Rasmussen H S, Cintin C, Aurup P, Breum L, McNair P
Medical Department P/Chest Clinic, Bispebjerg Hospital.
Arch Intern Med. 1988 Aug;148(8):1801-5.
Serum concentrations of magnesium, potassium, calcium, and sodium were determined on admission of 224 patients to the hospital and after 2, 4, and 6 days in hospital; all were admitted to the hospital with suspected acute myocardial infarction (AMI). On admission, the patients were randomly allocated to 48 hours of treatment with magnesium intravenously or placebo. One hundred twenty-three patients had AMI (of whom 53 [43%] were treated with magnesium) and 101 had their suspected AMI disproven (of whom 51 [50%] were treated with magnesium). In a supplementary study, serum and urine levels of magnesium, potassium, calcium, and sodium, together with serum levels of parathyroid hormone, were determined before and after intravenous magnesium treatment in six patients with AMI and six patients with ischemic heart disease but without AMI. In both studies, magnesium therapy was associated with significant alterations in extracellular ion homeostasis. Serum concentrations of potassium decreased during the initial days of hospitalization in the patients treated with placebo, but increased slightly in the patients treated with magnesium infusions. These increments in the serum concentrations of magnesium and potassium correlated significantly. The increase in the serum concentration of potassium after magnesium infusions was due to a reduced renal potassium excretion level (from 71.3 to 49.4 mmol/24 h), indicating the existence of a divalent-monovalent cation exchange mechanism in the nephron. This hypothesis was supported by the observation that renal sodium excretion likewise decreased after magnesium infusions (from 83.2 to 59.2 mmol/24 h). Serum concentration of calcium decreased significantly after magnesium treatment (from 2.35 mmol/L on admission to 2.15 mmol/L after 24 hours in the hospital) in the AMI group, in contrast to the placebo-treated patients, where no significant fluctuations in serum concentration of calcium were detected during the initial six days. This decrease in serum concentration of calcium was due to a marked increase in renal calcium excretion (from 3.43 mmol/24 h before to 6.59 mmol/24 h after magnesium infusion). A correlation between increments in serum magnesium concentration and decrements in serum calcium concentration was detected. No change in serum levels of parathyroid hormone was found before and after magnesium infusions. Both serum and urine levels of magnesium significantly increased after magnesium treatment to levels above the upper normal limits (serum magnesium concentration increased from 0.81 to 1.21 mmol/L, urine magnesium excretion levels from 3.57 to 16.57 mmol/24 h for both serum and urine changes.(ABSTRACT TRUNCATED AT 400 WORDS)
对224例疑似急性心肌梗死（AMI）入院患者在入院时以及入院后2天、4天和6天测定了血清镁、钾、钙和钠浓度。入院时，患者被随机分配接受48小时静脉注射镁治疗或安慰剂治疗。123例患者确诊为AMI（其中53例[43%]接受了镁治疗），101例患者疑似AMI被排除（其中51例[50%]接受了镁治疗）。在一项补充研究中，测定了6例AMI患者和6例有缺血性心脏病但无AMI患者静脉注射镁治疗前后的血清和尿液中镁、钾、钙、钠水平以及血清甲状旁腺激素水平。在两项研究中，镁治疗均与细胞外离子稳态的显著改变有关。接受安慰剂治疗的患者在住院初期血清钾浓度降低，但接受镁输注治疗的患者血清钾浓度略有升高。血清镁和钾浓度的这些升高显著相关。镁输注后血清钾浓度升高是由于肾钾排泄水平降低（从71.3降至49.4 mmol/24 h），表明肾单位中存在二价-单价阳离子交换机制。这一假设得到了以下观察结果的支持：镁输注后肾钠排泄同样减少（从83.2降至59.2 mmol/24 h）。与安慰剂治疗的患者相比，AMI组镁治疗后血清钙浓度显著降低（入院时为2.35 mmol/L，住院24小时后为2.15 mmol/L），而安慰剂治疗的患者在最初6天内血清钙浓度未检测到显著波动。血清钙浓度降低是由于肾钙排泄显著增加（镁输注前为3.43 mmol/24 h，输注后为6.59 mmol/24 h）。检测到血清镁浓度升高与血清钙浓度降低之间存在相关性。镁输注前后血清甲状旁腺激素水平未发现变化。镁治疗后血清和尿液中镁水平均显著升高，高于正常上限（血清镁浓度从0.81 mmol/L升至1.21 mmol/L，尿液镁排泄水平从3.57 mmol/24 h升至16.57 mmol/24 h，血清和尿液均有变化）。（摘要截短至400字）
