Mouton Alan J, Maxi John K, Souza-Smith Flavia, Bagby Gregory J, Gilpin Nicholas W, Molina Patricia E, Gardner Jason D
Department of Physiology, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana.
Alcohol Clin Exp Res. 2016 Aug;40(8):1671-8. doi: 10.1111/acer.13133. Epub 2016 Jul 4.
Chronic intermittent ethanol vapor (CIEV) exposure has been used extensively to produce rodent models of alcohol dependence, but unlike other models of alcohol abuse, CIEV has not been assessed as a model of end-organ damage. The purpose of this study was to characterize the effects of CIEV on peripheral organ systems affected by alcohol abuse, including the liver, lungs, and cardiovascular system.
Adult male Sprague-Dawley rats were exposed to daily CIEV for a period of 8 weeks (14HR ON/10HR OFF), producing blood alcohol levels of ~200 mg/dl. Controls were exposed to room air. After 8 weeks, echocardiography was performed to assess cardiac function. Indices of liver injury (alanine and aspartate aminotransferases [ALT and AST]; cytochrome p450 2E1 [CYP2E1]; alcohol dehydrogenase [ADH]; Oil Red O and triglyceride content; lipid peroxidation; inflammatory cytokine expression; and macrophage infiltration), and lung inflammatory cell count, proinflammatory cytokine expression, and lipid peroxidation were measured.
Left ventricular posterior wall thickness was significantly decreased, and systolic blood pressure was significantly elevated by CIEV compared with air controls. CIEV led to a significant increase in plasma ALT and triglycerides compared with room air controls. CIEV did not affect liver triglyceride content, lipid staining or peroxidation, but increased CYP2E1 and chemokine (C-C motif) ligand 2 (CCL2) protein expression, while decreasing ADH expression. CIEV significantly increased numbers of both polymorphonuclear neutrophils and lymphocytes in the bronchoalveolar lavage fluid, indicative of pulmonary inflammation. However, CIEV did not produce significant changes in lung mass, pulmonary lipid peroxidation, inflammatory cytokine expression, or edema.
These results show that CIEV produces hepatic, pulmonary, and cardiovascular effects in rats similar to those found in other models of chronic alcohol administration. Alcohol vapor administration is a novel method of alcohol-induced tissue injury with high potential for widespread use in alcohol toxicology research.
慢性间歇性乙醇蒸汽(CIEV)暴露已被广泛用于建立酒精依赖的啮齿动物模型,但与其他酒精滥用模型不同,CIEV尚未被评估为终末器官损伤模型。本研究的目的是描述CIEV对受酒精滥用影响的外周器官系统的作用,包括肝脏、肺和心血管系统。
成年雄性Sprague-Dawley大鼠每天暴露于CIEV中8周(14小时开启/10小时关闭),使血液酒精水平达到约200mg/dl。对照组暴露于室内空气中。8周后,进行超声心动图检查以评估心脏功能。测量肝损伤指标(丙氨酸和天冬氨酸转氨酶[ALT和AST];细胞色素p450 2E1[CYP2E1];乙醇脱氢酶[ADH];油红O和甘油三酯含量;脂质过氧化;炎性细胞因子表达;以及巨噬细胞浸润),并测量肺炎症细胞计数、促炎细胞因子表达和脂质过氧化。
与空气对照组相比,CIEV使左心室后壁厚度显著降低,收缩压显著升高。与室内空气对照组相比,CIEV导致血浆ALT和甘油三酯显著增加。CIEV不影响肝脏甘油三酯含量、脂质染色或过氧化,但增加CYP2E1和趋化因子(C-C基序)配体2(CCL2)蛋白表达,同时降低ADH表达。CIEV显著增加支气管肺泡灌洗液中多形核中性粒细胞和淋巴细胞的数量,表明肺部有炎症。然而,CIEV未对肺质量、肺脂质过氧化、炎性细胞因子表达或水肿产生显著变化。
这些结果表明,CIEV在大鼠中产生的肝脏、肺部和心血管效应与其他慢性酒精给药模型中发现的效应相似。酒精蒸汽给药是一种新型的酒精诱导组织损伤方法,在酒精毒理学研究中具有广泛应用的高潜力。