Puzserova Angelika, Bernatova Iveta
Institute of Normal and Pathological Physiology, Centre of Excellence for Cardiovascular Research, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Interdiscip Toxicol. 2010 Dec;3(4):109-17. doi: 10.2478/v10102-010-0049-4.
The aim of this study was to examine oxidative load and endothelium-dependent vasorelaxation in the serotonin pre-constricted femoral artery (FA) of Wistar-Kyoto (WKY) rats exposed to chronic social stress produced by crowding in the presence or absence of ascorbic acid (AsA) in working solution. Adult male rats were randomly divided into control (living space: 480 cm(2)/rat) or stressed (living space: 200 cm(2)/rat) groups for 8 weeks. Blood pressure and heart rate, determined using tail-cuff plethysmography, were not influenced by stress vs. control. Conjugated dienes (CD) and concentrations of thiobarbituric acid-reactive substances (TBARS) were measured in the left ventricle and liver (for assessment of oxidative load) and were found unchanged by chronic crowding. The nitric oxide (NO)-dependent component of endothelium-dependent relaxation was investigated in the FA using a wire myograph. In both the presence and absence of AsA, acetylcholine-induced relaxation of the FA of stressed rats significantly exceeded that of the controls, which was associated with an increase of the NO-dependent component. In conclusion, the data showed that chronic crowding did not produce oxidative stress in the organs investigated and indicate that elevation of NO production during chronic stress is an important way of adaptation, which may prevent normotensive rats from the development of stress-induced hypertension.
本研究旨在检测工作溶液中存在或不存在抗坏血酸(AsA)时,暴露于拥挤所致慢性社会应激的Wistar-Kyoto(WKY)大鼠5-羟色胺预收缩股动脉(FA)中的氧化负荷和内皮依赖性血管舒张。成年雄性大鼠随机分为对照组(生活空间:480平方厘米/只)或应激组(生活空间:200平方厘米/只),持续8周。使用尾袖体积描记法测定的血压和心率不受应激组与对照组差异的影响。在左心室和肝脏中测量共轭二烯(CD)和硫代巴比妥酸反应性物质(TBARS)的浓度(用于评估氧化负荷),发现慢性拥挤对其无影响。使用线肌张力测定仪在FA中研究内皮依赖性舒张的一氧化氮(NO)依赖性成分。无论有无AsA,应激大鼠FA中乙酰胆碱诱导的舒张均显著超过对照组,这与NO依赖性成分的增加有关。总之,数据表明慢性拥挤在研究的器官中未产生氧化应激,并表明慢性应激期间NO产生的增加是一种重要的适应方式,这可能会防止正常血压大鼠发生应激性高血压。