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观察基础和卡维地洛干预条件下,自发性高血压大鼠和Wistar大鼠心肌成纤维细胞一氧化氮合酶-一氧化氤系统活性的变化。胰酶消化法分离、培养大鼠心肌成纤维细胞,采用硝酸还原酶法和分光光度法观察基础和卡维地洛干预条件下,培养基中一氧化氮合酶活性及一氧化氮含量的变化。结果发现,在基础状态下72 h,高血压大鼠组心肌成纤维细胞一氧化氮含量(66.6±3 5/μmol/L)及一氧化氮合酶活性(16.7±0.7 kU/L)较Wistar大鼠组(80.8±6.2/μmol/L和29.1±2.1 kU/L)显著降低,并有统计学意义(P<0.01);一氧化氮含量及一氧化氮合酶活性随卡维地洛浓度的增高而增加,均呈别量依赖性;另外,在不同浓度卡维地洛作用下,高血压大鼠组心肌成纤维细胞的一氧化氮含量随一氧化氮合酶活性的增强而增高,二者呈显著正相关(r=0.911,P<0.01)。结果提示,高血压大鼠心肌成纤维细胞的一氧化氮合酶一氧化氮系统功能异常,表现为一氧化氮合酶活性降低,一氧化氮含量减少。卡维地洛使心肌成纤维细胞内一氧化氯合酶一氧化氮系统活性显著增高,并呈浓度依赖性,其中对高血压大鼠的影响远远高于正常血压组,这可能是卡维地洛抑制血压增高的重要机制之一。
To observe the changes of nitric oxide synthase-monosodium glutamate system activity in spontaneously hypertensive rats and Wistar rats with basal and carvedilol interventions. The changes of nitric oxide synthase activity and nitric oxide content in culture medium were observed by nitric acid reductase method and spectrophotometry under the condition of intervention of carvedilol and pancreatic fibroblasts. . The results showed that at 72 h, the levels of nitric oxide (66.6 ± 3.5 / μmol / L) and nitric oxide synthase (16.7 ± 0.7 kU / L) in hypertensive rats were significantly higher than those in Wistar (80.8 ± 6.2 / μmol / L and 29.1 ± 2.1 kU / L) were significantly decreased in the rat group (P <0.01), while the levels of nitric oxide and nitric oxide synthase were significantly decreased with the increase of carvedilol In a dose-dependent manner. In addition, under the action of carvedilol at different concentrations, the content of nitric oxide in cardiac fibroblasts of hypertensive rats increased with the increase of nitric oxide synthase activity, There was a significant positive correlation between them (r = 0.911, P <0.01). The results suggest that nitric oxide synthase nitric oxide system in hypertensive rat cardiac fibroblasts dysfunction, manifested as nitric oxide synthase activity decreased, nitric oxide content decreased. Carvedilol enhanced the activity of nitric oxide synthase (NO) system in cardiac fibroblasts in a concentration-dependent manner. The effect of carvedilol on hypertensive rats was much higher than that of normotensive subjects, which may be Carve One of the important mechanisms of dexamethasone inhibiting blood pressure increase.