Fetal ethanol exposure represents a risk factor for the Sudden Infant Death Syndrome and its respiratory effects promote hypoxic ischemic consequences. This study analyzes central ethanol’s effects upon breathing plasticity during an ontogenetic stage equivalent to the third human gestational trimester. Ethanol’s unconditioned breathing effects and their intervention in learning processes were examined. Since central ethanol is primarily metabolized via the catalase system, we also examined the effects of early history with the drug upon this system. During postnatal days 3, 5 and 7 (PDs 3-7) pups were intracisternally administered with vehicle or ethanol (300 mg%). They were tested in a plethysmograph scented or not with ethanol odor. The state of intoxication attenuated the onset of apneas; a phenomenon suggestive of ethanol’s anxiolytic effects given the state of arousal caused by the novel environment and the stress of administrations. At PD9, pups were evaluated sober under sequential air conditions (initial-normoxia, hypoxia and recovery-normoxia) with or without the presence of ethanol odor. Initial apneic episodes increased when ethanol intoxication was previously associated with the odorant. Pups then ingested ethanol and brain catalase activity was determined. Pre-exposure to ethanol intoxication paired with the odor of the drug resulted in heightened enzymatic activity. Central ethanol exposure appears to exert antianxiety effects that attenuate apneic disruptions but under the state of withdrawal, the cues associated with such effects elicit an opposite reaction. The activity of the catalase system was also dependent upon learning processes determined by the association of environmental stimuli and ethanol intoxication.

胎儿乙醇暴露是婴儿猝死综合征的危险因素，其呼吸效应会导致缺氧缺血后果。这项研究分析了中央乙醇在个体发育阶段（相当于人类妊娠晚期）对呼吸可塑性的影响。检查了乙醇的无条件呼吸效应及其对学习过程的干预。由于中枢乙醇主要通过过氧化氢酶系统代谢，因此我们还检查了药物的早期历史对该系统的影响。在出生后第 3、5 和 7 天（PD 3-7），幼崽被脑池内注射载体或乙醇（300 毫克%）。它们在有或没有乙醇气味的体积描记器中进行了测试。醉酒状态减弱了呼吸暂停的发作；考虑到由新环境和管理压力引起的唤醒状态，一种暗示乙醇具有抗焦虑作用的现象。在 PD9 时，幼崽在连续的空气条件下（初始常氧、缺氧和恢复常氧）被评估为清醒，无论是否存在乙醇气味。当乙醇中毒之前与气味剂相关时，最初的呼吸暂停发作会增加。然后幼崽摄入乙醇并测定脑过氧化氢酶活性。预先暴露于乙醇中毒加上药物的气味导致酶活性增强。中枢乙醇暴露似乎发挥抗焦虑作用，减轻呼吸暂停中断，但在戒断状态下，与这种作用相关的线索会引起相反的反应。