Carlier P, Smelten N, Ciancabilla F, Rorive G
Service hospitalier Frédéric-Joliot, Commissariat à l'énergie atomique, Orsay.
Arch Mal Coeur Vaiss. 1994 Aug;87(8):1041-5.
In this study, we determined a) whether chronic antihypertensive treatment could alter myocardial free intracellular magnesium concentrations, b) whether changes in magnesium concentration would correlate with resistance to anoxia of hypertensive rat hearts. Six-month old male spontaneously hypertensive (HT) rats (n = 11) were compared to rats from the same strain treated with a calcium channel antagonist, nitrendipine (60 mg/kg/j; n = 11) or with a converting-enzyme inhibitor, perindopril (2 mg/kg/j; n = 9) during three months. The hearts were perfused in retrograde isovolumic mode and submitted to a standardized anoxia-recovery protocol. Aortic perfusion pressure and left ventricular pressure were constantly monitored. P-31 NMR spectra were simultaneously recorded and allowed to quantify the changes in myocardial inorganic phosphate, phosphocreatine and ATP. The pH was derived from the chemical shifts of inorganic phosphate and phosphocreatine, and the free intracellular magnesium concentration from the alpha-beta chemical shifts of ATP. Both treatments lowered systolic blood pressure and reversed left ventricular hypertrophy, perindopril being slightly more efficient at the dose administered. Intracellular magnesium concentration, calculated from the P-31 NMR spectra, was 277 +/- 17 microM in the untreated hypertensive group, 311 +/- 15 microM in the nitrendipine group and 401 +/- 17 microM in the perindopril group (p < 0.001 versus untreated and nitrendipine). There was a significant correlation between intracellular magnesium concentration and left ventricular developed pressure at the early stage of post-anoxic recovery (r = 0.61; p < 0.01). P-31 NMR spectroscopy demonstrates an increase in myocardial free intracellular magnesium concentration following chronic administration of an angiotensin-converting enzyme inhibitor, perindopril, spontaneously hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)
在本研究中,我们确定了:a)慢性抗高血压治疗是否会改变心肌细胞内游离镁浓度;b)镁浓度的变化是否与高血压大鼠心脏的缺氧耐受性相关。将6个月大的雄性自发性高血压(HT)大鼠(n = 11)与同一品系中在三个月内接受钙通道拮抗剂尼群地平(60 mg/kg/天;n = 11)或转化酶抑制剂培哚普利(2 mg/kg/天;n = 9)治疗的大鼠进行比较。心脏以逆行等容模式灌注,并接受标准化的缺氧-复氧方案。持续监测主动脉灌注压和左心室压力。同时记录P-31 NMR光谱,以量化心肌无机磷酸盐、磷酸肌酸和ATP的变化。pH值由无机磷酸盐和磷酸肌酸的化学位移得出,细胞内游离镁浓度由ATP的α-β化学位移得出。两种治疗均降低了收缩压并逆转了左心室肥厚,在所给药剂量下培哚普利的效果略好。根据P-31 NMR光谱计算,未治疗的高血压组细胞内镁浓度为277±17 μM,尼群地平组为311±15 μM,培哚普利组为401±17 μM(与未治疗组和尼群地平组相比,p < 0.001)。在缺氧后恢复的早期阶段,细胞内镁浓度与左心室舒张末压之间存在显著相关性(r = 0.61;p < 0.01)。P-31 NMR光谱显示,自发性高血压大鼠长期服用血管紧张素转化酶抑制剂培哚普利后,心肌细胞内游离镁浓度增加。(摘要截断于250字)