Kreusser W, Vetter H O, Mittmann U, Hörl W H, Ritz E
Eur J Clin Invest. 1982 Jun;12(3):219-28. doi: 10.1111/j.1365-2362.1982.tb00996.x.
The responses of arterial pressure and myocardial contractile force (VPM) to infusion of angiotensin II, noradrenaline and orciprenaline were examined in twelve dogs during a control phase, after 30 days of dietary phosphorus deprivation and after 21 days of phosphorus repletion. In the phosphorus depletion period, animals had low skeletal and heart muscle Pi content, low magnesium, ATP and creatine phosphate in skeletal and heart muscle with no change of ADP, AMP or energy charge. In the basal state, VPM was diminished with no change of end-diastolic and systolic pressure. Infusion of angiotensin II caused a significantly smaller rise of arterial pressure (angiotensin II resistance), and the stimulatory effect of noradrenaline and orciprenaline on VPM was diminished (catecholamine resistance). These effects were reversible with Pi repletion. In phosphorus depletion, arterial concentrations were increased for lactate, unchanged for FFA and decreased for acetoacetate/beta-hydroxybutyrate. Unchanged myocardial extraction of lactate or beta-hydroxybutyrate and preserved cell Pi uptake for glycogenolysis were observed. The initial rate of uptake of calcium and concentrating ability of myocardial sarcoplasmic reticulum were unchanged.
在12只犬的对照期、膳食磷缺乏30天后以及磷补充21天后,检测了动脉血压和心肌收缩力(VPM)对血管紧张素II、去甲肾上腺素和奥西那林输注的反应。在磷缺乏期,动物的骨骼肌和心肌磷含量低,骨骼肌和心肌中的镁、ATP和磷酸肌酸含量低,而ADP、AMP或能荷无变化。在基础状态下,VPM降低,舒张末期和收缩压无变化。输注血管紧张素II导致动脉压升高明显较小(血管紧张素II抵抗),去甲肾上腺素和奥西那林对VPM的刺激作用减弱(儿茶酚胺抵抗)。这些作用可通过磷补充逆转。在磷缺乏时,动脉血中乳酸浓度升高,游离脂肪酸浓度无变化,乙酰乙酸/β-羟丁酸浓度降低。观察到心肌对乳酸或β-羟丁酸的摄取无变化,且保存了用于糖原分解的细胞磷摄取。心肌对钙的初始摄取速率和肌浆网的浓缩能力无变化。