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Split-Dose Sparing of γ-Ray-Induced Pulmonary Endothelial Dysfunction in Rats
The purpose of this study was to determine whether radiation-induced pulmonary endothelial dysfunction exhibits split-dose sparing. Rats were sacrificed 2 months after a range of 60 Co γ-ray doses (0-40 Gy) delivered to the right hemithorax in either a single fraction or in two equal fractions separ...
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Published in: | Radiation research 1988-06, Vol.114 (3), p.627-633 |
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creator | Ward, William F. Hinz, Joann M. Molteni, Agostino Chung-hsin Ts'ao |
description | The purpose of this study was to determine whether radiation-induced pulmonary endothelial dysfunction exhibits split-dose sparing. Rats were sacrificed 2 months after a range of 60 Co γ-ray doses (0-40 Gy) delivered to the right hemithorax in either a single fraction or in two equal fractions separated by 24 h. Pulmonary angiotensin converting enzyme (ACE) activity, plasminogen activator (PLA) activity, and prostacyclin $({\rm PGI}_{2})$ and thromboxane $({\rm TXA}_{2})$ production served as indices of lung endothelial function. There were dose-dependent decreases in ACE and PLA activity and increases in PGI2 and TXA2 production after both single and split-dose exposures. The $D_{2}-D_{1}$ values determined from the two-fraction minus single-fraction isoeffective doses were 3.9 Gy for ACE activity, 7.2 Gy for PLA activity, 4.8 Gy for PGI2 production, and 4.7 Gy for TXA2 production. Thus these data demonstrate that over the present range of radiation doses approximately 4-7 Gy is repairable as subeffective endothelial damage during the 24-h interval between fractions. These values agree with previously published estimates of split-dose sparing in mouse lung based on lethality and breathing rate assays. |
doi_str_mv | 10.2307/3577133 |
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Rats were sacrificed 2 months after a range of 60 Co γ-ray doses (0-40 Gy) delivered to the right hemithorax in either a single fraction or in two equal fractions separated by 24 h. Pulmonary angiotensin converting enzyme (ACE) activity, plasminogen activator (PLA) activity, and prostacyclin $({\rm PGI}_{2})$ and thromboxane $({\rm TXA}_{2})$ production served as indices of lung endothelial function. There were dose-dependent decreases in ACE and PLA activity and increases in PGI2 and TXA2 production after both single and split-dose exposures. The $D_{2}-D_{1}$ values determined from the two-fraction minus single-fraction isoeffective doses were 3.9 Gy for ACE activity, 7.2 Gy for PLA activity, 4.8 Gy for PGI2 production, and 4.7 Gy for TXA2 production. Thus these data demonstrate that over the present range of radiation doses approximately 4-7 Gy is repairable as subeffective endothelial damage during the 24-h interval between fractions. These values agree with previously published estimates of split-dose sparing in mouse lung based on lethality and breathing rate assays.</description><identifier>ISSN: 0033-7587</identifier><identifier>EISSN: 1938-5404</identifier><identifier>DOI: 10.2307/3577133</identifier><identifier>PMID: 2836884</identifier><identifier>CODEN: RAREAE</identifier><language>eng</language><publisher>Oak Brook, Il: Academic Press, Inc</publisher><subject>Animals ; Biological and medical sciences ; Biological effects of radiation ; Cobalt Radioisotopes ; Endothelial cells ; Endothelium ; Endothelium - enzymology ; Endothelium - metabolism ; Endothelium - radiation effects ; Enzymes ; Epoprostenol - metabolism ; Fundamental and applied biological sciences. Psychology ; Gamma Rays ; Ionizing radiations ; Irradiation ; Lung - enzymology ; Lung - metabolism ; Lung - radiation effects ; Lungs ; Male ; Peptidyl-Dipeptidase A - metabolism ; Plasminogen activators ; Plasminogen Activators - metabolism ; Radiation damage ; Radiation Dosage ; Radiation injuries ; Rats ; Rats, Inbred Strains ; Thromboxane A2 - metabolism ; Thromboxanes ; Tissues, organs and organisms biophysics</subject><ispartof>Radiation research, 1988-06, Vol.114 (3), p.627-633</ispartof><rights>Copyright 1988 Academic Press, Inc.</rights><rights>1988 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c361t-3739fb592c96de132a29543dafe5423057e6f001befa19db9cbd0ccc2d723f473</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3577133$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3577133$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,58238,58471</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7758395$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2836884$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ward, William F.</creatorcontrib><creatorcontrib>Hinz, Joann M.</creatorcontrib><creatorcontrib>Molteni, Agostino</creatorcontrib><creatorcontrib>Chung-hsin Ts'ao</creatorcontrib><title>Split-Dose Sparing of γ-Ray-Induced Pulmonary Endothelial Dysfunction in Rats</title><title>Radiation research</title><addtitle>Radiat Res</addtitle><description>The purpose of this study was to determine whether radiation-induced pulmonary endothelial dysfunction exhibits split-dose sparing. Rats were sacrificed 2 months after a range of 60 Co γ-ray doses (0-40 Gy) delivered to the right hemithorax in either a single fraction or in two equal fractions separated by 24 h. Pulmonary angiotensin converting enzyme (ACE) activity, plasminogen activator (PLA) activity, and prostacyclin $({\rm PGI}_{2})$ and thromboxane $({\rm TXA}_{2})$ production served as indices of lung endothelial function. There were dose-dependent decreases in ACE and PLA activity and increases in PGI2 and TXA2 production after both single and split-dose exposures. The $D_{2}-D_{1}$ values determined from the two-fraction minus single-fraction isoeffective doses were 3.9 Gy for ACE activity, 7.2 Gy for PLA activity, 4.8 Gy for PGI2 production, and 4.7 Gy for TXA2 production. Thus these data demonstrate that over the present range of radiation doses approximately 4-7 Gy is repairable as subeffective endothelial damage during the 24-h interval between fractions. These values agree with previously published estimates of split-dose sparing in mouse lung based on lethality and breathing rate assays.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biological effects of radiation</subject><subject>Cobalt Radioisotopes</subject><subject>Endothelial cells</subject><subject>Endothelium</subject><subject>Endothelium - enzymology</subject><subject>Endothelium - metabolism</subject><subject>Endothelium - radiation effects</subject><subject>Enzymes</subject><subject>Epoprostenol - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gamma Rays</subject><subject>Ionizing radiations</subject><subject>Irradiation</subject><subject>Lung - enzymology</subject><subject>Lung - metabolism</subject><subject>Lung - radiation effects</subject><subject>Lungs</subject><subject>Male</subject><subject>Peptidyl-Dipeptidase A - metabolism</subject><subject>Plasminogen activators</subject><subject>Plasminogen Activators - metabolism</subject><subject>Radiation damage</subject><subject>Radiation Dosage</subject><subject>Radiation injuries</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Thromboxane A2 - metabolism</subject><subject>Thromboxanes</subject><subject>Tissues, organs and organisms biophysics</subject><issn>0033-7587</issn><issn>1938-5404</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1988</creationdate><recordtype>article</recordtype><recordid>eNp1kMtKw0AUhgdRaq3iEwizEFyNzuRkMpmltFULRaXVdZjMRVPSScgkiz6X7-EzGWmoK1eHw_9xLh9Cl4zeRkDFHXAhGMARGjMJKeExjY_RmFIAIngqTtFZCBva9yyRIzSKUkjSNB6j53VdFi2ZVcHida2awn_gyuHvL7JSO7LwptPW4Neu3FZeNTs896ZqP21ZqBLPdsF1XrdF5XHh8Uq14RydOFUGezHUCXp_mL9Nn8jy5XExvV8SDQlrCQiQLucy0jIxlkGkIsljMMpZHvf_cGETRynLrVNMmlzq3FCtdWREBC4WMEE3-7m6qUJorMvqptj2B2aMZr9CskFIT17tybrLt9YcuMFAn18PuQpala5RXhfhgIneHkj-h21CWzX_bvsBNhdyxw</recordid><startdate>19880601</startdate><enddate>19880601</enddate><creator>Ward, William F.</creator><creator>Hinz, Joann M.</creator><creator>Molteni, Agostino</creator><creator>Chung-hsin Ts'ao</creator><general>Academic Press, Inc</general><general>Radiation Research Society</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></search><sort><creationdate>19880601</creationdate><title>Split-Dose Sparing of γ-Ray-Induced Pulmonary Endothelial Dysfunction in Rats</title><author>Ward, William F. ; Hinz, Joann M. ; Molteni, Agostino ; Chung-hsin Ts'ao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c361t-3739fb592c96de132a29543dafe5423057e6f001befa19db9cbd0ccc2d723f473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1988</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biological effects of radiation</topic><topic>Cobalt Radioisotopes</topic><topic>Endothelial cells</topic><topic>Endothelium</topic><topic>Endothelium - enzymology</topic><topic>Endothelium - metabolism</topic><topic>Endothelium - radiation effects</topic><topic>Enzymes</topic><topic>Epoprostenol - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gamma Rays</topic><topic>Ionizing radiations</topic><topic>Irradiation</topic><topic>Lung - enzymology</topic><topic>Lung - metabolism</topic><topic>Lung - radiation effects</topic><topic>Lungs</topic><topic>Male</topic><topic>Peptidyl-Dipeptidase A - metabolism</topic><topic>Plasminogen activators</topic><topic>Plasminogen Activators - metabolism</topic><topic>Radiation damage</topic><topic>Radiation Dosage</topic><topic>Radiation injuries</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Thromboxane A2 - metabolism</topic><topic>Thromboxanes</topic><topic>Tissues, organs and organisms biophysics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ward, William F.</creatorcontrib><creatorcontrib>Hinz, Joann M.</creatorcontrib><creatorcontrib>Molteni, Agostino</creatorcontrib><creatorcontrib>Chung-hsin Ts'ao</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><jtitle>Radiation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ward, William F.</au><au>Hinz, Joann M.</au><au>Molteni, Agostino</au><au>Chung-hsin Ts'ao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Split-Dose Sparing of γ-Ray-Induced Pulmonary Endothelial Dysfunction in Rats</atitle><jtitle>Radiation research</jtitle><addtitle>Radiat Res</addtitle><date>1988-06-01</date><risdate>1988</risdate><volume>114</volume><issue>3</issue><spage>627</spage><epage>633</epage><pages>627-633</pages><issn>0033-7587</issn><eissn>1938-5404</eissn><coden>RAREAE</coden><abstract>The purpose of this study was to determine whether radiation-induced pulmonary endothelial dysfunction exhibits split-dose sparing. Rats were sacrificed 2 months after a range of 60 Co γ-ray doses (0-40 Gy) delivered to the right hemithorax in either a single fraction or in two equal fractions separated by 24 h. Pulmonary angiotensin converting enzyme (ACE) activity, plasminogen activator (PLA) activity, and prostacyclin $({\rm PGI}_{2})$ and thromboxane $({\rm TXA}_{2})$ production served as indices of lung endothelial function. There were dose-dependent decreases in ACE and PLA activity and increases in PGI2 and TXA2 production after both single and split-dose exposures. The $D_{2}-D_{1}$ values determined from the two-fraction minus single-fraction isoeffective doses were 3.9 Gy for ACE activity, 7.2 Gy for PLA activity, 4.8 Gy for PGI2 production, and 4.7 Gy for TXA2 production. Thus these data demonstrate that over the present range of radiation doses approximately 4-7 Gy is repairable as subeffective endothelial damage during the 24-h interval between fractions. These values agree with previously published estimates of split-dose sparing in mouse lung based on lethality and breathing rate assays.</abstract><cop>Oak Brook, Il</cop><pub>Academic Press, Inc</pub><pmid>2836884</pmid><doi>10.2307/3577133</doi><tpages>7</tpages></addata></record> |
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subjects | Animals Biological and medical sciences Biological effects of radiation Cobalt Radioisotopes Endothelial cells Endothelium Endothelium - enzymology Endothelium - metabolism Endothelium - radiation effects Enzymes Epoprostenol - metabolism Fundamental and applied biological sciences. Psychology Gamma Rays Ionizing radiations Irradiation Lung - enzymology Lung - metabolism Lung - radiation effects Lungs Male Peptidyl-Dipeptidase A - metabolism Plasminogen activators Plasminogen Activators - metabolism Radiation damage Radiation Dosage Radiation injuries Rats Rats, Inbred Strains Thromboxane A2 - metabolism Thromboxanes Tissues, organs and organisms biophysics |
title | Split-Dose Sparing of γ-Ray-Induced Pulmonary Endothelial Dysfunction in Rats |
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