碘缺乏和碘过量对大鼠心肌组织结构和电活动的影响

Effects of iodine deficiency and iodine excess on rat myocardial histology and electrical activity

目的:观察长期碘缺乏和碘过量对大鼠心肌组织结构和电活动的影响.方法:90只Wistar大鼠随机分为低碘(LI)饮食、适碘(NI)饮食和5,10,50,100倍高碘(HI)饮食6个组,每组15只.饲养6mo.测定大鼠尿碘中位数,血清甲状腺激素(TH)水平,记录大鼠心电图,心脏脏器指数,光镜下观察左心室心肌的病理改变.结果:与NI组相比,LI组尿碘始终低于2μg/L,而NI组为345μg/L,碘的排泄量维持在极低的水平,血清TT4,FT4,TT3,FT3分别降至(14.88±5.34)nmol/L,(0.10±0.07)pmol/L,(1.10±0.25)nmol/L,(2.10±0.55)pmol/L,而NI组TT4,FT4,TT3,FT3分别为(54.97±11.21)nmol/L,(30.11±4.20)pmol/L,(1.34±0.27)nmol/L,(5.47±1.21)pmol/L,两组差别有统计学意义(P<0.01).心脏脏器指数增至(0.48±0.04)g/100g,较NI组的(0.38±0.02)g/100g,差别有统计学意义(P<0.01);基本病理改变为左室心腔扩大,室壁变薄,心肌变性和局灶性坏死.各HI组大鼠尿碘水平显著增加,增加的幅度与碘摄入量的倍数基本平行;血清TH水平较NI组有下降趋势,10,50和100HI组血清TT3分别为(1.10±0.15)nmol/L,(1.10±0.15)nmol/L,(1.18±0.15)nmol/L与NI组(1.34±0.27)nmol/L比较差异有统计学意义(P<0.01,P<0.01和P<0.05).10,50HI组血清TT4分别为(45.60±9.85)nmol/L,(45.86±9.79)nmol/L与NI组(54.97±11.21)nmol/L比较也有降低(P<0.05).心电图各波段、心脏脏器指数与NI组之间差异无统计学意义(P>0.05).各HI组大鼠心脏的大体形态与正常组无明显差别,5和100HI组大鼠心脏有局灶性间质纤维化.结论:碘缺乏和碘过量均导致健康Wistar大鼠甲状腺机能低减(甲减),进而影响心肌的组织结构和电活动.

AIM： To observe the effects of iodine deficiency and iodine excess on rat myocardial histology and electrical activity. METHODS： Ninety Wistar rats were divided into 6 groups at random： low iodine （LI）, normal iodine （NI）, 5-fold iodine （5HI）, 10-fold iodine （10HI）, 50-fold iodine （50HI） and 100- fold iodine group （100HI） respectively and all fed with water containing various concentrations of KIO3. At 3 and 6 months after iodine administration, the median of urinary iodine was measured. At 6 months after iodine administration, the level of thyroid hormone （TH） in serum was measured by means of chemoluminescence. The electrocardiogram （ ECG）, the heart weight to body weight ratio （H/B ratio） were recorded. The histopathological changes of left ventricular myocardium were observed with light microscope. RESULTS： As compared with NI groups, the median of urinary iodine and the level of serum TH were decreased （ P 〈 0. 001 ） whereas H/B ratio was increased in LI group （ P 〈 0. 001 ）. The pathological changes of left ventricle were the increased inner diameter of left ventricular cavity, the decreased thickness of left ventricular free wall and the local necrosis. In response to various iodine treatment, the level of urinary iodine rose significantly with increasing concentration of iodine. Although the level of serum TH was not significantly changed in each iodine treatment group, there was a strong decreasing trend for serum TH among HI groups. The levels of TT3 declined in 10HI [ （1. 10 ± 0. 15 ） nmol/L], 50HI [ （1.10 ±0. 15） nmoL/L] and 100HI [ （1.18 ±0.15） nmoL/L] groups compared with NI [ （ 1.34 ± 0.27 ） nmol/L] group （ P 〈 0.01, P 〈0.01 and P 〈0. 05, respectively）. The levels of TT4 went down only in 10HI [ （45.60 ± 9.85 ） nmol/L] and 50HI [（45.86 ± 9. 79） nmol/L] groups compared with NI group [ （54.97 ± 11.21 ） nmol/L] （ P 〈 0.05 ）. In addition, wave patterns, intervals of ECG, H/B ratio and the histopathological changes of left ventricle were not significantly different among any HI groups （ P 〉 0.05 ）. Only in 5HI and 100HI groups, local myocardial fibrosis of left ventricle was found. CONCLUSION： Iodine deficiency and iodine excess could induce hypothyroidism in normal rats and affect their myocardial histology and electrical activity.