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首页> 外文期刊>Life sciences >The effect of aspirin and two nitric oxide donors on the infarcted heart in situ.
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The effect of aspirin and two nitric oxide donors on the infarcted heart in situ.

机译：阿司匹林和两个一氧化氮供体对梗死心脏的影响。

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Nitric oxide (NO) donors are heterogeneous substances which release NO, a biologically active compound. NO released by nitric oxide donors has important effects on the circulation by causing vasodilation, diminishing myocardial contractile force, inhibiting platelet aggregation, and counteracting the effects of thromboxane A2. In the infarcted heart, activation of the inducible form of nitric oxide synthase (iNOS) and the formation of prostacyclin and thromboxane A2 by cyclooxygenase (COX) were increased. Myocardial infarction also resulted in increased myocardial NO production. Aspirin (acetylsalicylic acid. ASA) at low concentration (35 mg/kg/day) fails to change iNOS production, in contrast to higher dose (150 mg/kg/day) which, as previously shown, inhibits iNOS activity. ASA at all doses also suppresses myocardial prostanoid formation because of inhibition of COX. Recently, two NO donors have been synthesized: NCX 4016 and Diethylenetriamine/NO (DETA/NO). NCX 4016 combines an NO-releasing moiety with a carboxylic residue via an esteric bond. We describe here that NCX 4016 (65 mg/kg/day) increased prostacyclin and thromboxane A2 production in the infarcted heart muscle, overcoming the inhibitory effects of ASA. As a result of nitric oxide release, oxidation products of NO (NO2- and NO3-; NOx) in arterial blood rose following administration of NCX 4016. On oral administration, NCX 4016 did not change systemic arterial pressure. The effects of a single NO donor, DETA/NO (1.0 mg/kg/day) on the infarcted heart were also investigated On intravenous administration, the compound increased NO concentration in arterial blood slightly but to a lesser degree than NCX 4016. Like NCX 4016, it raised myocardial production of prostacyclin and thromboxane A2 in the infarcted heart. However, it caused a severe fall in blood pressure. These findings demonstrate that newly-synthesized NO donors release nitric oxide in situ and increase myocardial production of prostanoids. NCX 4016 has therapeutic potential because it can be orally administered, lacks hypotensive effects, increases blood levels of nitric oxide and myocardial prostacyclin production.
机译：一氧化氮（NO）供体是释放NO（一种生物活性化合物）的异质物质。一氧化氮供体释放的NO通过引起血管舒张，减少心肌收缩力，抑制血小板聚集并抵消血栓烷A2的作用，对循环产生重要影响。在梗塞的心脏中，可诱导形式的一氧化氮合酶（iNOS）的活化以及环加氧酶（COX）增强前列环素和血栓烷A2的形成。心肌梗塞还导致心肌NO产生增加。如前所述，低浓度（35 mg / kg /天）的阿司匹林（乙酰水杨酸，ASA）不能改变iNOS的产生，而较高剂量（150 mg / kg /天）则抑制iNOS的活性。由于抑制COX，所有剂量的ASA还抑制心肌类前列腺素的形成。最近，已经合成了两种NO供体：NCX 4016和二亚乙基三胺/ NO（DETA / NO）。 NCX 4016通过酯键将释放NO的部分与羧基残基结合在一起。我们在这里描述了NCX 4016（65 mg / kg /天）增加了梗塞心肌中前列环素和血栓烷A2的产生，克服了ASA的抑制作用。由于释放一氧化氮，使用NCX 4016后动脉血中NO（NO2-和NO3-; NOx）的氧化产物增加。口服时，NCX 4016不会改变全身动脉压。还研究了单一NO供体DETA / NO（1.0 mg / kg / day）对梗塞心脏的影响。静脉内给药时，该化合物使动脉血中NO含量略有增加，但增幅低于NCX4016。与NCX相似。 4016年，它提高了梗塞心脏的前列环素和血栓烷A2的心肌产量。但是，它导致血压严重下降。这些发现表明，新合成的NO供体原位释放一氧化氮，并增加了前列腺素的心肌生成。 NCX 4016具有治疗潜力，因为它可以口服给药，没有降压作用，可以增加一氧化氮的血液水平和心肌前列环素的产生。

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