摘要
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 observe the effect of chronic salt loading on the remodeling of thoracic aorta in spontaneously hypertensive rats and to investigate possible mechanism.Methods Spontaneouly hypertensive rats（SHR）（n=80,male,4-5 weeks old） were assigned randomly to receive 4% high salt（HS group,n=45） and 0.4% low salt（LS group,n=35） for 16 weeks.Blood pressure,urine volume,and urinary sodium excretion were measured every four weeks.The rats were sacrificed randomly at the start,the 4th,8th,12th,16th week of the study.The aorta samples were collected and dyed with haematoxylin eosin（HE） to observe the change of aorta with microscope.The microholography system was used to measure the wall thickness（WT） and luminal diameter（LD） and to calculate the ratio of wall thickness to luminal diameter（WT/LD）.Expression of transforming growth factor-beta 1（TGF-β1） and endothelial nitric oxide synthase（eNOS） in the aorta were measured with immunohistochemistry method.Results The wall thickness（WT） in HS group were increased compared with that of LS group with significant differences between the two groups at 8th,12th,and 16th week（117.0±8.8 vs 100.5±9.1,124.7±8.8 vs 111.7±13.0,168.1±32.7 vs 132.5±32.6 μm;P0.05 for all） Compared with LS group,the TGF-β1 average light densities was increased at 4th,8th,12th,and 16th week（11795.8±1079.4 vs 9240.7±930.7,17773.8±928.3 vs 16608.5±620.2,6019.4±433.4 vs 5052.9±865.7,and 5455.6±380.2 vs 4372.8±579.1;P0.05 for all）.The eNOS average light densities were increased（14970.1±1249.2 vs 12638.1±1201.2,18236.6±2723.9 vs 14487.1±240.7,7201.9±1006.5 vs 5352.5±1251.5,and 8068.2±1418.2 vs 5213.1±2224.9;P0.05 for all）.Conclusion Chronic salt loading could aggravate the vascular remodeling in SHR.Local TGF-β1 induced by salt loading in SHR is probably involved in the development of the vascular remodeling.
出处
《中国公共卫生》
CAS
CSCD
北大核心
2011年第5期591-593,共3页
Chinese Journal of Public Health
基金
国家自然科学基金(30671160)
