Paquette N C, Tankersley C G, Zhang L Y, Kleeberger S R
Department of Environmental Health Sciences, Johns Hopkins University, School of Hygiene and Public Health, Baltimore, Maryland 21205.
Exp Lung Res. 1994 Nov-Dec;20(6):579-94. doi: 10.3109/01902149409031738.
The present study was designed to assess the effects of repeated subacute ozone (O3) exposure on pulmonary inflammation and ventilation in two inbred strains of mice differentially susceptible to a single O3 exposure. Susceptible C57BL/6J (B6) and resistant C3H/HeJ (C3) mice were exposed to 0.3 ppm O3 for 48 and 72 h and, after 14 days recovery, both strains were reexposed. Airway inflammation and lung injury were assessed by counting inflammatory cells and measuring total protein content and lactate dehydrogenase (LDH) activity in bronchoalveolar lavage (BAL) returns. Minute ventilation [VE, the product of breathing frequency (f), and tidal volume (VT)] was measured prior to and immediately following each exposure. After the initial exposure, B6 mice developed greater O3-induced increases in total protein, inflammatory cell influx, and LDH activity compared to C3 mice. In normal air, VE was also significantly elevated in B6, but not C3, mice after O3. The hypercapnic f of B6 and hypercapnic VT of C3 mice were significantly altered after O3 exposure. Reexposure to O3 caused a smaller increase in the numbers of macrophages, lymphocytes, epithelial cells, and BAL protein in both strains, and no changes in LDH activity. However, the number of polymorphonuclear leukocytes significantly increased in B6 and C3 mice as compared to the initial O3 exposure. In both strains, the ventilatory responses to normal air or hypercapnia were largely reproducible after O3 reexposure. Results indicated that differential susceptibility to O3-induced inflammation was maintained in B6 and C3 mice with O3 reexposure although the magnitude of the difference was reduced. Results also suggest that the ventilatory responses to O3 in B6 and C3 mice were reproducible with reexposure, and that airway inflammation and ventilation were not codependent.
本研究旨在评估反复亚急性臭氧（O3）暴露对两种对单次O3暴露敏感性不同的近交系小鼠肺部炎症和通气的影响。将易感的C57BL/6J（B6）小鼠和抗性的C3H/HeJ（C3）小鼠暴露于0.3 ppm O3中48小时和72小时，在恢复14天后，对两种品系的小鼠再次进行暴露。通过计数炎症细胞以及测量支气管肺泡灌洗（BAL）回收液中的总蛋白含量和乳酸脱氢酶（LDH）活性来评估气道炎症和肺损伤。在每次暴露之前和之后立即测量分钟通气量[VE，呼吸频率（f）与潮气量（VT）的乘积]。在初次暴露后，与C3小鼠相比，B6小鼠的O3诱导的总蛋白、炎症细胞流入和LDH活性增加更大。在正常空气中，O3暴露后B6小鼠的VE也显著升高，但C3小鼠没有。O3暴露后，B6小鼠的高碳酸血症呼吸频率和C3小鼠的高碳酸血症潮气量发生了显著变化。再次暴露于O3导致两种品系的巨噬细胞、淋巴细胞、上皮细胞和BAL蛋白数量增加较小，且LDH活性无变化。然而，与初次O3暴露相比，B6和C3小鼠中的多形核白细胞数量显著增加。在两种品系中，再次暴露于O3后对正常空气或高碳酸血症的通气反应在很大程度上是可重复的。结果表明，尽管差异程度有所降低，但B6和C3小鼠在再次暴露于O3时对O3诱导的炎症的不同易感性仍然存在。结果还表明，B6和C3小鼠对O3的通气反应在再次暴露时是可重复的，并且气道炎症和通气不是相互依赖的。
