کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10738852 | 1046838 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Oxidant stress but not thromboxane decreases with epoprostenol therapy
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کلمات کلیدی
RAPCOXPWPPPHET-1SvO2TxA2PAPcyclooxygenase - آنزیم سیکلواکسیژنازMixed venous saturation - اشباع وریدی مختلطendothelin-1 - اندوتلین-1Cardiac output - برون ده قلبیPulmonary heart disease - بیماری قلبی ریویThromboxane A2 - ترومبوکسیان A2Pulmonary artery pressure - فشار شریان ریویRight Atrial Pressure - فشار مستقیم دهلیزیPulmonary wedge pressure - فشار گوه ریهNitric oxide - نیتریک اکسیدLipid mediators - واسطه های لیپیدLipid peroxidation - پراکسیداسیون لیپیدprimary pulmonary hypertension - پرفشاری خون ریوی اولیهprostacyclin - پروستاسیکلینcreatine - کراتین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
Epoprostenol has improved the outcome of patients with primary pulmonary hypertension (PPH); however, its mechanism of action remains poorly understood. Isoprostanes are easily measured markers of oxidant stress and can activate platelets leading to increased thromboxane A2 (TxA2) production. We hypothesized that oxidant stress is associated with increased TxA2 synthesis and that epoprostenol decreases oxidant stress and TxA2 production in patients with PPH. Morning urine samples were obtained from 19 patients with PPH. We measured urinary metabolites of the isoprostane, 8-iso-PGF2α (F2-IsoP-M), and of TxA2 (Tx-M) before and after treatment with epoprostenol in patients with PPH. Mean (±SE) levels of F2-IsoP-M were elevated at baseline in our patients, 863 ± 97 pg/mg creatinine. During treatment with epoprostenol, values decreased to 636 ± 77 pg/mg creatinine (P = 0.011), and there was a strong correlation between the change in F2-IsoP-M and follow-up pulmonary vascular resistance (R2 = 0.69, P < 0.001). Tx-M levels were markedly elevated at baseline and were unchanged with therapy. These results indicate that oxidant stress decreases with epoprostenol therapy and is associated with hemodynamic and clinical improvement. The failure of Tx-M to decrease with therapy suggests that epoprostenol does not exert a beneficial effect through inhibition of TxA2 production in patients with PPH.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 38, Issue 5, 1 March 2005, Pages 568-574
Journal: Free Radical Biology and Medicine - Volume 38, Issue 5, 1 March 2005, Pages 568-574
نویسندگان
Ivan M. Robbins, Jason D. Morrow, Brian W. Christman,