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| 1 | 直接评估吗啡刺激糖尿病人隐静脉内皮一氧化氮释放减少显示文摘to directly measure in real time basal and stimulated levels of NO released from human saphenous vein endothelium and to quantify the expression of the μopiate receptor, which has been linked with NO release. METHODS: Saphenous vein segments from patients with type 2 diabetes ( n = 12) and patients without diabetes (n =8) were obtained. The release of NO was measured directly from the endothelium using a NO-specific amperometric probe. NΩ-nitro-L-arginine methyl ester (L-NAME, 0.1 mmol/L), a NO synthase (NOS) inhibitor, or morphine (1 μmol/L), a stimulant, was administered and the measurements were repeated. Values were reported relative to the mean initial measurement of NO release from diabetic endothelium, which was defined as the relative zero level of NO release. A RT-PCR was then performed on the endothelium to measureμ opiate receptor expression. RESULTS: Diabetic patients (n = 12) showed a relative and significantly diminished basal level of released NO, (0.049± 0.012) nmol/L, compared | Thomas V BILHNGER, James A VOSSWINKEL, Patrick CADET, Christos M RIALAS, Harold I MAGAZINE, George B STEFANO(Division of Cardiothoracic Surgery, Department of Surgery, University Hospital and Medical Center, HSC, T19-080, Stony Brook, New York 11794-8191 Neuroscience Research Institute, State University of New York College at Old Westbury, Old Westbury, New York , USA) | 2002 | Acta Pharmacologica Sinica2002，23，2： | 3 |
| 2 | Retroperitoneal ancient schwannoma:case report and analysis of clinico-radiological findings显示文摘 | Giglio M Giasotto V Medical M | 2002 | Ann Urol2002，36，： | 1 |
| 3 | In vitro evaluation of microleakage of various types of dental cements 显示文摘 | Medic V ObradovicDjurici K Dodic S | 2010 | Srp Arh Celok Lek2010，138，34： | 1 |
| 4 | Carbapenems resistance of Acinetobacter spp strains isolated from wound swabs during 2009-2010显示文摘 | Medic D Ukropina MM Gusman V | | 0，，11： | 1 |
| 5 | 乙醇心血管保护作用的潜在机制(英文)显示文摘Epidemiological studies demonstrate a significant protective effect of moderate alcohol consumption on the incidence of cardiovascular diseases which accounts for the majority of deaths in the Western world. In this review, possible mechanisms to explain the cardioprotective effect of ethanol are discussed. While the prevailing theory supported by a number of clinical and animal studies indicates that the ability of ethanol to elevate serum high-density lipoprotein (HDL) cholesterol levels is an important mechanism in ameliorating cardiovascular disease, other mechanisms whereby ethanol could exert its beneficial effect have been proposed. Namely, its ability to affect platelet function and endothelial cell and vascular smooth muscle cell function (In this review, the terms alcohol and ethanol are used interchangeably). | Eileen M REDMOND, James V SITZMANN, Paul A CAHILL (Department of Surgery, University of Rochester Medical Center, Box SURG, 601 Elmwood Avenue, Rochester NY 14642-8410, USA) | 2000 | Acta Pharmacologica Sinica2000，21，5： | 1 |
| 6 | Formu- Gel and its UV protective study of ina] flowers 显示文摘 | Patil S B lation of some medic 2011 1 (2) Patil V V Ghodke D S | 2011 | Asian J Pharm Ana2011，3435，： | 1 |
| 7 | Academic Press limited 显示文摘 | Daviodo W Frank J Medical V | 1993 | London1993，，： | 1 |
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