Nuclear magnetic resonance measurement of intracellular sodium in the perfused normotensive and spontaneously hypertensive rat heart.
Nuclear magnetic resonance measurement of intracellular sodium in the perfused normotensive and spontaneously hypertensive rat heart.
复制标题
核磁共振测量正常血压和自发性高血压大鼠心脏细胞内钠。
DOI：
10.1093/ajh/7.5.429
复制
发表时间：
1994
影响因子：
3.2
通讯作者：
Gupta,RK
中科院分区：
文献类型：
--
作者：
Jelicks,LA;Gupta,RK
我们用23 Na核磁共振波谱检查遗传性高血压患者细胞内钠离子与心肌改变之间的关系。在自发性高血压大鼠（SHR）与血压正常的Wistar-Kyoto大鼠（WKY）（15 - 19周龄）中，平均收缩压（使用尾袖法测量）显著（P<0.05）不同（WKY：118 ± 8 mm Hg，n = 5; SHR：185 ± 9 mm Hg，n = 5）。SHR的心脏重量也显著增加（P<0.05）（SHR的心脏干重/千克体重比为0.73 ± 0.04，n = 5，WKY的心脏干重/千克体重比为0.55 ± 0.02，n = 5）。采用位移试剂辅助和三重量子滤波（TQF）核磁共振技术测量的离体Langendorff灌注的高血压大鼠心脏（17.3 ± 3.6 mmol/L，n = 5）细胞内钠水平与正常血压大鼠心脏（8.4 ± 2.3 mmol/L，n = 5）相比显著增加（P<0.05）。这些数据表明，在原发性高血压心肌钠增加。我们还研究了起搏对心脏TQF 23 Na核磁共振的影响，发现在WKY和SHR心脏中TQF Na+含量在加速起搏时增加。这些结果支持在生理Ca 2+浓度下灌注的大鼠心脏中存在钠泵滞后，并表明高血压大鼠心脏已适应于补偿增加的基础细胞内Na+并维持对心率增加的正常反应。我们的数据似乎表明，在大鼠遗传性高血压的心脏肥大的离子的贡献。美国高血压杂志1994;7：429-435
We have used23Na nuclear magnetic resonance spectroscopy to examine the relationship between intracellular sodium and cardiac muscle alterations in genetic hypertension. In the spontaneously hypertensive rat (SHR) compared with the normotensive Wistar-Kyoto rat (WKY) (aged 15 to 19 weeks), mean systolic blood pressures (measured using the tail-cuff method) were significantly (P< .05) different (WKY: 118 ± 8 mm Hg, n = 5; SHR: 185 ± 9 mm Hg, n = 5). Heart weights were also increased significantly (P< .05) in SHR (grams dry heart to kilograms body weight ratio was 0.73 ± 0.04, n = 5, for SHR and 0.55 ± 0.02, n = 5, for WKY). Intracellular sodium levels, measured using shift-reagent-aided and triple quantum filtered (TQF) nuclear magnetic resonance techniques, were significantly increased (P< .05) in the isolated Langendorff perfused hypertensive rat hearts (17.3 ± 3.6 mmol/L, n = 5) compared with normotensive rat hearts (8.4 ± 2.3 mmol/L, n = 5). These data demonstrate increased sodium in cardiac muscle in essential hypertension. We also investigated the effect of pacing on cardiac TQF23Na nuclear magnetic resonance and found an increase in TQF Na+content in both WKY and SHR hearts on stepped up pacing. These results support the existence of sodium pump lag in the rat heart perfused at physiologic Ca2+concentration and suggest that the hypertensive rat heart has adapted to compensate for increased basal intracellular Na+and maintain a normal response to increased heart rate. Our data appear to suggest an ionic contribution to the cardiac hypertrophy of genetic hypertension in the rat. Am J Hypertens 1994;7:429–435