Development and assesment of the animal model for "sudden infant death syndrom".

“婴儿猝死综合症”动物模型的开发和评估。

基本信息

批准号：
08557067
负责人：
KAWAHARA Koichi
金额：
$ 1.15万
依托单位：
HOKKAIDO UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (A)
财政年份：
1996
资助国家：
日本
起止时间：
1996 至 1997
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08557067/
关键词：
sudden infant death sleep apnea newborn rat CO2 sensitivity brainstem-spinal cord preparation

项目摘要

Based on our previous findings in decerebrated cats, we have proposed the hypothesis that dysfunction in the central chemosensitivity in the ventrolateral medulla induces "sleep apnea" and "sudden infant death" when the descending inhibitory system for the generalized suppression of postural muscle tone is activated during REM sleep.In this research project, we have tried to elucidate the rostral pontine neuronal mechanisms activated during REM sleep for the regulation of respiratory rhythm using brainstem-spinal cord preparations from neonatal rats. The results obtained from this study are summarized as follows :(1) Postnatal 0-to 3-day-old Wistar rats were anesthetized with ether, and the spinal cord was transected at the most caudal cervical cord. The rostral transection was done at the level of the rostral border of the pons.(2) The respiratory bursting discharges were recorded by a suction electrode from the fourth or fifth cervical ventral root containing the phrenic nerve.(3) A tungsten microelectrode was inserted into the ipsilateral or the contralateral pons to the recording sites for microstimulation. In order to identify the brainstem sites for the suppression of the respiratory discharges, the stimulation electrode was systematically moved within the pons, and the stimulus effects elicited were analyzed. However, we never induced the suppressive effects on respiration by stimulating the pons.(4) Loading of carbachol, an Ach agonist, to the perfusion solution resulted in the increase of the respiratory frequency. CO2 loading also increased the respiratory frequency.All the above results suggested the possibility that the chemical regulation mechanism for respiration originating from the central chemoreceptor is completed at this developmental stage, but the inhibitory system originating from the rostral pons is not yet fully developed.

根据我们先前在雌性养猫中的发现，我们提出了这样的假说，即腹侧髓质的中心化学敏感性功能障碍会引起“睡眠呼吸呼吸呼吸呼吸呼吸症”和“猝死”和“突然的婴儿死亡”，当降低抑制性抑制姿势的抑制在此过程中，在这种研究过程中激活了NERIS的抑制作用，我们已经尝试了NERIS的整体抑制作用。在REM睡眠期间，使用新生大鼠的脑肺脊髓制剂来调节呼吸节奏。从这项研究中获得的结果总结如下：（1）用乙醚麻醉的产后0至3天大的Wistar大鼠，脊髓以最尾端的宫颈索转移。（2）通过从第四或第五宫颈腹侧根部的吸力电极记录呼吸爆发放电的鼻伸向。为了识别抑制呼吸放应的脑干部位，系统地将刺激电极移动到PON中，并分析了引起的刺激效应。但是，我们从未通过刺激PON诱导对呼吸的抑制作用。（4）Carbachol（ACH激动剂）的灌注溶液的加载导致呼吸频率的增加。二氧化碳加载还增加了呼吸频率。上述所有结果表明，在此发育阶段完成了源自中央化学感受器的呼吸机制的可能性，但是源自鼻pon的抑制系统尚未得到充分发达。