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用31P核磁共振研究镁缺乏、钾缺乏和氯噻嗪对大鼠细胞内pH值的影响。

Effect of magnesium depletion and potassium depletion and chlorothiazide on intracellular pH in the rat, studied by 31P NMR.

作者信息

Adam W R, Craik D J, Kneen M, Wellard R M

机构信息

Renal Unit, Repatriation General Hospital, West Heidelberg, Victoria, Australia.

出版信息

Clin Exp Pharmacol Physiol. 1989 Jan;16(1):33-40. doi: 10.1111/j.1440-1681.1989.tb01906.x.

Abstract
  1. Both dietary magnesium depletion and potassium depletion (confirmed by tissue analysis) were induced in rats which were then compared with rats treated with chlorothiazide (250 mg/kg diet) and rats on a control synthetic diet. 2. Brain and muscle intracellular pH was measured by using a surface coil and [31P]-NMR to measure the chemical shift of inorganic phosphate. pH was also measured in isolated perfused hearts from control and magnesium-deficient rats. Intracellular magnesium status was assessed by measuring the chemical shift of beta-ATP in brain. 3. There was no evidence for magnesium deficiency in the chlorothiazide-treated rats on tissue analysis or on chemical shift of beta-ATP in brain. Both magnesium and potassium deficiency, but not chlorothiazide treatment, were associated with an extracellular alkalosis. 4. Magnesium deficiency led to an intracellular alkalosis in brain, muscle and heart. Chlorothiazide treatment led to an alkalosis in brain. Potassium deficiency was associated with a normal intracellular pH in brain and muscle. 5. Magnesium depletion and chlorothiazide treatment produce intracellular alkalosis by unknown mechanism(s).
摘要
  1. 在大鼠中诱导出饮食性镁缺乏和钾缺乏(经组织分析证实),然后将这些大鼠与用氯噻嗪(250毫克/千克饮食)处理的大鼠以及食用对照合成饮食的大鼠进行比较。2. 使用表面线圈和[31P]-核磁共振来测量无机磷酸盐的化学位移,从而测定脑和肌肉细胞内的pH值。还对对照大鼠和缺镁大鼠的离体灌注心脏进行了pH值测定。通过测量脑中β-ATP的化学位移来评估细胞内镁状态。3. 经组织分析或脑中β-ATP化学位移检测,未发现氯噻嗪处理的大鼠存在镁缺乏证据。镁缺乏和钾缺乏均与细胞外碱中毒有关,但氯噻嗪处理未导致此情况。4. 镁缺乏导致脑、肌肉和心脏细胞内碱中毒。氯噻嗪处理导致脑内碱中毒。钾缺乏与脑和肌肉细胞内pH值正常有关。5. 镁缺乏和氯噻嗪处理通过未知机制导致细胞内碱中毒。

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