Continuous inhalation of carbon monoxide induces right ventricle ischemia and dysfunction in rats with hypoxic pulmonary hypertension
1 University Francois Rabelais of Tours, IFR 135, Labpart EA 3852, Tours Cedex; and 2 Pfizer Global Research and Development, Centre de Recherche, Amboise Cedex, France Submitted 22 September 2006 ; accepted in final form 3 May 2007 We aimed to investigate the toxicity of carbon monoxide (CO) in rat...
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| creator | Gautier, Mathieu Antier, Daniel Bonnet, Pierre Net, Jean-Loic Le Hanton, Gilles Eder, Veronique |
| description | 1 University Francois Rabelais of Tours, IFR 135, Labpart EA 3852, Tours Cedex; and 2 Pfizer Global Research and Development, Centre de Recherche, Amboise Cedex, France
Submitted 22 September 2006
; accepted in final form 3 May 2007
We aimed to investigate the toxicity of carbon monoxide (CO) in rats with right ventricle (RV) remodeling induced by hypoxic pulmonary hypertension (PHT). A group of Wistar rats was exposed to 3-wk hypobaric hypoxia (H). A second group was exposed to 50 ppm CO for 1 wk (CO). A third group was exposed to chronic hypoxia including 50 ppm CO during the third week (H+CO). These groups were compared with controls. RV and left ventricle (LV) functions were assessed by echocardiography and transparietal catheterization. Ventricular perfusion was estimated with the fluorescent microsphere method. Results were confirmed by histology. PHT induced RV hypertrophy and function enhancement. In the H group, RV shortening fraction (RVSF; 71 ± 12% vs. 41 ± 2%) and RV end-systolic pressure (RVESP; 54 ± 6 vs. 19 ± 2 mmHg) were increased compared with controls. Moreover, myocardial perfusion was increased in the RV (36 ± 2% vs. 22 ± 2%) and decreased in the LV (64 ± 3% vs. 78 ± 2%). In the H+CO group, RVSF (45 ± 3% vs. 71 ± 12%) and RVESP (38 ± 3 vs. 54 ± 6 mmHg) were decreased compared with the H group. RV perfusion was decreased in the H+CO group compared with the H group (21 ± 5% vs. 36 ± 2%), and LV perfusion was increased (79 ± 5% vs. 64 ± 3%). PHT and RV hypertrophy were still present in the H+CO group, and fibroses localized in the RV were detected. Similar lesions were observed in an additional group exposed simultaneously to hypoxia and 50 ppm CO over 3 wk. We demonstrated that rats with established PHT were more sensitive to CO, which dramatically alters the RV adaptive response to PHT, leading to ischemic lesions.
right ventricle remodeling; right ventricle perfusion
Address for reprint requests and other correspondence: V. Eder, Labpart EA 3852, Fac. of Medicine, Univ. Francois Rabelais, 10 Bld Tonnelle, BP 3223, 37032 Tours Cedex 1, France (e-mail: eder{at}med.univ-tours.fr ) |
| doi_str_mv | 10.1152/ajpheart.01040.2006 |
| format | Article |
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Submitted 22 September 2006
; accepted in final form 3 May 2007
We aimed to investigate the toxicity of carbon monoxide (CO) in rats with right ventricle (RV) remodeling induced by hypoxic pulmonary hypertension (PHT). A group of Wistar rats was exposed to 3-wk hypobaric hypoxia (H). A second group was exposed to 50 ppm CO for 1 wk (CO). A third group was exposed to chronic hypoxia including 50 ppm CO during the third week (H+CO). These groups were compared with controls. RV and left ventricle (LV) functions were assessed by echocardiography and transparietal catheterization. Ventricular perfusion was estimated with the fluorescent microsphere method. Results were confirmed by histology. PHT induced RV hypertrophy and function enhancement. In the H group, RV shortening fraction (RVSF; 71 ± 12% vs. 41 ± 2%) and RV end-systolic pressure (RVESP; 54 ± 6 vs. 19 ± 2 mmHg) were increased compared with controls. Moreover, myocardial perfusion was increased in the RV (36 ± 2% vs. 22 ± 2%) and decreased in the LV (64 ± 3% vs. 78 ± 2%). In the H+CO group, RVSF (45 ± 3% vs. 71 ± 12%) and RVESP (38 ± 3 vs. 54 ± 6 mmHg) were decreased compared with the H group. RV perfusion was decreased in the H+CO group compared with the H group (21 ± 5% vs. 36 ± 2%), and LV perfusion was increased (79 ± 5% vs. 64 ± 3%). PHT and RV hypertrophy were still present in the H+CO group, and fibroses localized in the RV were detected. Similar lesions were observed in an additional group exposed simultaneously to hypoxia and 50 ppm CO over 3 wk. We demonstrated that rats with established PHT were more sensitive to CO, which dramatically alters the RV adaptive response to PHT, leading to ischemic lesions.
right ventricle remodeling; right ventricle perfusion
Address for reprint requests and other correspondence: V. Eder, Labpart EA 3852, Fac. of Medicine, Univ. Francois Rabelais, 10 Bld Tonnelle, BP 3223, 37032 Tours Cedex 1, France (e-mail: eder{at}med.univ-tours.fr )</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.01040.2006</identifier><identifier>PMID: 17483237</identifier><identifier>CODEN: AJPPDI</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Administration, Inhalation ; Animals ; Blood Flow Velocity - drug effects ; Blood Pressure - drug effects ; Carbon monoxide ; Carbon Monoxide - administration & dosage ; Carbon Monoxide - toxicity ; Carboxyhemoglobin - metabolism ; Cardiac Catheterization ; Cardiovascular system ; Comparative analysis ; Coronary Circulation - drug effects ; Disease Models, Animal ; Echocardiography ; Fibrosis ; Heart Ventricles - drug effects ; Heart Ventricles - physiopathology ; Hematocrit ; Hypertension ; Hypertension, Pulmonary - blood ; Hypertension, Pulmonary - complications ; Hypertension, Pulmonary - etiology ; Hypertension, Pulmonary - physiopathology ; Hypertrophy, Right Ventricular - blood ; Hypertrophy, Right Ventricular - etiology ; Hypertrophy, Right Ventricular - physiopathology ; Hypoxia ; Hypoxia - blood ; Hypoxia - complications ; Hypoxia - physiopathology ; Laser-Doppler Flowmetry ; Life Sciences ; Male ; Myocardial Contraction - drug effects ; Myocardial Ischemia - chemically induced ; Myocardial Ischemia - complications ; Myocardial Ischemia - pathology ; Myocardial Ischemia - physiopathology ; Pulmonary Artery - drug effects ; Pulmonary Artery - physiopathology ; Rats ; Rats, Wistar ; Rodents ; Toxicity ; Ventricular Function, Left - drug effects ; Ventricular Function, Right - drug effects ; Ventricular Pressure - drug effects ; Ventricular Remodeling - drug effects</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2007-08, Vol.293 (2), p.H1046-H1052</ispartof><rights>Copyright American Physiological Society Aug 2007</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-ccd19535a4dcccb204a2d2e68cf4564d5af94030055237a5fbc182bfbbfe774d3</citedby><cites>FETCH-LOGICAL-c456t-ccd19535a4dcccb204a2d2e68cf4564d5af94030055237a5fbc182bfbbfe774d3</cites><orcidid>0000-0001-8971-5683</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17483237$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-04542586$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Gautier, Mathieu</creatorcontrib><creatorcontrib>Antier, Daniel</creatorcontrib><creatorcontrib>Bonnet, Pierre</creatorcontrib><creatorcontrib>Net, Jean-Loic Le</creatorcontrib><creatorcontrib>Hanton, Gilles</creatorcontrib><creatorcontrib>Eder, Veronique</creatorcontrib><title>Continuous inhalation of carbon monoxide induces right ventricle ischemia and dysfunction in rats with hypoxic pulmonary hypertension</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>1 University Francois Rabelais of Tours, IFR 135, Labpart EA 3852, Tours Cedex; and 2 Pfizer Global Research and Development, Centre de Recherche, Amboise Cedex, France
Submitted 22 September 2006
; accepted in final form 3 May 2007
We aimed to investigate the toxicity of carbon monoxide (CO) in rats with right ventricle (RV) remodeling induced by hypoxic pulmonary hypertension (PHT). A group of Wistar rats was exposed to 3-wk hypobaric hypoxia (H). A second group was exposed to 50 ppm CO for 1 wk (CO). A third group was exposed to chronic hypoxia including 50 ppm CO during the third week (H+CO). These groups were compared with controls. RV and left ventricle (LV) functions were assessed by echocardiography and transparietal catheterization. Ventricular perfusion was estimated with the fluorescent microsphere method. Results were confirmed by histology. PHT induced RV hypertrophy and function enhancement. In the H group, RV shortening fraction (RVSF; 71 ± 12% vs. 41 ± 2%) and RV end-systolic pressure (RVESP; 54 ± 6 vs. 19 ± 2 mmHg) were increased compared with controls. Moreover, myocardial perfusion was increased in the RV (36 ± 2% vs. 22 ± 2%) and decreased in the LV (64 ± 3% vs. 78 ± 2%). In the H+CO group, RVSF (45 ± 3% vs. 71 ± 12%) and RVESP (38 ± 3 vs. 54 ± 6 mmHg) were decreased compared with the H group. RV perfusion was decreased in the H+CO group compared with the H group (21 ± 5% vs. 36 ± 2%), and LV perfusion was increased (79 ± 5% vs. 64 ± 3%). PHT and RV hypertrophy were still present in the H+CO group, and fibroses localized in the RV were detected. Similar lesions were observed in an additional group exposed simultaneously to hypoxia and 50 ppm CO over 3 wk. We demonstrated that rats with established PHT were more sensitive to CO, which dramatically alters the RV adaptive response to PHT, leading to ischemic lesions.
right ventricle remodeling; right ventricle perfusion
Address for reprint requests and other correspondence: V. Eder, Labpart EA 3852, Fac. of Medicine, Univ. Francois Rabelais, 10 Bld Tonnelle, BP 3223, 37032 Tours Cedex 1, France (e-mail: eder{at}med.univ-tours.fr )</description><subject>Administration, Inhalation</subject><subject>Animals</subject><subject>Blood Flow Velocity - drug effects</subject><subject>Blood Pressure - drug effects</subject><subject>Carbon monoxide</subject><subject>Carbon Monoxide - administration & dosage</subject><subject>Carbon Monoxide - toxicity</subject><subject>Carboxyhemoglobin - metabolism</subject><subject>Cardiac Catheterization</subject><subject>Cardiovascular system</subject><subject>Comparative analysis</subject><subject>Coronary Circulation - drug effects</subject><subject>Disease Models, Animal</subject><subject>Echocardiography</subject><subject>Fibrosis</subject><subject>Heart Ventricles - drug effects</subject><subject>Heart Ventricles - physiopathology</subject><subject>Hematocrit</subject><subject>Hypertension</subject><subject>Hypertension, Pulmonary - blood</subject><subject>Hypertension, Pulmonary - complications</subject><subject>Hypertension, Pulmonary - etiology</subject><subject>Hypertension, Pulmonary - physiopathology</subject><subject>Hypertrophy, Right Ventricular - blood</subject><subject>Hypertrophy, Right Ventricular - etiology</subject><subject>Hypertrophy, Right Ventricular - physiopathology</subject><subject>Hypoxia</subject><subject>Hypoxia - blood</subject><subject>Hypoxia - complications</subject><subject>Hypoxia - physiopathology</subject><subject>Laser-Doppler Flowmetry</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardial Ischemia - chemically induced</subject><subject>Myocardial Ischemia - complications</subject><subject>Myocardial Ischemia - pathology</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Pulmonary Artery - drug effects</subject><subject>Pulmonary Artery - physiopathology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rodents</subject><subject>Toxicity</subject><subject>Ventricular Function, Left - drug effects</subject><subject>Ventricular Function, Right - drug effects</subject><subject>Ventricular Pressure - drug effects</subject><subject>Ventricular Remodeling - drug effects</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1uEzEUhS0EoqHwBEjIYsdiUv-M50esqoiSSpHYlLXlsT0dRxN7sD1t8wC8NzdNGtiwsnXvOZ_uvQehj5QsKRXsSm2nwaqYl4SSkiwZIdUrtIAOK6jg7Wu0ILziRUW5uEDvUtoSQkRd8bfogtZlwxmvF-j3Kvjs_BzmhJ0f1KiyCx6HHmsVO_jtgg9PzljomlnbhKO7HzJ-sD5Hp0eoJz3YnVNYeYPNPvWz188M53FUOeFHlwc87CfAaDzNIxBV3B8qNmbrE2jfoze9GpP9cHov0c-bb3erdbH58f12db0pdCmqXGhtaCu4UKXRWneMlIoZZqtG99AvjVB9WxIOawpYTom-07RhXd91va3r0vBL9OXIhUXlFN0OBpFBObm-3shDjZSiZKKpHihoPx-1Uwy_Zpuy3IY5ehhPMtZWomrrBkT8KNIxpBRtf6ZSIg8pyZeU5HNK8pASuD6d0HO3s-av5xQLCL6e5oRjP7po5TTs4VBjuN_Lm3kc7-xTPqNZyyWTa-BXcjI9uK_-7z7P84-L_wEfi7nE</recordid><startdate>20070801</startdate><enddate>20070801</enddate><creator>Gautier, Mathieu</creator><creator>Antier, Daniel</creator><creator>Bonnet, Pierre</creator><creator>Net, Jean-Loic Le</creator><creator>Hanton, Gilles</creator><creator>Eder, Veronique</creator><general>American Physiological Society</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>7QP</scope><scope>7QR</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0001-8971-5683</orcidid></search><sort><creationdate>20070801</creationdate><title>Continuous inhalation of carbon monoxide induces right ventricle ischemia and dysfunction in rats with hypoxic pulmonary hypertension</title><author>Gautier, Mathieu ; Antier, Daniel ; Bonnet, Pierre ; Net, Jean-Loic Le ; Hanton, Gilles ; Eder, Veronique</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-ccd19535a4dcccb204a2d2e68cf4564d5af94030055237a5fbc182bfbbfe774d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Administration, Inhalation</topic><topic>Animals</topic><topic>Blood Flow Velocity - drug effects</topic><topic>Blood Pressure - drug effects</topic><topic>Carbon monoxide</topic><topic>Carbon Monoxide - administration & dosage</topic><topic>Carbon Monoxide - toxicity</topic><topic>Carboxyhemoglobin - metabolism</topic><topic>Cardiac Catheterization</topic><topic>Cardiovascular system</topic><topic>Comparative analysis</topic><topic>Coronary Circulation - drug effects</topic><topic>Disease Models, Animal</topic><topic>Echocardiography</topic><topic>Fibrosis</topic><topic>Heart Ventricles - drug effects</topic><topic>Heart Ventricles - physiopathology</topic><topic>Hematocrit</topic><topic>Hypertension</topic><topic>Hypertension, Pulmonary - blood</topic><topic>Hypertension, Pulmonary - complications</topic><topic>Hypertension, Pulmonary - etiology</topic><topic>Hypertension, Pulmonary - physiopathology</topic><topic>Hypertrophy, Right Ventricular - blood</topic><topic>Hypertrophy, Right Ventricular - etiology</topic><topic>Hypertrophy, Right Ventricular - physiopathology</topic><topic>Hypoxia</topic><topic>Hypoxia - blood</topic><topic>Hypoxia - complications</topic><topic>Hypoxia - physiopathology</topic><topic>Laser-Doppler Flowmetry</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardial Ischemia - chemically induced</topic><topic>Myocardial Ischemia - complications</topic><topic>Myocardial Ischemia - pathology</topic><topic>Myocardial Ischemia - physiopathology</topic><topic>Pulmonary Artery - drug effects</topic><topic>Pulmonary Artery - physiopathology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Rodents</topic><topic>Toxicity</topic><topic>Ventricular Function, Left - drug effects</topic><topic>Ventricular Function, Right - drug effects</topic><topic>Ventricular Pressure - drug effects</topic><topic>Ventricular Remodeling - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gautier, Mathieu</creatorcontrib><creatorcontrib>Antier, Daniel</creatorcontrib><creatorcontrib>Bonnet, Pierre</creatorcontrib><creatorcontrib>Net, Jean-Loic Le</creatorcontrib><creatorcontrib>Hanton, Gilles</creatorcontrib><creatorcontrib>Eder, Veronique</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gautier, Mathieu</au><au>Antier, Daniel</au><au>Bonnet, Pierre</au><au>Net, Jean-Loic Le</au><au>Hanton, Gilles</au><au>Eder, Veronique</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Continuous inhalation of carbon monoxide induces right ventricle ischemia and dysfunction in rats with hypoxic pulmonary hypertension</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2007-08-01</date><risdate>2007</risdate><volume>293</volume><issue>2</issue><spage>H1046</spage><epage>H1052</epage><pages>H1046-H1052</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><coden>AJPPDI</coden><abstract>1 University Francois Rabelais of Tours, IFR 135, Labpart EA 3852, Tours Cedex; and 2 Pfizer Global Research and Development, Centre de Recherche, Amboise Cedex, France
Submitted 22 September 2006
; accepted in final form 3 May 2007
We aimed to investigate the toxicity of carbon monoxide (CO) in rats with right ventricle (RV) remodeling induced by hypoxic pulmonary hypertension (PHT). A group of Wistar rats was exposed to 3-wk hypobaric hypoxia (H). A second group was exposed to 50 ppm CO for 1 wk (CO). A third group was exposed to chronic hypoxia including 50 ppm CO during the third week (H+CO). These groups were compared with controls. RV and left ventricle (LV) functions were assessed by echocardiography and transparietal catheterization. Ventricular perfusion was estimated with the fluorescent microsphere method. Results were confirmed by histology. PHT induced RV hypertrophy and function enhancement. In the H group, RV shortening fraction (RVSF; 71 ± 12% vs. 41 ± 2%) and RV end-systolic pressure (RVESP; 54 ± 6 vs. 19 ± 2 mmHg) were increased compared with controls. Moreover, myocardial perfusion was increased in the RV (36 ± 2% vs. 22 ± 2%) and decreased in the LV (64 ± 3% vs. 78 ± 2%). In the H+CO group, RVSF (45 ± 3% vs. 71 ± 12%) and RVESP (38 ± 3 vs. 54 ± 6 mmHg) were decreased compared with the H group. RV perfusion was decreased in the H+CO group compared with the H group (21 ± 5% vs. 36 ± 2%), and LV perfusion was increased (79 ± 5% vs. 64 ± 3%). PHT and RV hypertrophy were still present in the H+CO group, and fibroses localized in the RV were detected. Similar lesions were observed in an additional group exposed simultaneously to hypoxia and 50 ppm CO over 3 wk. We demonstrated that rats with established PHT were more sensitive to CO, which dramatically alters the RV adaptive response to PHT, leading to ischemic lesions.
right ventricle remodeling; right ventricle perfusion
Address for reprint requests and other correspondence: V. Eder, Labpart EA 3852, Fac. of Medicine, Univ. Francois Rabelais, 10 Bld Tonnelle, BP 3223, 37032 Tours Cedex 1, France (e-mail: eder{at}med.univ-tours.fr )</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>17483237</pmid><doi>10.1152/ajpheart.01040.2006</doi><orcidid>https://orcid.org/0000-0001-8971-5683</orcidid></addata></record> |
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| identifier | ISSN: 0363-6135 |
| ispartof | American journal of physiology. Heart and circulatory physiology, 2007-08, Vol.293 (2), p.H1046-H1052 |
| issn | 0363-6135 1522-1539 |
| language | eng |
| recordid | cdi_pubmed_primary_17483237 |
| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Administration, Inhalation Animals Blood Flow Velocity - drug effects Blood Pressure - drug effects Carbon monoxide Carbon Monoxide - administration & dosage Carbon Monoxide - toxicity Carboxyhemoglobin - metabolism Cardiac Catheterization Cardiovascular system Comparative analysis Coronary Circulation - drug effects Disease Models, Animal Echocardiography Fibrosis Heart Ventricles - drug effects Heart Ventricles - physiopathology Hematocrit Hypertension Hypertension, Pulmonary - blood Hypertension, Pulmonary - complications Hypertension, Pulmonary - etiology Hypertension, Pulmonary - physiopathology Hypertrophy, Right Ventricular - blood Hypertrophy, Right Ventricular - etiology Hypertrophy, Right Ventricular - physiopathology Hypoxia Hypoxia - blood Hypoxia - complications Hypoxia - physiopathology Laser-Doppler Flowmetry Life Sciences Male Myocardial Contraction - drug effects Myocardial Ischemia - chemically induced Myocardial Ischemia - complications Myocardial Ischemia - pathology Myocardial Ischemia - physiopathology Pulmonary Artery - drug effects Pulmonary Artery - physiopathology Rats Rats, Wistar Rodents Toxicity Ventricular Function, Left - drug effects Ventricular Function, Right - drug effects Ventricular Pressure - drug effects Ventricular Remodeling - drug effects |
| title | Continuous inhalation of carbon monoxide induces right ventricle ischemia and dysfunction in rats with hypoxic pulmonary hypertension |
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