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慢性维生素E缺乏和高多不饱和脂肪酸饮食对大鼠肠系膜动脉功能的影响。

Effects of chronic vitamin E deficiency and a high polyunsaturated fatty acid diet on rat mesenteric arterial function.

作者信息

Ralevic V, Milla P J, Burnstock G

机构信息

Department of Anatomy and Developmental Biology, University College London.

出版信息

Br J Pharmacol. 1995 Dec;116(7):3075-81. doi: 10.1111/j.1476-5381.1995.tb15966.x.

Abstract
  1. Male rats were deprived as weanlings of dietary vitamin E and fed on a high polyunsaturated fatty acid (PUFA) diet for 6 months. Rats fed on a high PUFA or on an untreated diet served as controls. Mesenteric arterial beds were isolated and perfused at a constant flow rate (5 ml min-1) and the function of sympathetic nerves, smooth muscle and endothelium was assessed. 2. Electrical field stimulation (4-32 Hz, 90 V, 1 ms, for 30 s) elicited frequency-dependent vasoconstriction of the mesenteric arterial preparations. Response curves were similar between untreated control and PUFA-fed control groups. Maximum vasoconstrictor responses (at 24 and 32 Hz) were significantly attenuated in rats deprived of vitamin E and on a high PUFA diet compared to the PUFA-fed controls (P < 0.05). 3. Exogenous noradrenaline (NA; 0.15-500 nmol) elicited dose-dependent constriction of the mesenteric arterial beds. Preparations from rats fed on a high PUFA diet elicited significantly smaller responses compared to the control group. There was no significant difference in constrictor responses of PUFA rats deprived of vitamin E compared to the PUFA controls. Vasoconstrictor responses to doses of adenosine 5'-triphosphate (ATP) (5-5000 nmol) were significantly impaired in vitamin E-deficiency with a high PUFA diet compared to a high PUFA diet alone (P < < 0.001). Constrictor responses to potassium chloride (0.15 mmol) were significantly impaired in vitamin E-deficient PUFA rats compared to the PUFA-fed control group (P < 0.05). 4. Vasodilator responses were assessed in preparations in which tone was raised by continuous perfusion with methoxamine (4-25 microM). Mesenteric arterial beds from PUFA-fed rats deprived of vitamin E acquired significantly less tone, 59.8 +/- 4.6 mmHg (n = 7), than PUFA-fed controls 116.9 +/- 7.6 mmHg (n = 7) (P < 0.001) and were refractory to further increases in tone with further additions of methoxamine. Methoxamine-induced tone of PUFA-fed controls was greater than in P that in the untreated controls (83.9 +/- 7.4 mmHg; n = 5) (P < 0.05). Responses to the endothelium-dependent vasodilators acetylcholine (ACh) and ATP were significantly reduced in preparations from rats fed on the vitamin E-deficient high-PUFA diet compared to PUFA controls. Vasodilator responses to ACh were greater in PUFA controls than in untreated controls and this reached statistical significance at 5 nmol ACh. 5. Vasodilator responses to sodium nitroprusside, which acts directly on the vascular smooth muscle, were similar in untreated control and PUFA control groups. Responses were significantly attenuated in vitamin E-deficient PUFA rats compared to the PUFA control group (P < < 0.001). 6. These results indicate that a combination of a high PUFA diet and vitamin E deficiency impairs mesenteric arterial function at the level of the vascular smooth muscle. A high PUFA diet alone attenuates responses to NA and augments endothelium-dependent vasodilation. The detrimental effects of loss of antioxidant activity due to vitamin E-deficiency on vascular function may be exacerbated by a high PUFA diet.
摘要
  1. 雄性大鼠在断奶时被剥夺膳食维生素E,并喂食高多不饱和脂肪酸(PUFA)饮食6个月。喂食高PUFA饮食或未处理饮食的大鼠作为对照。分离肠系膜动脉床并以恒定流速(5 ml min-1)灌注,评估交感神经、平滑肌和内皮的功能。

  2. 电场刺激(4 - 32 Hz,90 V,1 ms,持续30 s)引起肠系膜动脉制剂的频率依赖性血管收缩。未处理对照组和喂食PUFA对照组之间的反应曲线相似。与喂食PUFA的对照组相比,缺乏维生素E且喂食高PUFA饮食的大鼠的最大血管收缩反应(在24和32 Hz时)显著减弱(P < 0.05)。

  3. 外源性去甲肾上腺素(NA;0.15 - 500 nmol)引起肠系膜动脉床的剂量依赖性收缩。与对照组相比,喂食高PUFA饮食的大鼠的制剂引起的反应明显较小。与PUFA对照组相比,缺乏维生素E的PUFA大鼠的收缩反应没有显著差异。与单独的高PUFA饮食相比,在维生素E缺乏且高PUFA饮食的情况下,对5'-三磷酸腺苷(ATP)(5 - 5000 nmol)剂量的血管收缩反应显著受损(P << 0.001)。与喂食PUFA的对照组相比,维生素E缺乏的PUFA大鼠对氯化钾(0.15 mmol)的收缩反应显著受损(P < 0.05)。

  4. 在通过用甲氧明(4 - 25 microM)持续灌注来升高张力的制剂中评估血管舒张反应。与喂食PUFA的对照组116.9±7.6 mmHg(n = 7)相比,缺乏维生素E的喂食PUFA大鼠的肠系膜动脉床获得的张力显著较小,为59.8±4.6 mmHg(n = 7)(P < 0.001),并且对进一步添加甲氧明导致的张力进一步增加无反应。甲氧明诱导的喂食PUFA对照组的张力大于未处理对照组(83.9±7.4 mmHg;n = 5)(P < 0.05)。与PUFA对照组相比,在喂食维生素E缺乏的高PUFA饮食的大鼠的制剂中,对内皮依赖性血管舒张剂乙酰胆碱(ACh)和ATP的反应显著降低。在PUFA对照组中,对ACh的血管舒张反应大于未处理对照组,并且在5 nmol ACh时达到统计学显著性。

  5. 对直接作用于血管平滑肌的硝普钠的血管舒张反应在未处理对照组和PUFA对照组中相似。与PUFA对照组相比,维生素E缺乏的PUFA大鼠的反应显著减弱(P << 0.001)。

  6. 这些结果表明,高PUFA饮食和维生素E缺乏的组合在血管平滑肌水平损害肠系膜动脉功能。单独的高PUFA饮食减弱对NA的反应并增强内皮依赖性血管舒张。高PUFA饮食可能会加剧由于维生素E缺乏导致的抗氧化活性丧失对血管功能的有害影响。

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