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兔心肌梗死后心肌中诱导型一氧化氮合酶活性

Inducible nitric oxide synthase activity in myocardium after myocardial infarction in rabbit.

作者信息

Dudek R R, Wildhirt S, Conforto A, Pinto V, Suzuki H, Winder S, Bing R J

机构信息

Department of Experimental Cardiology, Huntington Medical Research Institutes, Pasadena, CA 91101.

出版信息

Biochem Biophys Res Commun. 1994 Dec 30;205(3):1671-80. doi: 10.1006/bbrc.1994.2860.

Abstract

The activity of nitric oxide synthase (NOS) in infarcted and noninfarcted rabbit myocardium was determined. NOS activity, as measured by conversion of [14C]arginine to [14C]citrulline, was significantly higher in the infarcted area of myocardium (22.7 +/- 3.7 fmol/mg as compared to 7.67 +/- 1.0 in noninfarcted area). NOS activity within the area of risk remained on control level. Increased inducible NOS activity was observed on the first postoperative day and persisted for at least 14 days; it declined 3 weeks after infarction. Citrulline formation was inhibited by N-omega-nitro-L-arginine and N-omega-monomethyl-L-arginine The localization of NOS by monoclonal anti-NOS antibody indicates mononuclear cells/macrophages as the likely source of the enzyme. The concentrations of tumor necrosis factor-alpha and interleukin-1 beta were not increased in peripheral blood or myocardium.

摘要

测定了梗死和未梗死兔心肌中一氧化氮合酶(NOS)的活性。通过[14C]精氨酸转化为[14C]瓜氨酸来测量,梗死心肌区域的NOS活性显著更高(梗死区域为22.7±3.7 fmol/mg,未梗死区域为7.67±1.0 fmol/mg)。危险区域内的NOS活性维持在对照水平。术后第一天观察到诱导型NOS活性增加,并持续至少14天;梗死3周后其活性下降。N-ω-硝基-L-精氨酸和N-ω-单甲基-L-精氨酸可抑制瓜氨酸的形成。用单克隆抗NOS抗体对NOS进行定位显示,单核细胞/巨噬细胞可能是该酶的来源。外周血或心肌中肿瘤坏死因子-α和白细胞介素-1β的浓度没有升高。

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