覃燕青，沈洁，黄世园，蒋贤逊，王小同.神经肌肉电刺激对慢性低氧高二氧化碳模型大鼠肺动脉高压的影响[J].中华物理医学与康复杂志,2017,39(3):165-169
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| 神经肌肉电刺激对慢性低氧高二氧化碳模型大鼠肺动脉高压的影响 |
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| DOI： |
| 中文关键词: 低氧高二氧化碳 肺动脉高压 神经肌肉电刺激 低氧诱导因子-1α 大鼠 |
| 英文关键词: Hypoxic hypercapnia Pulmonary arterial hypertension Neuromuscular electrical stimulation Hypoxia-inducible factor-1α |
| 基金项目:浙江省自然科学基金（Y2080503） |
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| 摘要点击次数: 2436 |
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| 中文摘要: |
| 目的观察神经肌肉电刺激对慢性低氧高二氧化碳大鼠肺动脉高压的影响。 方法选取雄性SD大鼠18只，按随机数字表法分为正常对照组(对照组)、低氧高二氧化碳组（模型组）和低氧高二氧化碳+神经肌肉电刺激组（电刺激组），每组6只大鼠。模型组和电刺激组每天置于氧舱内（O2浓度9%至11%,CO2浓度5%至6%）8h进行造模，连续4周，对照组则吸入普通空气。每天造模结束后对电刺激组大鼠双侧腓肠肌进行神经肌肉电刺激30min。4周后,处死大鼠，分离右心室(RV)和左心室加室间隔(LV+S),计算右心肥厚指数RVHI［RVHI=RV/(LV+S)］,光镜下观察大鼠肺细小动脉结构形态变化，计算出管壁厚度占血管外径的百分比（WT%）和管壁面积占血管总面积的百分比（WA%）；采用蛋白质印迹法检测低氧诱导因子-1α(HIF-1α)、丙酮酸脱氢酶-E1(PDH-E1)、3-磷酸肌醇依赖性蛋白激酶1（PDK1）蛋白表达；同时采用微量酶标法检测(LDH)活性，采用ELISA法检测丙酮酸脱氢酶(PDH)的浓度。 结果与对照组比较，模型组的RVHI、WT％、WA％值均升高（P<0.01），HIF-1α、PDK1蛋白表达水平增高（P<0.01），PDH-1Eα蛋白表达下降（P<0.01），LDH活性提高（P<0.01），PDH浓度未见明显差异（P>0.05）。与模型组相比较，电刺激组的RVHI、WT％、WA％值均显著降低（P<0.01），HIF-1α，PDK1蛋白表达明显下降（P<0.01），PDH-E1α蛋白表达明显增高（P<0.01），LDH活性显著下降（P<0.01），PDH浓度未见明显差异（P>0.05）。 结论神经肌肉电刺激可能通过抑制HIF-1α蛋白表达，抑制PDK1、PDH-E1α活性、LDH活性，抑制肺组织氧化磷酸化向糖酵解转变，从而减轻肺血管重塑，改善慢性低氧高二氧化碳所致的大鼠肺动脉高压。 |
| 英文摘要: |
| Objective To investigate effects of neuromuscular electrical stimulation (NMES) on pulmonary arterial hypertension induced by chronic hypoxic hypercapnia in rats. MethodsEighteen male Sprague-Dawley rats were randomly divided into a normal control group (the control group), a hypoxic hypercapnia group (the model group), and a hypoxic hypercapnia + NMES group (the NMES group), each of 6. The rats in both the model and NMES groups were placed in an isobaric cabin with an O2 concentration of 9% to 11% and a CO2 concentration of 5% to 6% for 8 hours a day for 4 weeks. After leaving the cabin, NMES was performed on the NMES group′s bilateral calf muscles for 30 minutes every day. The heart was removed, and the right ventricle (RV) and the left ventricle plus the septum (LV+S) were dissected. An index of right ventricular hypertrophy was calculated as RVHI=RV/(LV+S). Any changes in the pulmonary vasculature were observed using an optical microscope. WT% and WA% were calculated. The expression of hypoxia-inducible factor-1α (HIF-1α), PDH-E1α and PDK1 in the lung tissue were determined using western blotting. The LDH activity and the concentration of PDH in the lung tissue homogenate were measured was measured by spectrophotometric method using the LDH assay kit and ELISA , respectively. ResultsCompared with the control group, the average RVHI, WT% and WA%, the protein expression of HIF-1α and PDK1, and LDH activity had all increased significantly in the NMES group, while the average expression of PDH-1Eα had decreased significantly. Compared with the model group, significant decrease was observed in the average RVHI, WT%, WA%, protein expression of HIF-1α and PDK1, and LDH activity in the NMES group, but the average expression of PDH-1Eα increased significantly. No significant differences in PDH concentration were detected among the 3 groups. ConclusionsNMES may alleviate pulmonary artery hypertension induced by chronic hypoxic hypercapnia, at least in rats. The mechanism may be attributed to inhibiting the expression of HIF-1α protein, which may inhibit the activity of PDH-E1α and LDH, then the aerobic metabolism into glycolysis, finally improving the remodeling of the pulmonary vascular structure. |
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