{"title":"肝硬化胃食管静脉曲张和静脉曲张出血的预防和处理:指南","authors":"J. F. Botha","doi":"10.4314/SAGR.V6I1.30746","DOIUrl":null,"url":null,"abstract":"Portal hypertension, the end stage of any chronic liver disease, is caused by (1) an increased resistance to blood flow due to (a) architectural distortion of the liver by fibrous tissue and regenerative nodules (b) active intra-hepatic vaso-constriction due to decreased endogenous production of NO (2) increased portal venous inflow due to splanchnic arteriolar vasodilatation and (3) insufficient portal de-compression through collaterals which offer greater resistance to flow than does the normal liver.","PeriodicalId":39144,"journal":{"name":"South African Gastroenterology Review","volume":"6 1","pages":"23-25"},"PeriodicalIF":0.0000,"publicationDate":"2008-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"SAGES Guidelines Prevention and management of gastro-oesophageal varices and variceal haemorrhage in cirrhosis : guidelines\",\"authors\":\"J. F. Botha\",\"doi\":\"10.4314/SAGR.V6I1.30746\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Portal hypertension, the end stage of any chronic liver disease, is caused by (1) an increased resistance to blood flow due to (a) architectural distortion of the liver by fibrous tissue and regenerative nodules (b) active intra-hepatic vaso-constriction due to decreased endogenous production of NO (2) increased portal venous inflow due to splanchnic arteriolar vasodilatation and (3) insufficient portal de-compression through collaterals which offer greater resistance to flow than does the normal liver.\",\"PeriodicalId\":39144,\"journal\":{\"name\":\"South African Gastroenterology Review\",\"volume\":\"6 1\",\"pages\":\"23-25\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2008-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"South African Gastroenterology Review\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4314/SAGR.V6I1.30746\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"South African Gastroenterology Review","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4314/SAGR.V6I1.30746","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
SAGES Guidelines Prevention and management of gastro-oesophageal varices and variceal haemorrhage in cirrhosis : guidelines
Portal hypertension, the end stage of any chronic liver disease, is caused by (1) an increased resistance to blood flow due to (a) architectural distortion of the liver by fibrous tissue and regenerative nodules (b) active intra-hepatic vaso-constriction due to decreased endogenous production of NO (2) increased portal venous inflow due to splanchnic arteriolar vasodilatation and (3) insufficient portal de-compression through collaterals which offer greater resistance to flow than does the normal liver.
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