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首页> 外文期刊>Biology of Sex Differences >Ovarian status modulates cardiovascular autonomic control and oxidative stress in target organs
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Ovarian status modulates cardiovascular autonomic control and oxidative stress in target organs

机译:卵巢状态调节靶器官的心血管自主控制和氧化应激

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Studies have presented conflicting findings regarding the association between both fluctuation and deprivation of ovarian hormones and cardiovascular autonomic modulation and oxidative stress and their potential impact on resting arterial pressure (AP) and cardiovascular risk. This study aimed to assess cardiovascular autonomic modulation, baroreflex sensitivity (BRS), and oxidative stress in male rats (M) and in female rats during ovulatory (FOV) and non-ovulatory phases (FNOV) of the estrous cycle and after deprivation of ovarian hormones (FO). Direct AP was recorded, and BRS was assessed by using increasing doses of phenylephrine and sodium nitroprusside. AP and heart rate variability were assessed by spectral analysis. Oxidative stress profile was evaluated in cardiac, renal, and muscle tissues. In females, the ovulatory phase and ovarian hormone deprivation induced an increase in AP (FOV and FO ~?9?mmHg) when compared to the non-ovulatory phase. Ovariectomy promoted increased cardiac sympathovagal balance (~?17–37%) when compared to other groups. Both FOV and FO groups presented impaired BRS, associated with higher AP variability. In general, antioxidant capacity was higher in the FNOV than in the M group. Ovarian hormone deprivation induced a decrease in catalase activity in cardiac and renal tissues and an increase in lipid peroxidation in all tissues analyzed. Positive correlations (p 0.05) were found between vascular sympathetic modulation and lipid peroxidation in cardiac (r = 0.60), renal (r = 0.60), and muscle (r = 0.57) tissues. In conclusion, both oscillation and deprivation of ovarian hormones play an important role in cardiovascular autonomic control and oxidative stress profile in target organs, which is reflected in AP changes.
机译:研究表现出关于卵巢激素和心血管自主调节和氧化应激的波动和剥夺之间的关联的相互关系的调查结果及其对静息动脉压(AP)和心血管风险的潜在影响。本研究旨在评估雄性大鼠(M)和雌性循环(FOV)和非排卵期(FNOV)的雄性大鼠(M)和雌性大鼠中的心血管自主调制,Baroreflex敏感性(BRS)和氧化应激,并在卵巢剥夺卵巢后激素(FO)。记录直接AP,通过使用增加剂量的苯肾上腺素和硝普钠来评估BRS。通过光谱分析评估AP和心率变异性。在心脏,肾和肌肉组织中评估氧化应激谱。在雌性中,与非排卵期相比,排卵期和卵巢激素剥夺诱导AP(FOV和FO〜9〜9?mmHg)的增加。与其他群体相比,卵巢切除术促进了心脏病伴患者的伴随(〜17-37%)。 FOV和FO组均呈现出受损的BRS,与高度的AP变异性相关联。通常,FNOV中的抗氧化能力比在M组中更高。卵巢激素剥夺诱导心脏和肾组织中的过氧化氢酶活性和分析的所有组织中的脂质过氧化的增加。在心脏(r = 0.60),肾(r = 0.60)和肌肉(r = 0.57)组织之间存在血管交感神经调节和脂质过氧化之间的阳性相关性(p <0.05)。总之,卵巢激素的振荡和剥夺在靶器官中的心血管自主控制和氧化应激型中发挥着重要作用,其反映在AP变化中。

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