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自发性高血压大鼠低镁血症的血流动力学和代谢影响

Hemodynamic and metabolic effects of hypomagnesemia in spontaneously hypertensive rats.

作者信息

Chrysant S G, Ganousis L, Chrysant C

机构信息

Department of Medicine, University of Kansas, Kansas City, Mo.

出版信息

Cardiology. 1988;75(2):81-9. doi: 10.1159/000174354.

Abstract

The hemodynamic and metabolic effects of dietary induced hypomagnesemia were studied in two groups of 2-month-old male spontaneously hypertensive rats (SHR). All rats were given distilled water to drink ad libitum and were followed for 2 months. However, control rats (n = 12) were given a regular rat diet to eat, whereas the experimental (hypomagnesemic; HM) rats (n = 12) were given a magnesium-free diet. Metabolic and hemodynamic studies were done at the end of the 2-month observation period in the awake state. HM rats had higher mean arterial pressure, total peripheral resistance, renal vascular resistance, heart rate, UNaV, UKV and serum Na, and lower hematocrit, renal blood flow, serum K and serum Mg than the controls. No differences were observed among the two groups of rats with respect to weight, fluid intake, urine volume, serum calcium, blood urea nitrogen, cardiac index and glomerular filtration rate. In addition, HM rats had widespread myocardial and renal tissue calcification in contrast to controls, which did not show any tissue calcification. We conclude: (1) dietary-induced hypomagnesemia aggravated the hypertension of SHR; (2) it caused widespread tissue calcification; (3) the adverse effects of hypomagnesemia on arterial pressure were possibly produced through calcium-mediated systemic vasoconstriction and increase in peripheral vascular resistance.

摘要

在两组2个月大的雄性自发性高血压大鼠(SHR)中研究了饮食诱导的低镁血症的血流动力学和代谢效应。所有大鼠随意饮用蒸馏水,持续观察2个月。然而,对照组大鼠(n = 12)给予常规大鼠饮食,而实验组(低镁血症;HM)大鼠(n = 12)给予无镁饮食。在2个月观察期结束时,对清醒状态的大鼠进行代谢和血流动力学研究。与对照组相比,HM大鼠的平均动脉压、总外周阻力、肾血管阻力、心率、尿钠排泄量、尿钾排泄量和血清钠更高,而血细胞比容、肾血流量、血清钾和血清镁更低。两组大鼠在体重、液体摄入量、尿量、血清钙、血尿素氮、心脏指数和肾小球滤过率方面未观察到差异。此外,与未出现任何组织钙化的对照组相比,HM大鼠出现广泛的心肌和肾组织钙化。我们得出结论:(1)饮食诱导的低镁血症加重了SHR的高血压;(2)它导致广泛的组织钙化;(3)低镁血症对动脉压的不利影响可能是通过钙介导的全身血管收缩和外周血管阻力增加产生的。

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