异仅在心肌梗塞后2天才显着。血管肽酶抑制剂omapatrilat的治疗表明，梗塞后心脏中ACE和NEP的相对贡献随着时间的推移而增加，与心梗后2天相比，明显增加了36。最后，在36天的梗塞性和非梗塞性心脏中使用ACE抑制剂（依那普利拉）和NEP抑制剂（逆转录硫吗啡）治疗表明，ACE在梗塞性心脏中的相对贡献与未梗塞性心脏相当，而梗死心脏的NEP明显增加。总之，大鼠的实验性MI诱导外源BK代谢的复杂变化。这些变化导致梗死后36天NEP的相对贡献增加。

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