摘要
目的:探讨腹内压力对高血压相关指标肾素、血管紧张素Ⅰ(AngⅠ)、血管紧张素Ⅱ(AngⅡ)和葡萄糖代谢相关指标空腹血糖、糖耐量、胰岛素的影响。方法:将19只大鼠随机分成生理盐水组(对照组)和矿物油组(实验组),实验组腹腔连续间断注射矿物油建立慢性腹水大鼠模型,对照组连续间断注射相同量的生理盐水,5周后测量腹内压,检测肾素、AngⅠ、AngⅡ、胰岛素、空腹血糖水平和糖耐量功能。结果:与对照组相比,实验组肾素与AngⅠ水平明显降低(P<0.05或P<0.01),胰岛素及AngⅡ比较,差异无统计学意义,空腹血糖水平明显降低(P<0.01),葡萄糖激发后的30 min及1 h血糖水平明显升高(P<0.05或P<0.01),2 h血糖水平无显著差异。结论:单独增加腹内压力可能在该动物模型中引起肾素-血管紧张素系统紊乱和葡萄糖代谢异常。
Objective: Overweight and obesity,especially those with abdominal obesity,are more likely to have metabolic diseases.Studies have also shown that pregnant women are more prone to metabolic diseases than non-pregnant women. To investigate the relationship between metabolic diseases and increase in intra-abdominal pressure (IAP),this study investigated the effects of increased IAP on fasting blood glucose,glucose tolerance,and insulin in glucose metabolism and the indicators of hypertension,such as renin,angiotensinⅠ (Ang Ⅰ),angiotensin Ⅱ (Ang Ⅱ). Methods: Nineteen rats were randomly divided into normal saline group and mineral oil group.The experimental group was treated with intermittent intraperitoneal injection of mineral oil to establish a chronic ascites rat model. The control group was continuously injected with the same amount of saline continuously. The intra-abdominal pressure renin,angiotensin Ⅰ,angiotensin Ⅱ,insulin,fasting glucose levels,glucose levels at half an hour and glucose at 1 and 2 hours after glucose challenge were measured after 5 weeks. Results: Compared with the control group,the levels of renin and angiotensin I were significantly lower in the experimental group (P<0.05 or P<0.01). There was no significant difference in insulin and angiotensin II between the two groups,and the fasting blood glucose level was significantly reduced (P<0.01). Glucose levels were significantly increased at half an hour and 1 hour after glucose challenge (P<0.05 or P<0.01),and there was no significant difference in blood glucose level at 2 hours. Conclusion: Increasing intra-abdominal pressure alone may cause renin-angiotensin system disorders and abnormal glucose metabolism in this animal model.
引文
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