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尼古丁和内毒素介导的仔猪长时间呼吸暂停和缺氧

Prolonged apneas and hypoxia mediated by nicotine and endotoxin in piglets.

作者信息

Frøen J Frederik, Akre Harriet, Stray-Pedersen Babill, Saugstad Ola Didrik

机构信息

Department of Pediatric Research, The National Hospital, University of Oslo, Norway.

出版信息

Biol Neonate. 2002;81(2):119-25. doi: 10.1159/000047196.

DOI:10.1159/000047196
PMID:11844882
Abstract

OBJECTIVE

Infections and maternal smoking are risk factors for SIDS, and toxins from common bacteria have been proposed as a causative link between infections and SIDS. Nicotine can be transferred in significant amounts postnatally to the infant through environmental tobacco smoke or maternal smoking before nursing. We investigated the acute effects of nicotine and endotoxin on repeated apnea by laryngeal reflex stimulation and the following autoresuscitation.

DESIGN

Thirty-four 1-week-old (+/- 1 day) piglets were sedated and randomized to 1 of 4 pretreatment groups: (1) 1 microg endotoxin i.v./kg; (2) 5 microg nicotine i.v./kg; (3) 1 microg endotoxin i.v./kg and 5 microg nicotine i.v./kg, and (4) placebo. Apnea was induced by insufflation of 0.1 ml of acidified saline (pH 2) in the subglottic space of the trachea three times with intervals of 2 min.

RESULTS

Pretreatment with endotoxin caused a significant increase in plasma TNF-alpha in the endotoxin groups (mean value +/- SEM 953 +/- 246 and 980 +/- 226 pg/ml, respectively) but no significant change in plasma IL-1 beta. Blood pressure, respiratory rate or S(a)O(2) was not significantly affected before induced apnea. Both pretreatment with nicotine and endotoxin caused prolonged apneas by 35-45%, a complete loss of normal hyperventilation during autoresuscitation, and prolonged hypoxia after apnea.

CONCLUSIONS

Nicotine and endotoxin interferes with autoresuscitation after apnea. This experimental model on piglets may shed light over important mechanisms involved in the causation of SIDS.

摘要

目的

感染和母亲吸烟是婴儿猝死综合征(SIDS)的危险因素,常见细菌产生的毒素被认为是感染与SIDS之间的因果联系。尼古丁可在出生后通过环境烟草烟雾或母亲在哺乳前吸烟大量转移至婴儿体内。我们通过喉反射刺激及随后的自主复苏研究了尼古丁和内毒素对反复呼吸暂停的急性影响。

设计

34只1周龄(±1天)的仔猪接受镇静,并随机分为4个预处理组中的1组:(1)静脉注射1微克/千克内毒素;(2)静脉注射5微克/千克尼古丁;(3)静脉注射1微克/千克内毒素和5微克/千克尼古丁;(4)安慰剂组。通过向气管声门下间隙注入0.1毫升酸化盐水(pH 2)诱导呼吸暂停,间隔2分钟进行3次。

结果

内毒素预处理使内毒素组血浆肿瘤坏死因子-α(TNF-α)显著升高(平均值±标准误分别为953±246和980±226皮克/毫升),但血浆白细胞介素-1β(IL-1β)无显著变化。在诱导呼吸暂停前,血压、呼吸频率或血氧饱和度(S(a)O(2))均未受到显著影响。尼古丁和内毒素预处理均使呼吸暂停时间延长35%-45%,自主复苏期间正常过度通气完全丧失,呼吸暂停后缺氧时间延长。

结论

尼古丁和内毒素干扰呼吸暂停后的自主复苏。这个仔猪实验模型可能有助于揭示SIDS发病机制中的重要机制。

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