失弛缓症发病机制的实验研究

T. Hara
{"title":"失弛缓症发病机制的实验研究","authors":"T. Hara","doi":"10.1540/JSMR1965.5.33","DOIUrl":null,"url":null,"abstract":"The pathognesis of achalasia has not yet been entirely clarified. The author undertook animal experiments in order to study the role of the central nervous system concerning the pathognesis. In 49 adult eats, destructive lesions were made bilaterally in the hypothalamus either with carbolic acid (Phenol) or with electrocoagulation. In those cats that had survived for more than 7 days, the esophageal movements were studied with X-ray, electromyogram and intraluminal pressure curve, and the extent of the hypothalamic lesions was identified histologically by serial sections. Seven eats were used as controls.The 10% phenol solution was injected into 8 animals among which 7 survived for more than 7 days. Serial sections performed in 2 cats did not disclose any destructive lesions in which cases any signs of diglutition or any X-ray abnormalities of the esophagus could not be observed.Electrocoagulation was used to make lesions in 34 cats among which 24 survived for more than 7 days. Serial sections revealed lesions involving the ventromedial nucleus of the hypothalamus bilaterally in 3 cats which showed signs of diglutition and radiographie evidence of passage disturbance of the esophagus. In contrast, in those 17 cats in which the lesion failed to involve the ventromedial nucleus, no signs of diglutition or motion disturbance of the sophagus were observed.It is thus possible to produce achalasia in cats by bilateral electrocoagulation of the ventromedial nucleus of the hypothalamus. This suggests the possible role of the central nervous system in the pathognesis of achalasia.","PeriodicalId":156233,"journal":{"name":"Japanese Journal of Smooth Muscle Research","volume":"22 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"EX PERIMENTAL STUDY ON THE PATHOGENESIS OF ACHALASIA\",\"authors\":\"T. Hara\",\"doi\":\"10.1540/JSMR1965.5.33\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The pathognesis of achalasia has not yet been entirely clarified. The author undertook animal experiments in order to study the role of the central nervous system concerning the pathognesis. In 49 adult eats, destructive lesions were made bilaterally in the hypothalamus either with carbolic acid (Phenol) or with electrocoagulation. In those cats that had survived for more than 7 days, the esophageal movements were studied with X-ray, electromyogram and intraluminal pressure curve, and the extent of the hypothalamic lesions was identified histologically by serial sections. Seven eats were used as controls.The 10% phenol solution was injected into 8 animals among which 7 survived for more than 7 days. Serial sections performed in 2 cats did not disclose any destructive lesions in which cases any signs of diglutition or any X-ray abnormalities of the esophagus could not be observed.Electrocoagulation was used to make lesions in 34 cats among which 24 survived for more than 7 days. Serial sections revealed lesions involving the ventromedial nucleus of the hypothalamus bilaterally in 3 cats which showed signs of diglutition and radiographie evidence of passage disturbance of the esophagus. In contrast, in those 17 cats in which the lesion failed to involve the ventromedial nucleus, no signs of diglutition or motion disturbance of the sophagus were observed.It is thus possible to produce achalasia in cats by bilateral electrocoagulation of the ventromedial nucleus of the hypothalamus. This suggests the possible role of the central nervous system in the pathognesis of achalasia.\",\"PeriodicalId\":156233,\"journal\":{\"name\":\"Japanese Journal of Smooth Muscle Research\",\"volume\":\"22 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1900-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Japanese Journal of Smooth Muscle Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1540/JSMR1965.5.33\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Japanese Journal of Smooth Muscle Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1540/JSMR1965.5.33","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1

摘要

贲门失弛缓症的发病机制尚未完全阐明。为了研究中枢神经系统在发病机制中的作用,笔者进行了动物实验。在49例成人实验中,用石炭酸(苯酚)或电凝在双侧下丘脑造成破坏性病变。对存活7天以上的猫,采用x线、肌电图、腔内压曲线观察其食管运动,并通过连续切片组织学检查下丘脑病变的范围。7只作为对照。将10%苯酚溶液注射到8只动物体内,其中7只存活7天以上。对2只猫进行的连续切片未发现任何破坏性病变,其中任何稀释迹象或任何食管x线异常均未观察到。采用电凝法制备病灶34只,其中存活7天以上的24只。连续切片显示3只猫双侧下丘脑腹内侧核病变,表现为稀释迹象和食道通道障碍的x线片证据。相比之下,在17只未累及腹内侧核的猫中,没有观察到食道稀释或运动障碍的迹象。因此,可以通过双侧电凝下丘脑腹内侧核产生猫的失弛缓症。这提示中枢神经系统在失弛缓症发病机制中的可能作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
EX PERIMENTAL STUDY ON THE PATHOGENESIS OF ACHALASIA
The pathognesis of achalasia has not yet been entirely clarified. The author undertook animal experiments in order to study the role of the central nervous system concerning the pathognesis. In 49 adult eats, destructive lesions were made bilaterally in the hypothalamus either with carbolic acid (Phenol) or with electrocoagulation. In those cats that had survived for more than 7 days, the esophageal movements were studied with X-ray, electromyogram and intraluminal pressure curve, and the extent of the hypothalamic lesions was identified histologically by serial sections. Seven eats were used as controls.The 10% phenol solution was injected into 8 animals among which 7 survived for more than 7 days. Serial sections performed in 2 cats did not disclose any destructive lesions in which cases any signs of diglutition or any X-ray abnormalities of the esophagus could not be observed.Electrocoagulation was used to make lesions in 34 cats among which 24 survived for more than 7 days. Serial sections revealed lesions involving the ventromedial nucleus of the hypothalamus bilaterally in 3 cats which showed signs of diglutition and radiographie evidence of passage disturbance of the esophagus. In contrast, in those 17 cats in which the lesion failed to involve the ventromedial nucleus, no signs of diglutition or motion disturbance of the sophagus were observed.It is thus possible to produce achalasia in cats by bilateral electrocoagulation of the ventromedial nucleus of the hypothalamus. This suggests the possible role of the central nervous system in the pathognesis of achalasia.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信