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Oxidative stress triggers hyperdynamic circulation via central neural activation in portal hypertensive rats
Background Hyperdynamic circulation in portal hypertension (PHT) depends on central neural activation. However, the initiating mechanism that signals PHT to the central neural cardiovascular-regulatory centers remains unclear. We aimed to test the hypothesis that oxidative stress in the gut initiate...
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| Published in: | Hepatology international 2023-06, Vol.17 (3), p.689-697 |
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| container_title | Hepatology international |
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| creator | Liu, Hongqun Alhassan, Noura Yoon, Ki Tae Almutlaq, Lamees Lee, Samuel S. |
| description | Background
Hyperdynamic circulation in portal hypertension (PHT) depends on central neural activation. However, the initiating mechanism that signals PHT to the central neural cardiovascular-regulatory centers remains unclear. We aimed to test the hypothesis that oxidative stress in the gut initiates the signal that activates central cardiovascular nuclei in portal hypertensive rats.
Methods
Two groups of rats were used. One had portal hypertension produced by partial portal vein ligation, while controls underwent sham operation. Hemodynamics including portal pressure, cardiac output, mean arterial pressure (MAP) and peripheral vascular resistance were measured. Activation of central cardiovascular nuclei was determined by immunohistochemical Fos expression in the paraventricular nucleus (PVN) of the hypothalamus. Myeloperoxidase activity, an oxidative stress marker, was measured in the jejunum. Hydrogen peroxide, the antioxidant
N
-acetyl-cysteine (NAC) or saline controls were administered for 12–14 days by gavage or osmotic minipumps placed in the peritoneal cavity.
Results
Compared with controls, PHT rats showed increased cardiac output (54.2 ± 9.5 vs 33.6 ± 2.4 ml/min/100 g BW,
p
|
| doi_str_mv | 10.1007/s12072-023-10481-5 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2771637420</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2819851699</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-db5b11e405af94c177d7d13b772555ff765868d548b6e176e16610959c7b009d3</originalsourceid><addsrcrecordid>eNp9kU1PJCEQhslGs37s_gEPphMvXnqtgga6j8b4lZh40TOhaXrE9NAj0Gbn38tMj5rsYQ-kCPXwQOol5AThDwLIi4gUJC2BshKhqrHkP8ghNkyUwCvc-9ozdkCOYnwF4Fyg-EkOmJCU1QCHZHj86zqd3LstYgo2xiIFt1jYEIuX9cqGbu310pnCuGCmIYOjL96dLoz1Keih8HbaFG2yYu46X6zGkPLhVpCsjxt70Cn-Ivu9HqL9vavH5Pnm-unqrnx4vL2_unwoDZM8lV3LW0RbAdd9UxmUspMdslZKyjnveyl4LeqOV3UrLMq8hEBoeGNkC9B07Jicz95VGN8mG5NaumjsMGhvxykqKiUKJisKGT37B30dp-Dz7xStsak5iqbJFJ0pE8YYg-3VKrilDmuFoDZZqDkLlbNQ2ywUz5dOd-qpXdru68rn8DPAZiDmls8z_377P9oPZ7OVbA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2819851699</pqid></control><display><type>article</type><title>Oxidative stress triggers hyperdynamic circulation via central neural activation in portal hypertensive rats</title><source>Springer Nature</source><creator>Liu, Hongqun ; Alhassan, Noura ; Yoon, Ki Tae ; Almutlaq, Lamees ; Lee, Samuel S.</creator><creatorcontrib>Liu, Hongqun ; Alhassan, Noura ; Yoon, Ki Tae ; Almutlaq, Lamees ; Lee, Samuel S.</creatorcontrib><description>Background
Hyperdynamic circulation in portal hypertension (PHT) depends on central neural activation. However, the initiating mechanism that signals PHT to the central neural cardiovascular-regulatory centers remains unclear. We aimed to test the hypothesis that oxidative stress in the gut initiates the signal that activates central cardiovascular nuclei in portal hypertensive rats.
Methods
Two groups of rats were used. One had portal hypertension produced by partial portal vein ligation, while controls underwent sham operation. Hemodynamics including portal pressure, cardiac output, mean arterial pressure (MAP) and peripheral vascular resistance were measured. Activation of central cardiovascular nuclei was determined by immunohistochemical Fos expression in the paraventricular nucleus (PVN) of the hypothalamus. Myeloperoxidase activity, an oxidative stress marker, was measured in the jejunum. Hydrogen peroxide, the antioxidant
N
-acetyl-cysteine (NAC) or saline controls were administered for 12–14 days by gavage or osmotic minipumps placed in the peritoneal cavity.
Results
Compared with controls, PHT rats showed increased cardiac output (54.2 ± 9.5 vs 33.6 ± 2.4 ml/min/100 g BW,
p
< 0.01), decreased MAP (96.2 ± 6.4 mmHg vs 103.2 ± 7.8,
p
< 0.01) and systemic vascular resistance (1.84 ± 0.28 vs 3.14 ± 0.19 mmHg/min/ml/100 g BW,
p
< 0.01). PHT rats had increased jejunal myeloperoxidase and PVN Fos expression. NAC treatment eliminated the hyperdynamic circulation, decreased jejunal myeloperoxidase and PVN Fos expression in PHT rats, but had no effect on sham controls. H
2
O
2
significantly increased PVN Fos expression and decreased MAP.
Conclusion
These results indicate that in PHT, mesenteric oxidative stress is the initial signal that activates chemoreceptors and triggers hyperdynamic circulation by central neural cardiovascular-regulatory centers.</description><identifier>ISSN: 1936-0533</identifier><identifier>EISSN: 1936-0541</identifier><identifier>DOI: 10.1007/s12072-023-10481-5</identifier><identifier>PMID: 36723800</identifier><language>eng</language><publisher>New Delhi: Springer India</publisher><subject>Acetylcysteine ; Animals ; Blood circulation ; Blood pressure ; Cardiac output ; Chemoreceptors ; Colorectal Surgery ; Heart ; Hemodynamics ; Hepatology ; Hydrogen peroxide ; Hydrogen Peroxide - pharmacology ; Hypertension ; Hypertension, Portal ; Hypothalamus ; Jejunum ; Medicine ; Medicine & Public Health ; Nuclei ; Original Article ; Oxidation ; Oxidative Stress ; Paraventricular nucleus ; Peroxidase ; Peroxidase - metabolism ; Peroxidase - pharmacology ; Portal Vein ; Rats ; Rats, Sprague-Dawley ; Surgery</subject><ispartof>Hepatology international, 2023-06, Vol.17 (3), p.689-697</ispartof><rights>Asian Pacific Association for the Study of the Liver 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. Asian Pacific Association for the Study of the Liver.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-db5b11e405af94c177d7d13b772555ff765868d548b6e176e16610959c7b009d3</citedby><cites>FETCH-LOGICAL-c375t-db5b11e405af94c177d7d13b772555ff765868d548b6e176e16610959c7b009d3</cites><orcidid>0000-0003-4431-272X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36723800$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Hongqun</creatorcontrib><creatorcontrib>Alhassan, Noura</creatorcontrib><creatorcontrib>Yoon, Ki Tae</creatorcontrib><creatorcontrib>Almutlaq, Lamees</creatorcontrib><creatorcontrib>Lee, Samuel S.</creatorcontrib><title>Oxidative stress triggers hyperdynamic circulation via central neural activation in portal hypertensive rats</title><title>Hepatology international</title><addtitle>Hepatol Int</addtitle><addtitle>Hepatol Int</addtitle><description>Background
Hyperdynamic circulation in portal hypertension (PHT) depends on central neural activation. However, the initiating mechanism that signals PHT to the central neural cardiovascular-regulatory centers remains unclear. We aimed to test the hypothesis that oxidative stress in the gut initiates the signal that activates central cardiovascular nuclei in portal hypertensive rats.
Methods
Two groups of rats were used. One had portal hypertension produced by partial portal vein ligation, while controls underwent sham operation. Hemodynamics including portal pressure, cardiac output, mean arterial pressure (MAP) and peripheral vascular resistance were measured. Activation of central cardiovascular nuclei was determined by immunohistochemical Fos expression in the paraventricular nucleus (PVN) of the hypothalamus. Myeloperoxidase activity, an oxidative stress marker, was measured in the jejunum. Hydrogen peroxide, the antioxidant
N
-acetyl-cysteine (NAC) or saline controls were administered for 12–14 days by gavage or osmotic minipumps placed in the peritoneal cavity.
Results
Compared with controls, PHT rats showed increased cardiac output (54.2 ± 9.5 vs 33.6 ± 2.4 ml/min/100 g BW,
p
< 0.01), decreased MAP (96.2 ± 6.4 mmHg vs 103.2 ± 7.8,
p
< 0.01) and systemic vascular resistance (1.84 ± 0.28 vs 3.14 ± 0.19 mmHg/min/ml/100 g BW,
p
< 0.01). PHT rats had increased jejunal myeloperoxidase and PVN Fos expression. NAC treatment eliminated the hyperdynamic circulation, decreased jejunal myeloperoxidase and PVN Fos expression in PHT rats, but had no effect on sham controls. H
2
O
2
significantly increased PVN Fos expression and decreased MAP.
Conclusion
These results indicate that in PHT, mesenteric oxidative stress is the initial signal that activates chemoreceptors and triggers hyperdynamic circulation by central neural cardiovascular-regulatory centers.</description><subject>Acetylcysteine</subject><subject>Animals</subject><subject>Blood circulation</subject><subject>Blood pressure</subject><subject>Cardiac output</subject><subject>Chemoreceptors</subject><subject>Colorectal Surgery</subject><subject>Heart</subject><subject>Hemodynamics</subject><subject>Hepatology</subject><subject>Hydrogen peroxide</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>Hypertension</subject><subject>Hypertension, Portal</subject><subject>Hypothalamus</subject><subject>Jejunum</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Nuclei</subject><subject>Original Article</subject><subject>Oxidation</subject><subject>Oxidative Stress</subject><subject>Paraventricular nucleus</subject><subject>Peroxidase</subject><subject>Peroxidase - metabolism</subject><subject>Peroxidase - pharmacology</subject><subject>Portal Vein</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Surgery</subject><issn>1936-0533</issn><issn>1936-0541</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNp9kU1PJCEQhslGs37s_gEPphMvXnqtgga6j8b4lZh40TOhaXrE9NAj0Gbn38tMj5rsYQ-kCPXwQOol5AThDwLIi4gUJC2BshKhqrHkP8ghNkyUwCvc-9ozdkCOYnwF4Fyg-EkOmJCU1QCHZHj86zqd3LstYgo2xiIFt1jYEIuX9cqGbu310pnCuGCmIYOjL96dLoz1Keih8HbaFG2yYu46X6zGkPLhVpCsjxt70Cn-Ivu9HqL9vavH5Pnm-unqrnx4vL2_unwoDZM8lV3LW0RbAdd9UxmUspMdslZKyjnveyl4LeqOV3UrLMq8hEBoeGNkC9B07Jicz95VGN8mG5NaumjsMGhvxykqKiUKJisKGT37B30dp-Dz7xStsak5iqbJFJ0pE8YYg-3VKrilDmuFoDZZqDkLlbNQ2ywUz5dOd-qpXdru68rn8DPAZiDmls8z_377P9oPZ7OVbA</recordid><startdate>20230601</startdate><enddate>20230601</enddate><creator>Liu, Hongqun</creator><creator>Alhassan, Noura</creator><creator>Yoon, Ki Tae</creator><creator>Almutlaq, Lamees</creator><creator>Lee, Samuel S.</creator><general>Springer India</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-4431-272X</orcidid></search><sort><creationdate>20230601</creationdate><title>Oxidative stress triggers hyperdynamic circulation via central neural activation in portal hypertensive rats</title><author>Liu, Hongqun ; Alhassan, Noura ; Yoon, Ki Tae ; Almutlaq, Lamees ; Lee, Samuel S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-db5b11e405af94c177d7d13b772555ff765868d548b6e176e16610959c7b009d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Acetylcysteine</topic><topic>Animals</topic><topic>Blood circulation</topic><topic>Blood pressure</topic><topic>Cardiac output</topic><topic>Chemoreceptors</topic><topic>Colorectal Surgery</topic><topic>Heart</topic><topic>Hemodynamics</topic><topic>Hepatology</topic><topic>Hydrogen peroxide</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>Hypertension</topic><topic>Hypertension, Portal</topic><topic>Hypothalamus</topic><topic>Jejunum</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Nuclei</topic><topic>Original Article</topic><topic>Oxidation</topic><topic>Oxidative Stress</topic><topic>Paraventricular nucleus</topic><topic>Peroxidase</topic><topic>Peroxidase - metabolism</topic><topic>Peroxidase - pharmacology</topic><topic>Portal Vein</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Surgery</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Hongqun</creatorcontrib><creatorcontrib>Alhassan, Noura</creatorcontrib><creatorcontrib>Yoon, Ki Tae</creatorcontrib><creatorcontrib>Almutlaq, Lamees</creatorcontrib><creatorcontrib>Lee, Samuel S.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Hepatology international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Hongqun</au><au>Alhassan, Noura</au><au>Yoon, Ki Tae</au><au>Almutlaq, Lamees</au><au>Lee, Samuel S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidative stress triggers hyperdynamic circulation via central neural activation in portal hypertensive rats</atitle><jtitle>Hepatology international</jtitle><stitle>Hepatol Int</stitle><addtitle>Hepatol Int</addtitle><date>2023-06-01</date><risdate>2023</risdate><volume>17</volume><issue>3</issue><spage>689</spage><epage>697</epage><pages>689-697</pages><issn>1936-0533</issn><eissn>1936-0541</eissn><abstract>Background
Hyperdynamic circulation in portal hypertension (PHT) depends on central neural activation. However, the initiating mechanism that signals PHT to the central neural cardiovascular-regulatory centers remains unclear. We aimed to test the hypothesis that oxidative stress in the gut initiates the signal that activates central cardiovascular nuclei in portal hypertensive rats.
Methods
Two groups of rats were used. One had portal hypertension produced by partial portal vein ligation, while controls underwent sham operation. Hemodynamics including portal pressure, cardiac output, mean arterial pressure (MAP) and peripheral vascular resistance were measured. Activation of central cardiovascular nuclei was determined by immunohistochemical Fos expression in the paraventricular nucleus (PVN) of the hypothalamus. Myeloperoxidase activity, an oxidative stress marker, was measured in the jejunum. Hydrogen peroxide, the antioxidant
N
-acetyl-cysteine (NAC) or saline controls were administered for 12–14 days by gavage or osmotic minipumps placed in the peritoneal cavity.
Results
Compared with controls, PHT rats showed increased cardiac output (54.2 ± 9.5 vs 33.6 ± 2.4 ml/min/100 g BW,
p
< 0.01), decreased MAP (96.2 ± 6.4 mmHg vs 103.2 ± 7.8,
p
< 0.01) and systemic vascular resistance (1.84 ± 0.28 vs 3.14 ± 0.19 mmHg/min/ml/100 g BW,
p
< 0.01). PHT rats had increased jejunal myeloperoxidase and PVN Fos expression. NAC treatment eliminated the hyperdynamic circulation, decreased jejunal myeloperoxidase and PVN Fos expression in PHT rats, but had no effect on sham controls. H
2
O
2
significantly increased PVN Fos expression and decreased MAP.
Conclusion
These results indicate that in PHT, mesenteric oxidative stress is the initial signal that activates chemoreceptors and triggers hyperdynamic circulation by central neural cardiovascular-regulatory centers.</abstract><cop>New Delhi</cop><pub>Springer India</pub><pmid>36723800</pmid><doi>10.1007/s12072-023-10481-5</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-4431-272X</orcidid></addata></record> |
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| ispartof | Hepatology international, 2023-06, Vol.17 (3), p.689-697 |
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| subjects | Acetylcysteine Animals Blood circulation Blood pressure Cardiac output Chemoreceptors Colorectal Surgery Heart Hemodynamics Hepatology Hydrogen peroxide Hydrogen Peroxide - pharmacology Hypertension Hypertension, Portal Hypothalamus Jejunum Medicine Medicine & Public Health Nuclei Original Article Oxidation Oxidative Stress Paraventricular nucleus Peroxidase Peroxidase - metabolism Peroxidase - pharmacology Portal Vein Rats Rats, Sprague-Dawley Surgery |
| title | Oxidative stress triggers hyperdynamic circulation via central neural activation in portal hypertensive rats |
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