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目的探讨孕期脂多糖刺激对子代大鼠肠系膜血管功能的影响。方法将12只SD孕鼠随机分为脂多糖组(n=6)和对照组(n=6)。对照组腹腔注射无菌生理盐水0.5mL;脂多糖组腹腔注射脂多糖0.79mg/kg。分别在孕期第8、10、12天9:00-10:00进行腹腔注射。子代大鼠出生4周龄时断奶,每组均随机选择子代雄鼠6只,子代大鼠9、11、13、15周龄采用鼠尾无创血压测量方法进行尾动脉血压测量,观察子代大鼠肠系膜三级血管对血管紧张素Ⅱ(AngⅡ)(10-10~10-5 mol/L)的反应性和肠系膜动脉血管紧张素Ⅱ1型受体(AT1R)蛋白的表达。结果子代大鼠9、11、13、15周龄时,脂多糖组收缩压高于对照组[分别(109.6±2.6)比(102.9±2.5),(117.7±1.5)比(108.1±3.3),(128.1±3.6)比(117.2±2.1),(135.1±3.2)比(123.0±2.3)mm Hg,均P<0.01];脂多糖组肠系膜动脉对AngⅡ诱导的最大收缩反应、AT1R蛋白表达高于对照组[分别(8.5±0.4)比(3.5±0.3)mN,1.21±0.08比0.75±0.08,均P<0.05]。结论孕期脂多糖暴露导致子代大鼠肠系膜AngⅡ介导的血管收缩功能异常,血管阻力增加,可能是子代大鼠血压升高的重要原因。
Objective To investigate the effects of gestational lipopolysaccharide stimulation on mesenteric vascular function in offspring rats. Methods Twelve SD pregnant rats were randomly divided into lipopolysaccharide group (n = 6) and control group (n = 6). The control group was injected intraperitoneally with 0.5 mL of sterile saline; LPS was intraperitoneally injected with 0.79 mg / kg of LPS. Respectively, during pregnancy 8,10,12 days 9: 00-10: 00 for intraperitoneal injection. The offspring of the offspring were weaned at 4 weeks of age. Six male offspring were randomly selected in each group. Tail arterial blood pressure was measured at 9, 11, 13 and 15 weeks of age on the tail of the offspring rats by noninvasive blood pressure measurement Reactivity of mesenteric blood vessel of third generation to angiotensin Ⅱ (10-10 ~ 10-5 mol / L) and expression of mesenteric artery angiotensin Ⅱ type 1 receptor (AT1R) in offspring rats. Results Compared with the control group, the systolic blood pressure of the lipopolysaccharide group was significantly higher at the 9th, 11th, 13th and 15th weeks of age in the offspring rats [(109.6 ± 2.6) vs (102.9 ± 2.5), (117.7 ± 1.5) vs (108.1 ± 3.3) , (128.1 ± 3.6) vs (117.2 ± 2.1), (135.1 ± 3.2) vs (123.0 ± 2.3) mm Hg, all P <0.01]. The maximal contractile response induced by AngⅡ and the high expression of AT1R protein in the mesenteric artery of the lipopolysaccharide group In the control group [(8.5 ± 0.4) vs (3.5 ± 0.3) mN, 1.21 ± 0.08 vs. 0.75 ± 0.08, all P <0.05]. Conclusion Exposure to lipopolysaccharide during pregnancy leads to abnormal mesenteric angiotensin Ⅱ-mediated vasoconstriction and increased vascular resistance in the offspring rats, which may be an important reason for the increased blood pressure in offspring rats.