氯沙坦钾对大鼠全氟异丁烯吸入性急性肺损伤防治作用研究

发布时间：2018-04-20 12:59

  本文选题：急性肺损伤 + 全氟异丁烯　； 参考：《中国职业医学》2014年03期

【摘要】：目的探讨血管紧张素Ⅱ1型受体(AT1-R)阻断剂氯沙坦钾在全氟异丁烯(PFIB)急性肺损伤(ALI)中的防治作用。方法无特定病原体级成年雄性Wistar大鼠68只,分为17个组,每组4只。时间-效应关系研究中,设PFIB染毒前1.0、0.5 h与染毒后0.5、1.0、2.0、4.0、8.0 h氯沙坦钾干预组,并设氯沙坦钾对照组,上述8组固定氯沙坦钾给药剂量为10.00 mg/kg体质量;剂量-效应关系研究中,设氯沙坦钾给药剂量分别为1.25、2.50、5.00、10.00和15.00 mg/kg体质量的干预组,固定给药时间为染毒前1.0 h。上述2种关系研究中,均设空白对照组和PFIB染毒对照组。采用大鼠头部暴露动态吸入染毒法建立PFIB吸入性ALI模型,各干预组和PFIB染毒对照组染毒剂量均为145 mg/m3×8 min,空白对照组和氯沙坦钾对照组均行过滤空气暴露8 min。染毒后24 h处死动物,分别收集右肺组织及左肺支气管肺泡灌洗液(BALF),测定肺湿/干质量比、肺含水量、湿肺体比、干肺体比4个肺系数和BALF总蛋白水平。结果时间-效应关系研究中,PFIB染毒对照组肺湿/干质量比、肺含水量、湿肺体比3个肺系数以及BALF总蛋白水平均分别高于空白对照组、氯沙坦钾对照组(P0.05);7个时间氯沙坦钾干预组的4个肺系数指标以及BALF总蛋白水平分别与PFIB染毒对照组比较,差异均无统计学意义(P0.05)。剂量-效应关系研究中,PFIB染毒对照组的4个肺系数和BALF总蛋白水平均分别高于空白对照组(P0.05);5个剂量氯沙坦钾干预组的4个肺系数以及BALF总蛋白水平分别与PFIB染毒对照组比较,差异均无统计学意义(P0.05)。结论 AT1-R阻断剂氯沙坦钾对PFIB吸入性ALI无明显影响,提示血管紧张素Ⅱ在PFIB中毒性肺损伤中作用有限。
[Abstract]:Objective to investigate the protective effect of losartan potassium on acute lung injury of perfluoroisobutylene perfluorobutylene perfluorobutene (PFIBF). Methods 68 adult male Wistar rats without specific pathogens were divided into 17 groups with 4 rats in each group. In the study of time-effect relationship, the dosage of losartan potassium was 10.00 mg/kg body mass in the 8 groups, the dose of Losartan potassium was 10.00 mg/kg body mass in the control group, and the dosage of losartan potassium was 10.00 mg/kg body weight in the study of dose-effect relationship, the dosage of losartan potassium was 10.00 mg/kg body mass in the study of dose-effect relationship, and the dosage of losartan potassium was 10.00 mg/kg body weight in the study of dose-effect relationship. The dosage of losartan potassium was 1.25U 2.50m 5.0010.00 and 15.00 mg/kg body weight, respectively, and the fixed time was 1.0 h before exposure to Losartan. In the above two relation studies, there were blank control group and PFIB exposure control group. PFIB inhalation ALI model was established by dynamic inhalation of rat head exposure. The dose of each intervention group and PFIB control group was 145 mg/m3 脳 8 min, and the blank control group and losartan potassium control group were exposed to filtered air for 8 min. The right lung tissue and left lung bronchoalveolar lavage fluid (BALFN) were collected 24 hours after exposure. Lung wet / dry mass ratio, lung water content, wet lung body ratio, dry lung body ratio and BALF total protein level were measured. Results the lung wet / dry weight ratio, lung water content, three lung coefficients of wet lung to body ratio and the total protein level of BALF in the control group were higher than those in the blank control group, respectively. There was no significant difference in lung coefficient index and BALF total protein level between Losartan potassium control group and PFIB exposed control group at 7 hours after treatment with Losartan potassium, and there was no significant difference between Losartan potassium control group and PFIB exposed control group (P 0.05). In the dose-response study, the four lung coefficients and BALF total protein levels in the PFIB-exposed control group were higher than those in the blank control group, respectively, and the four lung coefficients and the BALF total protein levels in the five doses of losartan potassium intervention group were compared with those in the PFIB exposed control group, respectively. The difference was not statistically significant (P 0.05). Conclusion Losartan potassium, a AT1-R blocker, has no significant effect on PFIB inhaled ALI, suggesting that angiotensin 鈪，

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