CAJ | 학술논문

目的探讨大气细颗粒物(PM2.5,)水溶成分静脉染毒后1、6 h,对大鼠胸主动脉血管环收缩、舒张功能的影响.方法雄性Wistar大鼠30只,分为空白对照组、1 h对照组、6 h对照组、染毒1 h组、染毒6 h组,每组6只.染毒组以PM2.5水溶成分(1 ml/kg)尾静脉注射1、6 h后,分别以25%乌拉坦腹腔注射(0.4 ml/100 g)麻醉后,迅速开胸取大鼠胸主动脉,制备血管环,置于张力换能器进行实验.1 h,6 h对照组以0.9%氯化钠注射液(1 ml/kg)尾静脉注射,处理同染毒组.结果空白对照组、1 h对照组、6 h对照组三组间血管环舒缩反应差别无统计学意义.染毒1 h后,胸主动脉血管环对60 mmol/L KCi的收缩反应减弱,6 h后有升高趋势,但仍低于对照组.10-6mol/L去甲肾上腺素(NE)预收缩的血管环:乙酰胆碱(ACh)浓度在10-5moL/L、10-7moL/L水平,染毒后1 h舒张率降低.ACh浓度在10-5～10-7mol/L水平,染毒6 h组舒张率较染毒1 h组升高;硝普钠(SNP)浓度在10-5～10-9mol/L水平,染毒后1 h舒张率降低,在10-6mol/L、10-9mol/L水平,染毒后6 h组舒张率较染毒1 h组升高,在10-5～10-7moL/L水平,染毒6 h组舒张率仍低于对照组.结论 PM2.5水溶成分静脉染毒1 h后引起血管收缩抑制、舒张下降,6 h后该作用减弱.
목적탐토대기세과립물(PM2.5,)수용성분정맥염독후1、6 h,대대서흉주동맥혈관배수축、서장공능적영향.방법 웅성Wistar대서30지,분위공백대조조、1 h대조조、6 h대조조、염독1 h조、염독6 h조,매조6지.염독조이PM2.5수용성분(1 ml/kg)미정맥주사1、6 h후,분별이25%오랍탄복강주사(0.4 ml/100 g)마취후,신속개흉취대서흉주동맥,제비혈관배,치우장력환능기진행실험.1 h,6 h대조조이0.9%록화납주사액(1 ml/kg)미정맥주사,처리동염독조.결과 공백대조조、1 h대조조、6 h대조조삼조간혈관배서축반응차별무통계학의의.염독1 h후,흉주동맥혈관배대60 mmol/L KCi적수축반응감약,6 h후유승고추세,단잉저우대조조.10-6mol/L거갑신상선소(NE)예수축적혈관배:을선담감(ACh)농도재10-5moL/L、10-7moL/L수평,염독후1 h서장솔강저.ACh농도재10-5～10-7mol/L수평,염독6 h조서장솔교염독1 h조승고;초보납(SNP)농도재10-5～10-9mol/L수평,염독후1 h서장솔강저,재10-6mol/L、10-9mol/L수평,염독후6 h조서장솔교염독1 h조승고,재10-5～10-7moL/L수평,염독6 h조서장솔잉저우대조조.결론 PM2.5수용성분정맥염독1 h후인기혈관수축억제、서장하강,6 h후해작용감약.
Objective To compare the difference of vasomotor functions in aortas segments from Wistar rats between 1-hour and 6-hours after exposure of water-soluble components of fine particulate matter (PM2.5 ). Methods All 30 Wistar rats were assigned to five groups (n = 6 for each group) at random: the blank control group,control group for 1-hour and 6-hours, exposure group for 1-hour and 6-hours. The rats were sacrificed 1-hour or 6-hours later and aorta ring segments were mounted on wire myographs. Results ( 1 ) There was no significant difference in vasomotor functions among three control groups( P 0. 05 ). (2) 1-hour or 6-hours after exposure there was a decrease of contraction elicited by 60 mmol/L KCl in contrast to the control group(P<0. 05), whereas no significant change between the exposure group for 1-hour and 6-hours (P 0. 05). (3)On the level of 10-5 or 10-7 mol/L, 1-hour after exposure there was a decrease in endothelium-depondent acetylcholine(ACh) elcited relaxation precontracted by 10-6mol/L NE compared with the control group (P <0. 01 or P <0. 05), on the level from 10 -5 to 10-7 mol/L there was a decrease compared with the exposure group for 6-hours ( P < 0. 05 ), whereas no difference between the exposure group for 6-hours and the control group( P 0. 05). On the level from 10-5 to 10-9 mol/L, 1-hour after exposure there was a decrease in endothelium-independent sodium nitroprusside (SNP)elicited relaxation precontracted by 10-6 mol/L NE as compared with the control group( P < 0. 01 or P < 0. 05 )and a decrease on the level of 10-6or 10 -9 mol/L compared with the exposure group for 6-hours ( P < 0. 05 ), 6-hours after exposure a decrease was caused as compared with the control group on the level from 10-5 to 10-7 mol/L (P <0. 01 or P < 0. 05 ). Conclusions Inhibition of contraction and impairment of relaxation in aortas should be caused 1-hour after exposure to water-soluble components of PM2.5 in the air, which is weaken 6-hours after exposure.