Role of hydrogen sulfide in portal hypertension and esophagogastric junction vascular disease
AIM:To investigate the association between endogenous hydrogen sulfide(H2S)and portal hypertension as well as its effect on vascular smooth muscle cells.METHODS:Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels,prothrombin time,ascites and hepati...
Saved in:
Published in | World journal of gastroenterology : WJG Vol. 20; no. 4; pp. 1079 - 1087 |
---|---|
Main Author | |
Format | Journal Article |
Language | English |
Published |
United States
Baishideng Publishing Group Co., Limited
28.01.2014
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | AIM:To investigate the association between endogenous hydrogen sulfide(H2S)and portal hypertension as well as its effect on vascular smooth muscle cells.METHODS:Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels,prothrombin time,ascites and hepatic encephalopathy.Plasma H2S concentrations and portal vein diameters(PVDs)were compared between portal hypertension patients and control participants,as well as between portal hypertension patients with varying degrees of severity.In addition,we established a rabbit hepatic schistosomiasis portal hypertension(SPH)model and analyzed liver morphology,fibrosis grade,plasma and liver tissue H2S concentrations,as well as cystathionineγ-lyase(CSE)activity and phosphorylated extracellular signal-regulated kinase(pERK)1/2,B cell lymphoma(Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells,in addition to their H2S-induced apoptosis rates.RESULTS:In portal hypertension patients,endogenous H2S levels were significantly lower than those in healthy controls.The more severe the disease was,the lower were the H2S plasma levels,which were inversely correlated with PVD and Child-Pugh score.Liver tissue H2S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals,starting at 3 wk,whereas pERK 1/2expressions gradually increased 12-20 wk after SPH model establishment.In portal vein smooth muscle cells,increasing H2S levels led to increased apoptosis,while Bcl-2 and Bcl-XL expression decreased.CONCLUSION:H2S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction,which helps to maintain normal vascular structures. |
---|---|
AbstractList | To investigate the association between endogenous hydrogen sulfide (H₂S) and portal hypertension as well as its effect on vascular smooth muscle cells.AIMTo investigate the association between endogenous hydrogen sulfide (H₂S) and portal hypertension as well as its effect on vascular smooth muscle cells.Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels, prothrombin time, ascites and hepatic encephalopathy. Plasma H₂S concentrations and portal vein diameters (PVDs) were compared between portal hypertension patients and control participants, as well as between portal hypertension patients with varying degrees of severity. In addition, we established a rabbit hepatic schistosomiasis portal hypertension (SPH) model and analyzed liver morphology, fibrosis grade, plasma and liver tissue H₂S concentrations, as well as cystathionine γ-lyase (CSE) activity and phosphorylated extracellular signal-regulated kinase (pERK)1/2, B cell lymphoma (Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells, in addition to their H₂S-induced apoptosis rates.METHODSPortal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels, prothrombin time, ascites and hepatic encephalopathy. Plasma H₂S concentrations and portal vein diameters (PVDs) were compared between portal hypertension patients and control participants, as well as between portal hypertension patients with varying degrees of severity. In addition, we established a rabbit hepatic schistosomiasis portal hypertension (SPH) model and analyzed liver morphology, fibrosis grade, plasma and liver tissue H₂S concentrations, as well as cystathionine γ-lyase (CSE) activity and phosphorylated extracellular signal-regulated kinase (pERK)1/2, B cell lymphoma (Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells, in addition to their H₂S-induced apoptosis rates.In portal hypertension patients, endogenous H₂S levels were significantly lower than those in healthy controls. The more severe the disease was, the lower were the H₂S plasma levels, which were inversely correlated with PVD and Child-Pugh score. Liver tissue H₂S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals, starting at 3 wk, whereas pERK 1/2 expressions gradually increased 12-20 wk after SPH model establishment. In portal vein smooth muscle cells, increasing H₂S levels led to increased apoptosis, while Bcl-2 and Bcl-XL expression decreased.RESULTSIn portal hypertension patients, endogenous H₂S levels were significantly lower than those in healthy controls. The more severe the disease was, the lower were the H₂S plasma levels, which were inversely correlated with PVD and Child-Pugh score. Liver tissue H₂S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals, starting at 3 wk, whereas pERK 1/2 expressions gradually increased 12-20 wk after SPH model establishment. In portal vein smooth muscle cells, increasing H₂S levels led to increased apoptosis, while Bcl-2 and Bcl-XL expression decreased.H₂S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction, which helps to maintain normal vascular structures.CONCLUSIONH₂S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction, which helps to maintain normal vascular structures. To investigate the association between endogenous hydrogen sulfide (H₂S) and portal hypertension as well as its effect on vascular smooth muscle cells. Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels, prothrombin time, ascites and hepatic encephalopathy. Plasma H₂S concentrations and portal vein diameters (PVDs) were compared between portal hypertension patients and control participants, as well as between portal hypertension patients with varying degrees of severity. In addition, we established a rabbit hepatic schistosomiasis portal hypertension (SPH) model and analyzed liver morphology, fibrosis grade, plasma and liver tissue H₂S concentrations, as well as cystathionine γ-lyase (CSE) activity and phosphorylated extracellular signal-regulated kinase (pERK)1/2, B cell lymphoma (Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells, in addition to their H₂S-induced apoptosis rates. In portal hypertension patients, endogenous H₂S levels were significantly lower than those in healthy controls. The more severe the disease was, the lower were the H₂S plasma levels, which were inversely correlated with PVD and Child-Pugh score. Liver tissue H₂S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals, starting at 3 wk, whereas pERK 1/2 expressions gradually increased 12-20 wk after SPH model establishment. In portal vein smooth muscle cells, increasing H₂S levels led to increased apoptosis, while Bcl-2 and Bcl-XL expression decreased. H₂S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction, which helps to maintain normal vascular structures. AIM:To investigate the association between endogenous hydrogen sulfide(H2S)and portal hypertension as well as its effect on vascular smooth muscle cells.METHODS:Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels,prothrombin time,ascites and hepatic encephalopathy.Plasma H2S concentrations and portal vein diameters(PVDs)were compared between portal hypertension patients and control participants,as well as between portal hypertension patients with varying degrees of severity.In addition,we established a rabbit hepatic schistosomiasis portal hypertension(SPH)model and analyzed liver morphology,fibrosis grade,plasma and liver tissue H2S concentrations,as well as cystathionineγ-lyase(CSE)activity and phosphorylated extracellular signal-regulated kinase(pERK)1/2,B cell lymphoma(Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells,in addition to their H2S-induced apoptosis rates.RESULTS:In portal hypertension patients,endogenous H2S levels were significantly lower than those in healthy controls.The more severe the disease was,the lower were the H2S plasma levels,which were inversely correlated with PVD and Child-Pugh score.Liver tissue H2S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals,starting at 3 wk,whereas pERK 1/2expressions gradually increased 12-20 wk after SPH model establishment.In portal vein smooth muscle cells,increasing H2S levels led to increased apoptosis,while Bcl-2 and Bcl-XL expression decreased.CONCLUSION:H2S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction,which helps to maintain normal vascular structures. AIM: To investigate the association between endogenous hydrogen sulfide (H 2 S) and portal hypertension as well as its effect on vascular smooth muscle cells. METHODS: Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels, prothrombin time, ascites and hepatic encephalopathy. Plasma H 2 S concentrations and portal vein diameters (PVDs) were compared between portal hypertension patients and control participants, as well as between portal hypertension patients with varying degrees of severity. In addition, we established a rabbit hepatic schistosomiasis portal hypertension (SPH) model and analyzed liver morphology, fibrosis grade, plasma and liver tissue H 2 S concentrations, as well as cystathionine γ-lyase (CSE) activity and phosphorylated extracellular signal-regulated kinase (pERK)1/2, B cell lymphoma (Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells, in addition to their H 2 S-induced apoptosis rates. RESULTS: In portal hypertension patients, endogenous H 2 S levels were significantly lower than those in healthy controls. The more severe the disease was, the lower were the H 2 S plasma levels, which were inversely correlated with PVD and Child-Pugh score. Liver tissue H 2 S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals, starting at 3 wk, whereas pERK 1/2 expressions gradually increased 12-20 wk after SPH model establishment. In portal vein smooth muscle cells, increasing H 2 S levels led to increased apoptosis, while Bcl-2 and Bcl-XL expression decreased. CONCLUSION: H 2 S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction, which helps to maintain normal vascular structures. |
Author | Chao Wang Juan Han Liang Xiao Chang-E Jin Dong-Jian Li Zhen Yang |
AuthorAffiliation | Department of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Department of Biliary and Pancreatic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Department of Surgery and Biological Therapy, Shenzhen Second People’s Hospital the First Affiliated Hospital of Shenzhen University Department of Respiratory Medicine, Shenzhen People’s Hospital |
Author_xml | – sequence: 1 givenname: Chao surname: Wang fullname: Wang, Chao |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24574782$$D View this record in MEDLINE/PubMed |
BookMark | eNp1UV1rFDEUDVKx2-qzb5JHX2abT2fyIkixtlAQij5KSDM3s1myyTSZWem_b8Zuiwq9EMLl3HMO954TdBRTBITeU7LmrejOfm-H9Z6RtRdrSlr1Cq0Yo6phnSBHaEUJaRvFWXuMTkrZEsI4l-wNOmZCtqLt2Ar9ukkBcHJ4c9_nNEDEZQ7O94B9xGPKkwkVGiFPEItPEZvYYyhp3JghDaZM2Vu8naOdFnBvip2Dybj3BUyBt-i1M6HAu8N_in5efP1xftlcf_92df7lurGCt1PDnBNS3TKpnLDOcQU9cdIJ7lzreul66qQ1lHemk6IHUNC62n2qPXGcSX6KPj_qjvPtDnoLccom6DH7ncn3Ohmv_0Wi3-gh7TVXjErOq8DHg0BOdzOUSe98sRCCiZDmoqkkXIparI5--Nvr2eTppnVAPg7YnErJ4LT1k1nuU6190JToJTtds9M1O-2FXrKrvLP_eE_SLzP4gbFJcbjzcXimKNItpSQRnVCSie7PI3WPB2JksEE |
CitedBy_id | crossref_primary_10_1186_s12967_022_03631_0 crossref_primary_10_3390_jcm10051081 crossref_primary_10_1016_j_biochi_2022_04_013 crossref_primary_10_1042_BSR20221006 crossref_primary_10_1152_ajpheart_00303_2019 crossref_primary_10_3389_fphar_2022_911704 crossref_primary_10_1590_1414_431x20165592 crossref_primary_10_1016_j_phrs_2016_07_040 crossref_primary_10_1016_j_arr_2024_102515 crossref_primary_10_1097_FJC_0000000000000714 crossref_primary_10_1155_2015_593407 crossref_primary_10_1155_2017_1406726 crossref_primary_10_1152_ajpheart_00465_2016 crossref_primary_10_1016_j_phrs_2020_104677 crossref_primary_10_1089_ars_2023_0404 crossref_primary_10_3892_etm_2015_2823 crossref_primary_10_1007_s11596_017_1738_4 crossref_primary_10_1007_s11596_017_1792_y crossref_primary_10_1038_s41401_020_00549_5 crossref_primary_10_1111_liv_70024 crossref_primary_10_1161_JAHA_120_017544 crossref_primary_10_3390_biom13071023 crossref_primary_10_1155_2021_3206982 crossref_primary_10_1016_j_arres_2022_100030 crossref_primary_10_12688_f1000research_7987_1 crossref_primary_10_3389_fcimb_2020_586923 crossref_primary_10_1111_bph_14645 crossref_primary_10_1111_bph_12900 |
ContentType | Journal Article |
Copyright | 2014 Baishideng Publishing Group Co., Limited. All rights reserved. 2014 |
Copyright_xml | – notice: 2014 Baishideng Publishing Group Co., Limited. All rights reserved. 2014 |
DBID | 2RA 92L CQIGP W91 ~WA AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM |
DOI | 10.3748/wjg.v20.i4.1079 |
DatabaseName | 维普期刊资源整合服务平台 中文科技期刊数据库-CALIS站点 维普中文期刊数据库 中文科技期刊数据库-医药卫生 中文科技期刊数据库- 镜像站点 CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic PubMed Central (Full Participant titles) |
DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
DatabaseTitleList | MEDLINE - Academic MEDLINE |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
DeliveryMethod | fulltext_linktorsrc |
DocumentTitleAlternate | Role of hydrogen sulfide in portal hypertension and esophagogastric junction vascular disease |
EISSN | 2219-2840 |
EndPage | 1087 |
ExternalDocumentID | PMC3921533 24574782 10_3748_wjg_v20_i4_1079 90888889504849524852485050 |
Genre | Research Support, Non-U.S. Gov't Journal Article |
GroupedDBID | --- 123 29R 2B. 2C~ 2RA 2WC 36B 53G 5VR 8WL 92F 92I 92L 93N 93R AAKDD ACGFO AENEX AFUIB ALMA_UNASSIGNED_HOLDINGS CCEZO CHBEP CIEJG CQIGP CS3 CW9 DIK DU5 E3Z EBS EJD EMB F5P FA0 FRP GX1 HYE M~E OK1 P2P RNS RPM SV3 TCJ TGQ TR2 W91 WFFXF XSB ~WA AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM |
ID | FETCH-LOGICAL-c437t-2ff459b259f4cff39ed0f5f43ff7fd5fd1f5ca138a854dee9e7f13868a80f3253 |
ISSN | 1007-9327 2219-2840 |
IngestDate | Thu Aug 21 18:16:30 EDT 2025 Fri Jul 11 07:55:00 EDT 2025 Mon Jul 21 06:04:19 EDT 2025 Tue Jul 01 01:53:29 EDT 2025 Thu Apr 24 23:03:33 EDT 2025 Wed Feb 14 10:28:36 EST 2024 |
IsDoiOpenAccess | false |
IsOpenAccess | true |
IsPeerReviewed | false |
IsScholarly | true |
Issue | 4 |
Keywords | Hydrogen sulfide Cystathionine γ-lyase B-cell lymphoma-XL Portal hypertension B-cell lymphoma-2 pERK 1/2 Apoptosis |
Language | English |
LinkModel | OpenURL |
MergedId | FETCHMERGED-LOGICAL-c437t-2ff459b259f4cff39ed0f5f43ff7fd5fd1f5ca138a854dee9e7f13868a80f3253 |
Notes | Chao Wang;Juan Han;Liang Xiao;Chang-E Jin;Dong-Jian Li;Zhen Yang;Department of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology;Department of Biliary and Pancreatic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology;Department of Surgery and Biological Therapy, Shenzhen Second People’s Hospital, the First Affiliated Hospital of Shenzhen University;Department of Respiratory Medicine, Shenzhen People’s Hospital ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author contributions: Wang C, Han J and Xiao L designed the research; Wang C, Han J, Xiao L, Jin CE, Li DJ and Yang Z performed the research; Wang C, Han J, Xiao L and Jin CE analyzed the data; Wang C, Han J and Xiao L wrote the paper. Correspondence to: Chao Wang, PhD, Department of General Surgery, Tongji Hospital, Tongji Medical College, Science and Technology of Huazhong University, No. 1095, Jiefang Avenue, Wuhan 430030, Hubei Province, China. wangchao75@sina.com Telephone: +86-27-83663008 Fax: +86-27-83663039 |
OpenAccessLink | https://www.wjgnet.com/1007-9327/full/v20/i4/1079.htm |
PMID | 24574782 |
PQID | 1503544442 |
PQPubID | 23479 |
PageCount | 9 |
ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_3921533 proquest_miscellaneous_1503544442 pubmed_primary_24574782 crossref_citationtrail_10_3748_wjg_v20_i4_1079 crossref_primary_10_3748_wjg_v20_i4_1079 chongqing_primary_90888889504849524852485050 |
ProviderPackageCode | CITATION AAYXX |
PublicationCentury | 2000 |
PublicationDate | 2014-01-28 |
PublicationDateYYYYMMDD | 2014-01-28 |
PublicationDate_xml | – month: 01 year: 2014 text: 2014-01-28 day: 28 |
PublicationDecade | 2010 |
PublicationPlace | United States |
PublicationPlace_xml | – name: United States |
PublicationTitle | World journal of gastroenterology : WJG |
PublicationTitleAlternate | World Journal of Gastroenterology |
PublicationYear | 2014 |
Publisher | Baishideng Publishing Group Co., Limited |
Publisher_xml | – name: Baishideng Publishing Group Co., Limited |
References | 23675260 - Int J Biomed Sci. 2012 Jun;8(2):81-6 19402365 - Acta Gastroenterol Belg. 2009 Jan-Mar;72(1):9-16 8558235 - J Neurosci. 1996 Feb 1;16(3):1066-71 16108046 - Hepatology. 2005 Sep;42(3):539-48 23846016 - Biochim Biophys Acta. 2013 Dec;1832(12):1989-97 23129058 - Mol Med Rep. 2013 Jan;7(1):247-53 14628564 - Morfologiia. 2003;124(4):84-7 7150244 - Biochem J. 1982 Aug 15;206(2):267-77 20577128 - J Hypertens. 2010 Sep;28(9):1875-82 15951554 - Gut. 2005 Jul;54(7):1024-33 23131022 - Hepatol Res. 2013 Jun;43(6):670-8 10613719 - Hepatology. 2000 Jan;31(1):3-6 9299397 - Biochem Biophys Res Commun. 1997 Aug 28;237(3):527-31 19255435 - Proc Natl Acad Sci U S A. 2009 Mar 17;106(11):4513-8 15047144 - Biochem Biophys Res Commun. 2004 Apr 23;317(1):30-7 19821198 - Turk J Gastroenterol. 2009 Sep;20(3):171-9 23830348 - Int J Cardiol. 2013 Oct 9;168(4):3770-8 23493917 - Iran J Basic Med Sci. 2012 Jul;15(4):907-15 12392053 - Mol Neurobiol. 2002 Aug;26(1):13-9 16174660 - Gut. 2005 Dec;54(12):1668-71 12646242 - Biochem Biophys Res Commun. 2003 Mar 21;302(4):810-6 23660955 - Mol Cell Biochem. 2013 Sep;381(1-2):41-50 15303121 - Beijing Da Xue Xue Bao. 2004 Aug 18;36(4):341-4 |
References_xml | – reference: 23493917 - Iran J Basic Med Sci. 2012 Jul;15(4):907-15 – reference: 15047144 - Biochem Biophys Res Commun. 2004 Apr 23;317(1):30-7 – reference: 12646242 - Biochem Biophys Res Commun. 2003 Mar 21;302(4):810-6 – reference: 10613719 - Hepatology. 2000 Jan;31(1):3-6 – reference: 23675260 - Int J Biomed Sci. 2012 Jun;8(2):81-6 – reference: 9299397 - Biochem Biophys Res Commun. 1997 Aug 28;237(3):527-31 – reference: 23131022 - Hepatol Res. 2013 Jun;43(6):670-8 – reference: 23660955 - Mol Cell Biochem. 2013 Sep;381(1-2):41-50 – reference: 23846016 - Biochim Biophys Acta. 2013 Dec;1832(12):1989-97 – reference: 23830348 - Int J Cardiol. 2013 Oct 9;168(4):3770-8 – reference: 7150244 - Biochem J. 1982 Aug 15;206(2):267-77 – reference: 15303121 - Beijing Da Xue Xue Bao. 2004 Aug 18;36(4):341-4 – reference: 16108046 - Hepatology. 2005 Sep;42(3):539-48 – reference: 8558235 - J Neurosci. 1996 Feb 1;16(3):1066-71 – reference: 12392053 - Mol Neurobiol. 2002 Aug;26(1):13-9 – reference: 20577128 - J Hypertens. 2010 Sep;28(9):1875-82 – reference: 14628564 - Morfologiia. 2003;124(4):84-7 – reference: 23129058 - Mol Med Rep. 2013 Jan;7(1):247-53 – reference: 16174660 - Gut. 2005 Dec;54(12):1668-71 – reference: 15951554 - Gut. 2005 Jul;54(7):1024-33 – reference: 19821198 - Turk J Gastroenterol. 2009 Sep;20(3):171-9 – reference: 19402365 - Acta Gastroenterol Belg. 2009 Jan-Mar;72(1):9-16 – reference: 19255435 - Proc Natl Acad Sci U S A. 2009 Mar 17;106(11):4513-8 |
SSID | ssj0023352 |
Score | 2.2546365 |
Snippet | AIM:To investigate the association between endogenous hydrogen sulfide(H2S)and portal hypertension as well as its effect on vascular smooth muscle... To investigate the association between endogenous hydrogen sulfide (H₂S) and portal hypertension as well as its effect on vascular smooth muscle cells. Portal... To investigate the association between endogenous hydrogen sulfide (H₂S) and portal hypertension as well as its effect on vascular smooth muscle cells.AIMTo... AIM: To investigate the association between endogenous hydrogen sulfide (H 2 S) and portal hypertension as well as its effect on vascular smooth muscle cells.... |
SourceID | pubmedcentral proquest pubmed crossref chongqing |
SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
StartPage | 1079 |
SubjectTerms | Adult Animals Apoptosis B-cell Brief Case-Control Studies Cell Proliferation Cells, Cultured Disease Models, Animal Esophagogastric Junction - blood supply Esophagogastric Junction - metabolism Female Humans Hydrogen Sulfide - blood hypertension Hypertension, Portal - blood Hypertension, Portal - parasitology Hypertension, Portal - pathology Liver - metabolism Liver - pathology Liver Cirrhosis, Experimental - metabolism Liver Cirrhosis, Experimental - parasitology lymphoma-2 Male Middle Aged Muscle, Smooth, Vascular - metabolism Muscle, Smooth, Vascular - pathology Myocytes, Smooth Muscle - metabolism Myocytes, Smooth Muscle - pathology Portal Portal Vein - metabolism Portal Vein - pathology Rabbits Schistosomiasis - complications Severity of Illness Index Time Factors |
Title | Role of hydrogen sulfide in portal hypertension and esophagogastric junction vascular disease |
URI | http://lib.cqvip.com/qk/84123X/201404/90888889504849524852485050.html https://www.ncbi.nlm.nih.gov/pubmed/24574782 https://www.proquest.com/docview/1503544442 https://pubmed.ncbi.nlm.nih.gov/PMC3921533 |
Volume | 20 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3di9NAEF_0fPFFFL_qFyv4IGhimuwmzaMcPY7jPEFari-y5GMnzSHJWXuK_vXOZHfTtFY4LTQ0m82mZH6ZndnM_IaxV1kMBU1dXipC4Yk8jr0JTAJPyJys97GEMSU4fziLj-fiZCEXO9kl69wvfu3NK_kfqWIbypWyZP9Bsv2g2IC_Ub64RQnj9loy_mRDA5c_y1WLvSjWHOqy4wExdjUeutSrLkrdhh1rqluQVW2VUcWO4s0FTmwdBvqY1OE7G2u2mpCbActEd3ZLfJ4rQ-JEKwvnJ32hrnO7DH24zNqNkrN5IBtALuqsNSsDmZ1BKZindoEATeVNh8sSYwplcWnenfYKURVig-Fi8vWeNqt-w2AAMzHQpeiYpvuUPBHmoGR-XFT-9zDwa-G7ntt02mcf1dH89FTNpovZTXYrRD8idMs51iOnhDOqPuj-l-F-ogu82xmeqDeWbVN9RYNi24T5wy_ZDa8d2Cuzu-yOdTT4e4Oae-yGbu6zz4QY3gJ3iOEWMbxuuEEMHyKGI2L4DmK4Qwx3iOEWMQ_Y_Gg6Ozz2bIENrxBRsvZCACHTHD1gEAVAlOoyAAkiAkiglFCOQRbZOJpkEylKrVOdAO7FuB9AFMroITto2kY_ZjxKixL74JMdgaCX-Xi3kzhNRVCWmQQ5Ym_7-6cuDZGKohg7_KQSpxF01Ildj76BDEbMd7dYFZasnmqmfFHotJJ8FMpHoXxULRTJZ8Re9ye44f_a9aWTmUJdSi_Iska3V98UOkeRFPgJR-yRkWE_WCgklZrAI8mWdPsOxNO-faSplx1fO7og5FU9ucZ1n7Lbm4fpGTtYr670c7R61_mLDrm_AbDCsVQ |
linkProvider | National Library of Medicine |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Role+of+hydrogen+sulfide+in+portal+hypertension+and+esophagogastric+junction+vascular+disease&rft.jtitle=World+journal+of+gastroenterology+%3A+WJG&rft.au=Wang%2C+Chao&rft.au=Han%2C+Juan&rft.au=Xiao%2C+Liang&rft.au=Jin%2C+Chang-E&rft.date=2014-01-28&rft.issn=2219-2840&rft.eissn=2219-2840&rft.volume=20&rft.issue=4&rft.spage=1079&rft_id=info:doi/10.3748%2Fwjg.v20.i4.1079&rft.externalDBID=NO_FULL_TEXT |
thumbnail_s | http://utb.summon.serialssolutions.com/2.0.0/image/custom?url=http%3A%2F%2Fimage.cqvip.com%2Fvip1000%2Fqk%2F84123X%2F84123X.jpg |