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目的观察慢性盐负荷诱导高血压大鼠胸主动脉重构的影响并探讨其可能机制。方法雄性大鼠分为2组,分别采用4%高盐和0.4%低盐饮食持续诱导16周,每隔4周监测血压、尿量和尿钠;采集胸主动脉切片,观察病理变化,测量管壁厚度、管腔直径,比较管壁厚度/管腔直径比值;免疫组化法测定胸主动脉管壁转化生长因子β1(TGFβ1)、内皮型一氧化氮合酶(eNOS)的蛋白表达。结果观察期各周,高盐组收缩压、尿量及尿钠均高于低盐组,高盐摄入、大鼠周龄对血压变化有影响(P<0.05);2组大鼠胸主动脉管壁均随周龄增加逐渐增厚,管腔逐渐变狭窄;第8、12、16周时,高盐组胸主动脉管壁厚度分别为(117.0±8.8)、(124.7±8.8)、(168.1±32.7)μm,均高于低盐组(P<0.05或P<0.01);第4、8周时高盐组胸主动脉TGFβ1、eNOS表达明显增加,第12、16周时逐渐减少;各观察期内,高盐组TGFβ1表达的吸光度值分别为(11795.8±1079.4)、(17773.8±928.3)、(6019.4±433.4)、(5455.6±380.2);eNOS表达的吸光度值分别为(14970.1±1249.2)、(18236.6±2723.9)、(7201.9±1006.5)、(8068.2±1418.2),均高于低盐组(P<0.05或P<0.01)。结论慢性盐负荷可加重实验大鼠胸主动脉重构,盐负荷后大鼠胸主动脉局部TGFβ1含量的增加可能是其导致血管重构的原因之一。
Objective To investigate the effect of chronic salt stress-induced thoracic aorta remodeling in hypertensive rats and to explore its possible mechanism. Methods Male rats were divided into two groups. The rats were continuously induced by 4% high salt and 0.4% low salt diet for 16 weeks. Blood pressure, urine output and urinary sodium were monitored every 4 weeks. Thoracic aorta sections were collected to observe the pathological changes. The thickness of the wall, the diameter of the lumen and the ratio of the thickness of the lumen to the diameter of the lumen were compared. The protein expressions of the transforming growth factor β1 (TGFβ1) and endothelial nitric oxide synthase (eNOS) in the thoracic aorta were detected by immunohistochemistry. Results During the observation period, systolic blood pressure, urine volume and urinary sodium in high-salt group were significantly higher than those in low-salt group and high-salt diet. The changes of blood pressure were influenced by the age of rats (P <0.05) The arterial wall thickens gradually with the increase of the age, and the lumen gradually narrows. At the 8th, 12th and 16th week, the thoracic aortic wall thicknesses in the high salt group are (117.0 ± 8.8), (124.7 ± 8.8), (168.1 ± 32.7) μm, all higher than those in the low-salt group (P <0.05 or P <0.01). The expression of TGFβ1 and eNOS in the thoracic aorta increased significantly at the 4th and 8th week, ; The absorbance values of TGFβ1 expression in high salt group were (11795.8 ± 1079.4), (17773.8 ± 928.3), (6019.4 ± 433.4) and (5455.6 ± 380.2) respectively in each observation period; the absorbance values of eNOS expression were (14970.1 ± 1249.2), (18236.6 ± 2723.9), (7201.9 ± 1006.5) and (8068.2 ± 1418.2), respectively, were significantly higher than those in the low-salt group (P <0.05 or P <0.01). Conclusion Chronic salt stress may aggravate thoracic aorta remodeling in rats, and the increase of TGFβ1 in rat thoracic aorta after salt stress may be one of the reasons leading to vascular remodeling.