Hemodilution does not alter the coronary vasodilating effects of endogenous or exogenous nitric oxide
Introduction: It is well known that hemoglobin is a scavenger of nitric oxide (NO). The present study used a canine model to test the hypothesis that acute normovolemic hemodilution (ANH) affects NO-mediated coronary vasodilation. Methods: Studies were performed in 18 open-chest, anesthetized dogs....
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creator | Crystal, George J. El-Orbany, Mohammad Zhou, Xiping Salem, M. Ramez Kim, Song-Jung |
description | Introduction:
It is well known that hemoglobin is a scavenger of nitric oxide (NO). The present study used a canine model to test the hypothesis that acute normovolemic hemodilution (ANH) affects NO-mediated coronary vasodilation.
Methods:
Studies were performed in 18 open-chest, anesthetized dogs. In Series 1, the contribution of endogenous NO to coronary vasodilatation during ANH with 5% dextran-40 (reduction in hematocrit by 50%) was assessed. This was accomplished by comparing myocardial blood flow (MBF; radioactive microspheres) in the left anterior descending (LAD) region, which was treated with the NO synthase inhibitor, N
G
-nitro-Larginine methyl ester (L-NAME), to that in the circumflex (control) region. In Series 2, the LAD was perfused via a controlledpressure extracorporeal system with coronary blood flow (CBF) measured with an ultrasonic, transit-time flow transducer. The dose-dependent increases in CBF caused by acetylcholine (ACh), which releases endogenous NO from the vascular endothelium, and sodium nitroprusside (SNP), which provides exogenous NO, were compared before and during ANH.
Results:
Acute normovolemic hemodilution caused similar (approximately twofold) increases in MBF (
P |
doi_str_mv | 10.1007/BF03016670 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_69375702</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>69375702</sourcerecordid><originalsourceid>FETCH-LOGICAL-c414t-fda1f2949c03e45ab5430cdfc5b2b2354f7bd3440cdd1ecd3751bc7e685eb12a3</originalsourceid><addsrcrecordid>eNpt0E2LFDEQBuAgijuuXvwBEgQ9KK2Vz-4-6uK6woIXBW9NOqmMWXqSNUnL-u_NMKMD4ilU8qSqeAl5yuANA-jfvr8EAUzrHu6RDZOj7oaxV_fJBgbBO83g2xl5VMoNAAxaDQ_JGRt0r8WgNgSvcJdcWNYaUqQuYaExVWqWipnW70htyima_Iv-NGUPTQ1xS9F7tLXQ5ClGl7YY09qqTPHuTxFDzcHSdBccPiYPvFkKPjme5-Tr5YcvF1fd9eePny7eXXdWMlk77wzzfJSjBYFSmVlJAdZ5q2Y-c6Gk72cnpGx3jqF1oldstj3qQeHMuBHn5OWh721OP1YsddqFYnFZTMS206TH9qUH3uDzf-BNWnNsu00j55KBEGNDrw7I5lRKRj_d5rBrWUwMpn3y0yn5hp8dO67zDt2JHqNu4MURmGLN4rOJNpS_joNSTA_7qa8PrrSnuMV8Wu0_Y38D5euZ5A</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>922410339</pqid></control><display><type>article</type><title>Hemodilution does not alter the coronary vasodilating effects of endogenous or exogenous nitric oxide</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Crystal, George J. ; El-Orbany, Mohammad ; Zhou, Xiping ; Salem, M. Ramez ; Kim, Song-Jung</creator><creatorcontrib>Crystal, George J. ; El-Orbany, Mohammad ; Zhou, Xiping ; Salem, M. Ramez ; Kim, Song-Jung</creatorcontrib><description>Introduction:
It is well known that hemoglobin is a scavenger of nitric oxide (NO). The present study used a canine model to test the hypothesis that acute normovolemic hemodilution (ANH) affects NO-mediated coronary vasodilation.
Methods:
Studies were performed in 18 open-chest, anesthetized dogs. In Series 1, the contribution of endogenous NO to coronary vasodilatation during ANH with 5% dextran-40 (reduction in hematocrit by 50%) was assessed. This was accomplished by comparing myocardial blood flow (MBF; radioactive microspheres) in the left anterior descending (LAD) region, which was treated with the NO synthase inhibitor, N
G
-nitro-Larginine methyl ester (L-NAME), to that in the circumflex (control) region. In Series 2, the LAD was perfused via a controlledpressure extracorporeal system with coronary blood flow (CBF) measured with an ultrasonic, transit-time flow transducer. The dose-dependent increases in CBF caused by acetylcholine (ACh), which releases endogenous NO from the vascular endothelium, and sodium nitroprusside (SNP), which provides exogenous NO, were compared before and during ANH.
Results:
Acute normovolemic hemodilution caused similar (approximately twofold) increases in MBF (
P
<0.01) in the absence and presence of L-NAME, and it did not affect the dose-related increases in CBF caused by ACh and SNP.
Conclusions:
Series 1: under baseline conditions, hemoglobin in red blood cells does not limit the coronary vasodilatation resulting from tonic release of NO; NO does not mediate coronary vasodilation during ANH. Series 2: ANH does not influence the coronary vasodilating effects of increased levels of NO, whether due to endogenous release (ACh) or infusion of an NO donor (SNP).</description><identifier>ISSN: 0832-610X</identifier><identifier>EISSN: 1496-8975</identifier><identifier>DOI: 10.1007/BF03016670</identifier><identifier>PMID: 18676385</identifier><identifier>CODEN: CJOAEP</identifier><language>eng</language><publisher>New York: Springer-Verlag</publisher><subject>Acetylcholine - pharmacology ; Adenosine - pharmacology ; Anesthesia ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Anesthesiology ; Animals ; Biological and medical sciences ; Blood Gas Analysis ; Blood Pressure - drug effects ; Cardiology ; Circulatory system ; Coronary Vessels - diagnostic imaging ; Coronary Vessels - drug effects ; Critical Care Medicine ; Dogs ; Enzyme Inhibitors - pharmacology ; Female ; Free Radical Scavengers - pharmacology ; Heart Rate - drug effects ; Hemodilution - adverse effects ; Hemodilution - methods ; Intensive ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Models, Animal ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric oxide ; Nitric Oxide - pharmacology ; Nitric Oxide - physiology ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitroprusside - pharmacology ; Pain Medicine ; Pediatrics ; Pneumology/Respiratory System ; Radionuclide Imaging ; Reports Of Original Investigations ; Treatment Outcome ; Vasodilator Agents - pharmacology</subject><ispartof>Canadian journal of anesthesia, 2008-08, Vol.55 (8), p.507-514</ispartof><rights>Canadian Anesthesiologists 2008</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c414t-fda1f2949c03e45ab5430cdfc5b2b2354f7bd3440cdd1ecd3751bc7e685eb12a3</citedby><cites>FETCH-LOGICAL-c414t-fda1f2949c03e45ab5430cdfc5b2b2354f7bd3440cdd1ecd3751bc7e685eb12a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/BF03016670$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/BF03016670$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20551689$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18676385$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Crystal, George J.</creatorcontrib><creatorcontrib>El-Orbany, Mohammad</creatorcontrib><creatorcontrib>Zhou, Xiping</creatorcontrib><creatorcontrib>Salem, M. Ramez</creatorcontrib><creatorcontrib>Kim, Song-Jung</creatorcontrib><title>Hemodilution does not alter the coronary vasodilating effects of endogenous or exogenous nitric oxide</title><title>Canadian journal of anesthesia</title><addtitle>Can J Anesth</addtitle><addtitle>Can J Anaesth</addtitle><description>Introduction:
It is well known that hemoglobin is a scavenger of nitric oxide (NO). The present study used a canine model to test the hypothesis that acute normovolemic hemodilution (ANH) affects NO-mediated coronary vasodilation.
Methods:
Studies were performed in 18 open-chest, anesthetized dogs. In Series 1, the contribution of endogenous NO to coronary vasodilatation during ANH with 5% dextran-40 (reduction in hematocrit by 50%) was assessed. This was accomplished by comparing myocardial blood flow (MBF; radioactive microspheres) in the left anterior descending (LAD) region, which was treated with the NO synthase inhibitor, N
G
-nitro-Larginine methyl ester (L-NAME), to that in the circumflex (control) region. In Series 2, the LAD was perfused via a controlledpressure extracorporeal system with coronary blood flow (CBF) measured with an ultrasonic, transit-time flow transducer. The dose-dependent increases in CBF caused by acetylcholine (ACh), which releases endogenous NO from the vascular endothelium, and sodium nitroprusside (SNP), which provides exogenous NO, were compared before and during ANH.
Results:
Acute normovolemic hemodilution caused similar (approximately twofold) increases in MBF (
P
<0.01) in the absence and presence of L-NAME, and it did not affect the dose-related increases in CBF caused by ACh and SNP.
Conclusions:
Series 1: under baseline conditions, hemoglobin in red blood cells does not limit the coronary vasodilatation resulting from tonic release of NO; NO does not mediate coronary vasodilation during ANH. Series 2: ANH does not influence the coronary vasodilating effects of increased levels of NO, whether due to endogenous release (ACh) or infusion of an NO donor (SNP).</description><subject>Acetylcholine - pharmacology</subject><subject>Adenosine - pharmacology</subject><subject>Anesthesia</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Anesthesiology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Gas Analysis</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiology</subject><subject>Circulatory system</subject><subject>Coronary Vessels - diagnostic imaging</subject><subject>Coronary Vessels - drug effects</subject><subject>Critical Care Medicine</subject><subject>Dogs</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Female</subject><subject>Free Radical Scavengers - pharmacology</subject><subject>Heart Rate - drug effects</subject><subject>Hemodilution - adverse effects</subject><subject>Hemodilution - methods</subject><subject>Intensive</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Models, Animal</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - pharmacology</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitroprusside - pharmacology</subject><subject>Pain Medicine</subject><subject>Pediatrics</subject><subject>Pneumology/Respiratory System</subject><subject>Radionuclide Imaging</subject><subject>Reports Of Original Investigations</subject><subject>Treatment Outcome</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0832-610X</issn><issn>1496-8975</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNpt0E2LFDEQBuAgijuuXvwBEgQ9KK2Vz-4-6uK6woIXBW9NOqmMWXqSNUnL-u_NMKMD4ilU8qSqeAl5yuANA-jfvr8EAUzrHu6RDZOj7oaxV_fJBgbBO83g2xl5VMoNAAxaDQ_JGRt0r8WgNgSvcJdcWNYaUqQuYaExVWqWipnW70htyima_Iv-NGUPTQ1xS9F7tLXQ5ClGl7YY09qqTPHuTxFDzcHSdBccPiYPvFkKPjme5-Tr5YcvF1fd9eePny7eXXdWMlk77wzzfJSjBYFSmVlJAdZ5q2Y-c6Gk72cnpGx3jqF1oldstj3qQeHMuBHn5OWh721OP1YsddqFYnFZTMS206TH9qUH3uDzf-BNWnNsu00j55KBEGNDrw7I5lRKRj_d5rBrWUwMpn3y0yn5hp8dO67zDt2JHqNu4MURmGLN4rOJNpS_joNSTA_7qa8PrrSnuMV8Wu0_Y38D5euZ5A</recordid><startdate>20080801</startdate><enddate>20080801</enddate><creator>Crystal, George J.</creator><creator>El-Orbany, Mohammad</creator><creator>Zhou, Xiping</creator><creator>Salem, M. Ramez</creator><creator>Kim, Song-Jung</creator><general>Springer-Verlag</general><general>Canadian Anesthesiologists' Society</general><general>Springer Nature B.V</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8FQ</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20080801</creationdate><title>Hemodilution does not alter the coronary vasodilating effects of endogenous or exogenous nitric oxide</title><author>Crystal, George J. ; El-Orbany, Mohammad ; Zhou, Xiping ; Salem, M. Ramez ; Kim, Song-Jung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c414t-fda1f2949c03e45ab5430cdfc5b2b2354f7bd3440cdd1ecd3751bc7e685eb12a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Adenosine - pharmacology</topic><topic>Anesthesia</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Anesthesiology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Gas Analysis</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiology</topic><topic>Circulatory system</topic><topic>Coronary Vessels - diagnostic imaging</topic><topic>Coronary Vessels - drug effects</topic><topic>Critical Care Medicine</topic><topic>Dogs</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Female</topic><topic>Free Radical Scavengers - pharmacology</topic><topic>Heart Rate - drug effects</topic><topic>Hemodilution - adverse effects</topic><topic>Hemodilution - methods</topic><topic>Intensive</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Models, Animal</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - pharmacology</topic><topic>Nitric Oxide - physiology</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitroprusside - pharmacology</topic><topic>Pain Medicine</topic><topic>Pediatrics</topic><topic>Pneumology/Respiratory System</topic><topic>Radionuclide Imaging</topic><topic>Reports Of Original Investigations</topic><topic>Treatment Outcome</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Crystal, George J.</creatorcontrib><creatorcontrib>El-Orbany, Mohammad</creatorcontrib><creatorcontrib>Zhou, Xiping</creatorcontrib><creatorcontrib>Salem, M. Ramez</creatorcontrib><creatorcontrib>Kim, Song-Jung</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>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Canadian Business & Current Affairs Database</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Canadian journal of anesthesia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Crystal, George J.</au><au>El-Orbany, Mohammad</au><au>Zhou, Xiping</au><au>Salem, M. Ramez</au><au>Kim, Song-Jung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hemodilution does not alter the coronary vasodilating effects of endogenous or exogenous nitric oxide</atitle><jtitle>Canadian journal of anesthesia</jtitle><stitle>Can J Anesth</stitle><addtitle>Can J Anaesth</addtitle><date>2008-08-01</date><risdate>2008</risdate><volume>55</volume><issue>8</issue><spage>507</spage><epage>514</epage><pages>507-514</pages><issn>0832-610X</issn><eissn>1496-8975</eissn><coden>CJOAEP</coden><abstract>Introduction:
It is well known that hemoglobin is a scavenger of nitric oxide (NO). The present study used a canine model to test the hypothesis that acute normovolemic hemodilution (ANH) affects NO-mediated coronary vasodilation.
Methods:
Studies were performed in 18 open-chest, anesthetized dogs. In Series 1, the contribution of endogenous NO to coronary vasodilatation during ANH with 5% dextran-40 (reduction in hematocrit by 50%) was assessed. This was accomplished by comparing myocardial blood flow (MBF; radioactive microspheres) in the left anterior descending (LAD) region, which was treated with the NO synthase inhibitor, N
G
-nitro-Larginine methyl ester (L-NAME), to that in the circumflex (control) region. In Series 2, the LAD was perfused via a controlledpressure extracorporeal system with coronary blood flow (CBF) measured with an ultrasonic, transit-time flow transducer. The dose-dependent increases in CBF caused by acetylcholine (ACh), which releases endogenous NO from the vascular endothelium, and sodium nitroprusside (SNP), which provides exogenous NO, were compared before and during ANH.
Results:
Acute normovolemic hemodilution caused similar (approximately twofold) increases in MBF (
P
<0.01) in the absence and presence of L-NAME, and it did not affect the dose-related increases in CBF caused by ACh and SNP.
Conclusions:
Series 1: under baseline conditions, hemoglobin in red blood cells does not limit the coronary vasodilatation resulting from tonic release of NO; NO does not mediate coronary vasodilation during ANH. Series 2: ANH does not influence the coronary vasodilating effects of increased levels of NO, whether due to endogenous release (ACh) or infusion of an NO donor (SNP).</abstract><cop>New York</cop><pub>Springer-Verlag</pub><pmid>18676385</pmid><doi>10.1007/BF03016670</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acetylcholine - pharmacology Adenosine - pharmacology Anesthesia Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Anesthesiology Animals Biological and medical sciences Blood Gas Analysis Blood Pressure - drug effects Cardiology Circulatory system Coronary Vessels - diagnostic imaging Coronary Vessels - drug effects Critical Care Medicine Dogs Enzyme Inhibitors - pharmacology Female Free Radical Scavengers - pharmacology Heart Rate - drug effects Hemodilution - adverse effects Hemodilution - methods Intensive Male Medical sciences Medicine Medicine & Public Health Models, Animal NG-Nitroarginine Methyl Ester - pharmacology Nitric oxide Nitric Oxide - pharmacology Nitric Oxide - physiology Nitric Oxide Synthase - antagonists & inhibitors Nitroprusside - pharmacology Pain Medicine Pediatrics Pneumology/Respiratory System Radionuclide Imaging Reports Of Original Investigations Treatment Outcome Vasodilator Agents - pharmacology |
title | Hemodilution does not alter the coronary vasodilating effects of endogenous or exogenous nitric oxide |
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