Oldershaw P J, Cameron I R
Department of Medicine, St. Thomas' Hospital Medical School, London, U.K.
Int J Cardiol. 1988 Feb;18(2):143-9. doi: 10.1016/0167-5273(88)90159-3.
Experiments were performed to assess the effect of long-standing (4-8 weeks) left ventricular hypertrophy (induced by experimental hypertension) on intracellular pH (pHi) and intracellular electrolytes in left ventricular tissue. They were undertaken on: (1) hypertensive rats (hypertension being induced by either (a) subdiaphragmatic aortic constriction, (b) unilateral renal artery clipping, or (c) unilateral renal artery clipping with contralateral nephrectomy); (2) sham-operated rats for the above 3 subgroups; and (3) control (unoperated) rats. In this study the hypertension (and therefore the hypertrophy) was of long (4-8 weeks) duration. Intracellular pH and intracellular electrolytes were measured in left ventricular, right ventricular and skeletal muscle tissue from these animals. Intracellular pH control was assessed by exposing a number of animals in each group to a respiratory acidosis (by varying the concentration of inspired PCO2). As described previously [Oldershaw PJ, Cameron IR, Int J Cardiol 1988;18:131-141], in the earlier stages of left ventricular hypertrophy (1-4 weeks duration) left ventricular pHi was significantly alkaline at normal levels of extracellular pH. At this late stage, with the exception of animals with aortic constriction, pHi had returned to control values. There was no change in resting levels of pHi in right ventricular or skeletal muscle tissue in any hypertensive group. The improved control of pHi in left ventricular tissue observed with hypertrophy of short duration (1-4 weeks [Oldershaw PJ, Cameron IR. Int J Cardiol 1988;18:131-141]) persisted in all experimental groups at this stage (4-8 weeks) after the onset of development of left ventricular hypertrophy. There was no change in pHi control in right ventricular or skeletal muscle tissue. Neither was there any change in intracellular electrolyte concentrations or content in association with hypertension in any tissue or group studied.
进行实验以评估长期（4 - 8周）左心室肥厚（由实验性高血压诱导）对左心室组织细胞内pH值（pHi）和细胞内电解质的影响。实验对象包括：（1）高血压大鼠（高血压通过以下方式诱导：（a）膈下主动脉缩窄，（b）单侧肾动脉夹闭，或（c）单侧肾动脉夹闭并对侧肾切除术）；（2）上述3个亚组的假手术大鼠；以及（3）对照（未手术）大鼠。在本研究中，高血压（以及由此导致的肥厚）持续时间较长（4 - 8周）。测量了这些动物左心室、右心室和骨骼肌组织中的细胞内pH值和细胞内电解质。通过使每组中的一些动物暴露于呼吸性酸中毒（通过改变吸入的PCO2浓度）来评估细胞内pH值的控制情况。如先前所述[Oldershaw PJ, Cameron IR, Int J Cardiol 1988;18:131 - 141]，在左心室肥厚的早期阶段（持续1 - 4周），在细胞外pH值正常水平时，左心室pHi显著呈碱性。在这个后期阶段，除了主动脉缩窄的动物外，pHi已恢复到对照值。任何高血压组的右心室或骨骼肌组织中pHi的静息水平均无变化。在左心室肥厚发展到这个阶段（4 - 8周）后，所有实验组中，在左心室肥厚持续时间较短（1 - 4周[Oldershaw PJ, Cameron IR. Int J Cardiol 1988;18:131 - 141]）时观察到的左心室组织中pHi控制的改善情况仍然存在。右心室或骨骼肌组织中pHi的控制没有变化。在研究的任何组织或组中，与高血压相关的细胞内电解质浓度或含量也没有任何变化。
