Hormonal and Cardiac Effects of Converting Enzyme Inhibition in Rat Myocardial Infarction
Hormonal and Cardiac Effects of Converting Enzyme Inhibition in Rat Myocardial Infarction
复制标题
转化酶抑制对大鼠心肌梗死的激素和心脏影响
作者：
J. Michel;A. Lattion;J. Salzmann;Maria de Lourdes Cerol;M. Philippe;J. Camilleri;P. Corvol
为了解释转换酶抑制如何改善心功能不全的预后，我们在大鼠左心室梗死实验模型（未治疗的梗死，n = 18）和假手术对照组（n = 15）中研究了S9490-3（培哚普利）治疗2个月转换酶抑制（CEI）对激素血浆变量和心肌定量和质变的影响。心肌梗死的诱发与血压的短暂下降有关。在整个实验期间，CEI治疗维持了较低的血压。与假手术组（47.6±15.9 ng AI/ml/hr）相比，未治疗梗死组血浆肾素浓度（155.4±136.7 ng AI/ml/hr）无显著升高。血浆醛固酮在三个实验组中没有变化。与对照组（76±40 pg/ml）相比，未治疗梗死组血浆免疫反应性心房钠素水平升高（185±245 pg/ml），经CEI恢复正常（66±60 pg/ml）。与假手术对照组（1,071±80 mg）相比，治疗组和未治疗组的体重均略有下降，而未治疗组的心脏重量（1,540±310 mg）显著增加（1,145±180 mg），治疗后恢复正常（1,145±180 mg）。未经治疗的梗死组心房和右心室合并质量显著增加（660±210 mg），治疗后减少（443±106 mg），但未完全正常化（对照组，343±40 mg）。与对照组相比，心肌梗死改变了左心室异肌球蛋白谱：V1形态从假手术组的62.4±9.4%下降到梗死组的41.6±13.4%，V3形态从假手术组的13.0±4.7%上升到未治疗梗死组的27.4±11.8%。CEI治疗部分但显著地逆转了这种异肌球蛋白谱的修饰（V1, 53.0±14.4%;V1,17.5±8.0%）。未经治疗的梗死大鼠胶原体积密度显著增加（4.14±0.81%，对照组为2.68±0.49%），治疗后逆转（2.95±0.66%）。编码心房利钠因子的信使RNA，通过斑点杂交测量，在未治疗的梗死组的心房和心室中显著增加，CEI治疗部分逆转了这种增加。因此，心肌梗死深刻地改变了外周循环的几个变量以及心肌蛋白的定量和定性表达。CEI治疗在很大程度上逆转了这些变化，但可能没有使它们完全正常化。
To explain how converting enzyme inhibition could improve the prognosis in cardiac insufficiency, the effect of converting enzyme inhibition (CEI) by S9490–3 (Perindopril) treatment for 2 months (treated infarctions, n = 18) on hormonal plasma variables and the quantitative and qualitative changes in myocardium were studied in an experimental model of left ventricular infarction in rats (untreated infarctions, n = 18) and compared to a sham-operated control group (n = 15). Induction of myocardial infarction was associated with a transient decrease in blood pressure. CEI treatment maintained a lower blood pressure throughout the experimental period. Plasma renin concentration was not significantly increased in the untreated infarct group (155.4 ± 136.7 ng AI/ml/hr) as compared to the sham-operated group (47.6 ± 15.9 ng AI/ml/hr). Plasma aldosterone did not change in the three experimental groups. The plasma level of immunoreactive atrial natriuretic factor increased in the untreated infarct group (185 ± 245 pg/ml) as compared with the control group (76 ± 40 pg/ml) and was normalized by CEI (66 ± 60 pg/ml). Body weight was slightly decreased in both treated and untreated infarct groups, whereas the heart weight was significantly increased in the untreated group (1,540 ± 310 mg) and normalized by treatment (1,145 ± 180 mg) as compared with sham-operated controls (1,071 ± 80 mg). The combined atria and right ventricular mass was significantly increased in the untreated infarct group (660 ± 210 mg) and decreased by treatment (443 ± 106 mg) but was not completely normalized (controls, 343 ± 40 mg). Left ventricular isomyosin profiles were modified by myocardial infarction as compared with controls: V1 form decreased from 62.4 ± 9.4% in the sham-operated group to 41.6 ± 13.4% in the infarct group, and the V3 form increased from 13.0 ± 4.7% in sham-operated animals to 27.4 ± 11.8% in untreated infarct animals. CEI treatment partially, but significantly, reversed this modification of the isomyosin profile (V1, 53.0 ± 14.4%; V1,17.5 ± 8.0%). Volume density of collagen was significantly increased in the untreated infarct rats (4.14 ± 0.81% versus 2.68 ± 0.49% in controls), and this was reversed by treatment (2.95 ± 0.66%). Messenger RNA encoding for atrial natriuretic factor, measured by dot blot hybridization, was significantly increased in both the atria and the ventricles in the untreated infarct group, and treatment by CEI partially reversed this increase. Thus, myocardial infarction profoundly modified several variables of peripheral circulation and quantitative and qualitative myocardial protein expression. CEI treatment largely reversed these changes but probably did not completely normalize them.
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影响因子：
24
作者：
H. Weisman;D. Bush;J. Mannisi;B. H. Bulkley
通讯作者：
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影响因子：
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作者：
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影响因子：
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作者：
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影响因子：
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作者：
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通讯作者：
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