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目的探讨大气细颗粒物(PM2.5)对自发性高血压大鼠(SHR)心律的影响及其机制。方法将28只自发性高血压大鼠(SHR)随机分为4组,即空白膜对照组、7.5、15和30mg/kg剂量组。颗粒物采用一次性气管滴注染毒,染毒24h后处死动物。染毒30min、1h、24h后测定SHR大鼠心电图,采用间接免疫荧光细胞化学方法测定大鼠心脏缝隙连接蛋白Cx43的分布及表达密度,采用免疫印迹法测定连接蛋白Cx43的表达;采用试剂盒法测定心肌组织MDA和SOD水平。结果染毒30min后,各组SHR大鼠均较基础测量时心律失常发生率增加,染毒1h后对照组恢复正常心律,而染毒组仍显示异常心律,染毒24h后各组均恢复正常心律。Cx43免疫荧光结果显示,染毒24h后,15和30mg/kg剂量组SHR大鼠心肌连接蛋白Cx43荧光强度显著降低(P<0.01),其中30mg/kg剂量组心肌细胞闰盘处几乎未见荧光分布;Western blot测定结果显示,随着PM2.5染毒剂量的增加,心肌组织Cx43表达逐渐减少,尤其以15、30mg/kg剂量组蛋白水平降低最为显著(P<0.01),分别为对照的56%和45%;此外,随着PM2.5染毒剂量的增加,心肌组织丙二醛(MDA)含量有所增加,超氧化物歧化酶(SOD)活力逐渐减少,但与对照组相比,差异无统计学意义(P>0.05)。结论大气PM2.5可引起自发性高血压大鼠心律异常的发生,心肌组织Cx43表达的减少可能是其机制之一。
Objective To investigate the effect and mechanism of airborne particulate matter (PM2.5) on heart rhythm in spontaneously hypertensive rats (SHR). Methods Twenty-eight spontaneously hypertensive rats (SHR) were randomly divided into four groups: blank control group, 7.5, 15 and 30 mg / kg dose groups. One-time tracheal instillation of particles was used to infect the particles, and the animals were sacrificed 24h after exposure. The electrocardiogram of SHR rats was measured after 30min, 1h, 24h, and the distribution and expression density of Cx43 were detected by indirect immunofluorescence cytochemistry. The expression of connexins Cx43 was determined by immunoblotting method. Myocardial tissue MDA and SOD levels were measured. Results After 30 minutes of exposure, the incidence of arrhythmia in SHR rats was higher than that in the baseline measurement. After 1 hour of exposure, the control group returned to normal heart rhythm, while the poisoned rats still showed abnormal rhythm. After 24h of exposure, all the rats returned to normal Heart rate. Cx43 immunofluorescence results showed that the fluorescence intensity of myocardial connexin Cx43 was significantly decreased in SHR group (P <0.01) at 15 and 30 mg / kg dose for 24 h after exposure, in which the fluorescence of cardiomyocyte intercalated plate was almost not observed in the 30 mg / kg dose group The results of Western blot showed that the expression of Cx43 in myocardium decreased with the increase of PM2.5 dose, especially at the dose of 15 and 30 mg / kg (P <0.01) 56% and 45% respectively. In addition, the content of malondialdehyde (MDA) in myocardial tissue increased and the activity of superoxide dismutase (SOD) decreased gradually with the increase of PM2.5 dose, but compared with the control group , The difference was not statistically significant (P> 0.05). Conclusion Atmospheric PM2.5 can cause the occurrence of cardiac arrhythmia in spontaneously hypertensive rats. The decrease of Cx43 expression in myocardium may be one of its mechanisms.