Alterations in pulmonary vascular function in rats exposed to intermittent hypoxia
Vasoactive agents were examined in arteries from control rats and rats exposed to intermittent hypoxia (10% oxygen; 8 h/day) for 3, 5 or 20 days. Hypoxic rats developed right ventricular hypertrophy after 5 days, but became pulmonary hypertensive (elevated right ventricular systolic pressure; RVSP)...
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| Veröffentlicht in: | European journal of pharmacology 2003-09, Vol.477 (2), p.153-161 |
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| creator | Thomas, Bronwyn J. Wanstall, Janet C. |
| description | Vasoactive agents were examined in arteries from control rats and rats exposed to intermittent hypoxia (10% oxygen; 8 h/day) for 3, 5 or 20 days. Hypoxic rats developed right ventricular hypertrophy after 5 days, but became pulmonary hypertensive (elevated right ventricular systolic pressure; RVSP) only after 20 days. In pulmonary arteries (main and intralobar), responses to acetylcholine and ionomycin (endothelium-dependent vasodilators) were reduced after 20 and 5 days of intermittent hypoxia, whereas contractions to 5-hydroxytryptamine (5-HT) were enhanced (potency increase >10-fold) after 20, 5 and 3 days. Contractions to endothelin-1 and a thromboxane-mimetic, but not Ca
2+, were also increased. No changes in vascular function occurred in aorta. Since changes in pulmonary vascular function preceded the increase in RVSP they do not result from, but may contribute to, the development of hypoxia-induced pulmonary hypertension. If similar changes occur in humans, they may be important in conditions characterised by intermittent, as opposed to continuous, hypoxia. |
| doi_str_mv | 10.1016/j.ejphar.2003.08.015 |
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2+, were also increased. No changes in vascular function occurred in aorta. Since changes in pulmonary vascular function preceded the increase in RVSP they do not result from, but may contribute to, the development of hypoxia-induced pulmonary hypertension. If similar changes occur in humans, they may be important in conditions characterised by intermittent, as opposed to continuous, hypoxia.</description><subject>15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology</subject><subject>5-HT (5-hydroxytryptamine, serotonin)</subject><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Endothelin-1 - pharmacology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Endothelium-dependent vasodilatation</subject><subject>Hypoxia</subject><subject>Hypoxia - physiopathology</subject><subject>In Vitro Techniques</subject><subject>intermittent</subject><subject>Ionomycin - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - physiopathology</subject><subject>Pneumology</subject><subject>Potassium Chloride - pharmacology</subject><subject>Pulmonary artery</subject><subject>Pulmonary Artery - drug effects</subject><subject>Pulmonary Artery - metabolism</subject><subject>Pulmonary Artery - physiopathology</subject><subject>Pulmonary hypertension</subject><subject>Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Serotonin - analogs & derivatives</subject><subject>Serotonin - pharmacology</subject><subject>Vasoactive agent</subject><subject>Vasoconstrictor Agents - pharmacology</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFq3DAQhkVpabZp36AUX9qb3ZE9sq1LIYS0CQQKpT0LWRoTLbblSnJI3r4yu5BbTyNmvn8YfYx95FBx4O3XY0XH9UGHqgZoKugr4OIVO_C-kyV0vH7NDgAcy1pKecHexXgEACFr8ZZdcBRcIpcH9utqShR0cn6JhVuKdZtmv-jwXDzqaLZJh2LcFrPP93EmY0FPq49ki-RzK6dnlxItqXh4Xv2T0-_Zm1FPkT6c6yX78_3m9_Vtef_zx9311X1pUGAqsRU4YFMP2LZINSdE2QxC5LexOEprdS8bYbVu20FYOcDYQ9M1zah5KwU0l-zLae8a_N-NYlKzi4amSS_kt6g60dWyR8wgnkATfIyBRrUGN-c_Kg5qd6mO6uRS7S4V9Cq7zLFP5_3bMJN9CZ3lZeDzGciq9DQGvRgXXzjBEdp-P_TbiaNs49FRUNE4WgxZF8gkZb37_yX_AMYBlNk</recordid><startdate>20030912</startdate><enddate>20030912</enddate><creator>Thomas, Bronwyn J.</creator><creator>Wanstall, Janet C.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>20030912</creationdate><title>Alterations in pulmonary vascular function in rats exposed to intermittent hypoxia</title><author>Thomas, Bronwyn J. ; Wanstall, Janet C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-4654b432b4664e21e4493b554e2cd4f9dda8935daa66b5d9b0f803733fa169503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology</topic><topic>5-HT (5-hydroxytryptamine, serotonin)</topic><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Endothelin-1 - pharmacology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Endothelium-dependent vasodilatation</topic><topic>Hypoxia</topic><topic>Hypoxia - physiopathology</topic><topic>In Vitro Techniques</topic><topic>intermittent</topic><topic>Ionomycin - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - physiopathology</topic><topic>Pneumology</topic><topic>Potassium Chloride - pharmacology</topic><topic>Pulmonary artery</topic><topic>Pulmonary Artery - drug effects</topic><topic>Pulmonary Artery - metabolism</topic><topic>Pulmonary Artery - physiopathology</topic><topic>Pulmonary hypertension</topic><topic>Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Serotonin - analogs & derivatives</topic><topic>Serotonin - pharmacology</topic><topic>Vasoactive agent</topic><topic>Vasoconstrictor Agents - pharmacology</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Thomas, Bronwyn J.</creatorcontrib><creatorcontrib>Wanstall, Janet C.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Thomas, Bronwyn J.</au><au>Wanstall, Janet C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alterations in pulmonary vascular function in rats exposed to intermittent hypoxia</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2003-09-12</date><risdate>2003</risdate><volume>477</volume><issue>2</issue><spage>153</spage><epage>161</epage><pages>153-161</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>Vasoactive agents were examined in arteries from control rats and rats exposed to intermittent hypoxia (10% oxygen; 8 h/day) for 3, 5 or 20 days. Hypoxic rats developed right ventricular hypertrophy after 5 days, but became pulmonary hypertensive (elevated right ventricular systolic pressure; RVSP) only after 20 days. In pulmonary arteries (main and intralobar), responses to acetylcholine and ionomycin (endothelium-dependent vasodilators) were reduced after 20 and 5 days of intermittent hypoxia, whereas contractions to 5-hydroxytryptamine (5-HT) were enhanced (potency increase >10-fold) after 20, 5 and 3 days. Contractions to endothelin-1 and a thromboxane-mimetic, but not Ca
2+, were also increased. No changes in vascular function occurred in aorta. Since changes in pulmonary vascular function preceded the increase in RVSP they do not result from, but may contribute to, the development of hypoxia-induced pulmonary hypertension. If similar changes occur in humans, they may be important in conditions characterised by intermittent, as opposed to continuous, hypoxia.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>14519419</pmid><doi>10.1016/j.ejphar.2003.08.015</doi><tpages>9</tpages></addata></record> |
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| subjects | 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology 5-HT (5-hydroxytryptamine, serotonin) Acetylcholine - pharmacology Animals Biological and medical sciences Endothelin-1 - pharmacology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Endothelium, Vascular - physiopathology Endothelium-dependent vasodilatation Hypoxia Hypoxia - physiopathology In Vitro Techniques intermittent Ionomycin - pharmacology Male Medical sciences Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - physiopathology Pneumology Potassium Chloride - pharmacology Pulmonary artery Pulmonary Artery - drug effects Pulmonary Artery - metabolism Pulmonary Artery - physiopathology Pulmonary hypertension Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases Rats Rats, Wistar Serotonin - analogs & derivatives Serotonin - pharmacology Vasoactive agent Vasoconstrictor Agents - pharmacology Vasodilator Agents - pharmacology |
| title | Alterations in pulmonary vascular function in rats exposed to intermittent hypoxia |
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