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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 with
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 linked with NO release. METHODS: Saphenous vein segments from patients with type 2 diabetes (n = 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 Values were reported relative to the mean initial measurement of NO release from diabetic endothelium, which was defined as RESULTS: Diabetic patients (n = 12) showed a relative and significant diminished basal level of released NO, (0.049 ± 0.012) nmo l / L, compared with