F Rulli, M Muzzi, P D'Antini, M Melissari, M Sianesi, E Zanella
{"title":"[急性无结石性胆囊炎模型的组织病理学和微生物学方面:一项实验研究]。","authors":"F Rulli, M Muzzi, P D'Antini, M Melissari, M Sianesi, E Zanella","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The early stages of acute acalculous cholecystitis (ACC) have been difficult to investigate due to the animal models developed and utilized over the past years. A new model of animal AAC induced by intra-abdominal sepsis is presented. Under general anesthesia 35 guinea pigs underwent laparotomy. The designed model included ligation and prick of the caecum in 25 animals (group A), while 10 animals served as control group (group B). Seven days after these experimental procedures animals underwent relaparotomy and were submitted to cholecystectomy and sacrifice. Histological studies of the specimen revealed various degrees of cholecystitis in all the gallbladders of survived animals from group A. Gallbladders of animals from group B were histologically normal. Gallbladder bile of 15 survived animals from group A were cultured. Bile cultures were negative in 10, while culture of gallbladder bile were positive in 5; the pathogen cultured were Streptococcus Faecalis and Streptococcus Sp. The results of this study suggest that intra-abdominal sepsis induces gallbladder inflammation of various degrees. This directly supports the theoretical relationship indicating that sepsis and shock could produce AAC. Moreover this model proved that AAC, in early stages, is primarily induced by inflammatory processes, while infection of the bile do represent a late event.</p>","PeriodicalId":6943,"journal":{"name":"Acta bio-medica de L'Ateneo parmense : organo della Societa di medicina e scienze naturali di Parma","volume":"67 1-2","pages":"61-7"},"PeriodicalIF":0.0000,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[The histopathological and microbiological aspects in a model of acute acalculous cholecystitis: an experimental study].\",\"authors\":\"F Rulli, M Muzzi, P D'Antini, M Melissari, M Sianesi, E Zanella\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The early stages of acute acalculous cholecystitis (ACC) have been difficult to investigate due to the animal models developed and utilized over the past years. A new model of animal AAC induced by intra-abdominal sepsis is presented. Under general anesthesia 35 guinea pigs underwent laparotomy. The designed model included ligation and prick of the caecum in 25 animals (group A), while 10 animals served as control group (group B). Seven days after these experimental procedures animals underwent relaparotomy and were submitted to cholecystectomy and sacrifice. Histological studies of the specimen revealed various degrees of cholecystitis in all the gallbladders of survived animals from group A. Gallbladders of animals from group B were histologically normal. Gallbladder bile of 15 survived animals from group A were cultured. Bile cultures were negative in 10, while culture of gallbladder bile were positive in 5; the pathogen cultured were Streptococcus Faecalis and Streptococcus Sp. The results of this study suggest that intra-abdominal sepsis induces gallbladder inflammation of various degrees. This directly supports the theoretical relationship indicating that sepsis and shock could produce AAC. Moreover this model proved that AAC, in early stages, is primarily induced by inflammatory processes, while infection of the bile do represent a late event.</p>\",\"PeriodicalId\":6943,\"journal\":{\"name\":\"Acta bio-medica de L'Ateneo parmense : organo della Societa di medicina e scienze naturali di Parma\",\"volume\":\"67 1-2\",\"pages\":\"61-7\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1996-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Acta bio-medica de L'Ateneo parmense : organo della Societa di medicina e scienze naturali di Parma\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta bio-medica de L'Ateneo parmense : organo della Societa di medicina e scienze naturali di Parma","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
[The histopathological and microbiological aspects in a model of acute acalculous cholecystitis: an experimental study].
The early stages of acute acalculous cholecystitis (ACC) have been difficult to investigate due to the animal models developed and utilized over the past years. A new model of animal AAC induced by intra-abdominal sepsis is presented. Under general anesthesia 35 guinea pigs underwent laparotomy. The designed model included ligation and prick of the caecum in 25 animals (group A), while 10 animals served as control group (group B). Seven days after these experimental procedures animals underwent relaparotomy and were submitted to cholecystectomy and sacrifice. Histological studies of the specimen revealed various degrees of cholecystitis in all the gallbladders of survived animals from group A. Gallbladders of animals from group B were histologically normal. Gallbladder bile of 15 survived animals from group A were cultured. Bile cultures were negative in 10, while culture of gallbladder bile were positive in 5; the pathogen cultured were Streptococcus Faecalis and Streptococcus Sp. The results of this study suggest that intra-abdominal sepsis induces gallbladder inflammation of various degrees. This directly supports the theoretical relationship indicating that sepsis and shock could produce AAC. Moreover this model proved that AAC, in early stages, is primarily induced by inflammatory processes, while infection of the bile do represent a late event.