Interaction of glutamine and arginine on cerebrovascular reactivity to hypercapnia
Department of Anesthesiology and Critical Care Medicine and Department of Pediatrics, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205 Glutamine is purported to inhibit recycling of citrulline to arginine and to limit nitric oxide release in vitro. However, vasoactive effects of glutami...
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container_title | American journal of physiology. Heart and circulatory physiology |
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creator | Okada, Toshiki Watanabe, Yukinaga Brusilow, Saul W Traystman, Richard J Koehler, Raymond C |
description | Department of Anesthesiology and Critical Care Medicine and
Department of Pediatrics, Johns Hopkins Medical Institutions,
Baltimore, Maryland 21205
Glutamine is
purported to inhibit recycling of citrulline to arginine and to limit
nitric oxide release in vitro. However, vasoactive effects of glutamine
have not been clearly demonstrated in vivo. During hyperammonemia,
impaired cerebrovascular reactivity to CO 2 is related to
glutamine accumulation. We tested the hypotheses that 1 )
glutamine infusion in the absence of hyperammonemia impairs cerebrovascular CO 2 reactivity and 2 ) arginine
infusion preserves CO 2 reactivity during glutamine infusion
and during hyperammonemia. Pentobarbital sodium-anesthetized rats were
equipped with a closed cranial window for measuring pial arteriolar
diameter. Intravenous infusion of 3 mmol · kg 1 · h 1
of L -glutamine for 6 h produced threefold increases in
plasma and cerebrospinal fluid concentrations. Dilation to hypercapnia was reduced by 45% compared with that of a time control group at 6 h
but not at 3 h of glutamine infusion. Coinfusion of 2 mmol · kg 1 · h 1
of L -arginine with glutamine maintained the hypercapnic
vasodilation at the control value. Infusion of ammonium acetate at a
rate known to produce threefold increases in cortical tissue glutamine
concentration resulted in no significant hypercapnic vasodilation.
Coinfusion of arginine with ammonium acetate maintained hypercapnic
vasodilation at 60% of the control value. Arginine infusion did not
augment hypercapnic vasodilation in a control group. We conclude that glutamine modulates cerebrovascular CO 2 reactivity in vivo.
Glutamine probably acts by limiting arginine availability because the
vascular inhibitory effect required >3 h to develop and because
arginine infusion counteracted the vascular effect of both endogenously and exogenously produced increases in glutamine.
ammonia; carbon dioxide; cerebral blood vessels; nitric oxide; rat |
doi_str_mv | 10.1152/ajpheart.2000.278.5.h1577 |
format | Article |
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Department of Pediatrics, Johns Hopkins Medical Institutions,
Baltimore, Maryland 21205
Glutamine is
purported to inhibit recycling of citrulline to arginine and to limit
nitric oxide release in vitro. However, vasoactive effects of glutamine
have not been clearly demonstrated in vivo. During hyperammonemia,
impaired cerebrovascular reactivity to CO 2 is related to
glutamine accumulation. We tested the hypotheses that 1 )
glutamine infusion in the absence of hyperammonemia impairs cerebrovascular CO 2 reactivity and 2 ) arginine
infusion preserves CO 2 reactivity during glutamine infusion
and during hyperammonemia. Pentobarbital sodium-anesthetized rats were
equipped with a closed cranial window for measuring pial arteriolar
diameter. Intravenous infusion of 3 mmol · kg 1 · h 1
of L -glutamine for 6 h produced threefold increases in
plasma and cerebrospinal fluid concentrations. Dilation to hypercapnia was reduced by 45% compared with that of a time control group at 6 h
but not at 3 h of glutamine infusion. Coinfusion of 2 mmol · kg 1 · h 1
of L -arginine with glutamine maintained the hypercapnic
vasodilation at the control value. Infusion of ammonium acetate at a
rate known to produce threefold increases in cortical tissue glutamine
concentration resulted in no significant hypercapnic vasodilation.
Coinfusion of arginine with ammonium acetate maintained hypercapnic
vasodilation at 60% of the control value. Arginine infusion did not
augment hypercapnic vasodilation in a control group. We conclude that glutamine modulates cerebrovascular CO 2 reactivity in vivo.
Glutamine probably acts by limiting arginine availability because the
vascular inhibitory effect required >3 h to develop and because
arginine infusion counteracted the vascular effect of both endogenously and exogenously produced increases in glutamine.
ammonia; carbon dioxide; cerebral blood vessels; nitric oxide; rat</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.2000.278.5.h1577</identifier><identifier>PMID: 10775136</identifier><language>eng</language><publisher>United States</publisher><subject>Acetates - administration & dosage ; Ammonia - blood ; Analysis of Variance ; Animals ; Arginine - administration & dosage ; Arginine - metabolism ; Arterioles - drug effects ; Blood Pressure - drug effects ; Carbon Dioxide - metabolism ; Cerebrovascular Circulation - drug effects ; Cerebrovascular Circulation - physiology ; Drug Synergism ; Glutamic Acid - blood ; Glutamic Acid - cerebrospinal fluid ; Glutamine - administration & dosage ; Glutamine - blood ; Glutamine - cerebrospinal fluid ; Glutamine - metabolism ; Hypercapnia - blood ; Hypercapnia - metabolism ; Infusions, Intravenous ; Male ; Pia Mater - blood supply ; Pia Mater - drug effects ; Rats ; Rats, Wistar ; Sodium Acetate - administration & dosage</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2000-05, Vol.278 (5), p.H1577-H1584</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-9ba7e89640b5f7d6d3303e6d44557eaa4128924f0167c895109daf27966997eb3</citedby><cites>FETCH-LOGICAL-c405t-9ba7e89640b5f7d6d3303e6d44557eaa4128924f0167c895109daf27966997eb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3026,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10775136$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Okada, Toshiki</creatorcontrib><creatorcontrib>Watanabe, Yukinaga</creatorcontrib><creatorcontrib>Brusilow, Saul W</creatorcontrib><creatorcontrib>Traystman, Richard J</creatorcontrib><creatorcontrib>Koehler, Raymond C</creatorcontrib><title>Interaction of glutamine and arginine on cerebrovascular reactivity to hypercapnia</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>Department of Anesthesiology and Critical Care Medicine and
Department of Pediatrics, Johns Hopkins Medical Institutions,
Baltimore, Maryland 21205
Glutamine is
purported to inhibit recycling of citrulline to arginine and to limit
nitric oxide release in vitro. However, vasoactive effects of glutamine
have not been clearly demonstrated in vivo. During hyperammonemia,
impaired cerebrovascular reactivity to CO 2 is related to
glutamine accumulation. We tested the hypotheses that 1 )
glutamine infusion in the absence of hyperammonemia impairs cerebrovascular CO 2 reactivity and 2 ) arginine
infusion preserves CO 2 reactivity during glutamine infusion
and during hyperammonemia. Pentobarbital sodium-anesthetized rats were
equipped with a closed cranial window for measuring pial arteriolar
diameter. Intravenous infusion of 3 mmol · kg 1 · h 1
of L -glutamine for 6 h produced threefold increases in
plasma and cerebrospinal fluid concentrations. Dilation to hypercapnia was reduced by 45% compared with that of a time control group at 6 h
but not at 3 h of glutamine infusion. Coinfusion of 2 mmol · kg 1 · h 1
of L -arginine with glutamine maintained the hypercapnic
vasodilation at the control value. Infusion of ammonium acetate at a
rate known to produce threefold increases in cortical tissue glutamine
concentration resulted in no significant hypercapnic vasodilation.
Coinfusion of arginine with ammonium acetate maintained hypercapnic
vasodilation at 60% of the control value. Arginine infusion did not
augment hypercapnic vasodilation in a control group. We conclude that glutamine modulates cerebrovascular CO 2 reactivity in vivo.
Glutamine probably acts by limiting arginine availability because the
vascular inhibitory effect required >3 h to develop and because
arginine infusion counteracted the vascular effect of both endogenously and exogenously produced increases in glutamine.
ammonia; carbon dioxide; cerebral blood vessels; nitric oxide; rat</description><subject>Acetates - administration & dosage</subject><subject>Ammonia - blood</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Arginine - administration & dosage</subject><subject>Arginine - metabolism</subject><subject>Arterioles - drug effects</subject><subject>Blood Pressure - drug effects</subject><subject>Carbon Dioxide - metabolism</subject><subject>Cerebrovascular Circulation - drug effects</subject><subject>Cerebrovascular Circulation - physiology</subject><subject>Drug Synergism</subject><subject>Glutamic Acid - blood</subject><subject>Glutamic Acid - cerebrospinal fluid</subject><subject>Glutamine - administration & dosage</subject><subject>Glutamine - blood</subject><subject>Glutamine - cerebrospinal fluid</subject><subject>Glutamine - metabolism</subject><subject>Hypercapnia - blood</subject><subject>Hypercapnia - metabolism</subject><subject>Infusions, Intravenous</subject><subject>Male</subject><subject>Pia Mater - blood supply</subject><subject>Pia Mater - drug effects</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Sodium Acetate - administration & dosage</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kNFOgzAUhhujcXP6CgYfANZS2tJ4ZRbnliwxMfO6KXCALgxIgSlvLwQ188Krk5P___6LD6EHgj1CmL_UhzoHbVvPxxh7vgg95uWECXGB5kPuu4RReYnmmHLqckLZDN00zWEoM8HpNZoRLAQjlM_R27Zsweq4NVXpVKmTFV2rj6YER5eJo21myvEZwhgsRLY66SbuCm0dCyN1Mm3vtJWT9zXYWNel0bfoKtVFA3ffd4He18_71cbdvb5sV087Nw4wa10ZaQGh5AGOWCoSnlCKKfAkCBgToHVA_FD6QYoJF3EoGcEy0akvJOdSCojoAslpN7ZV01hIVW3NUdteEaxGT-rHkxo9qcGTYmozehrY-4mtu-gIyRk5iRkKy6mQmyz_MBZUnfeNqYoq6892_0w-_k-su6LYw2f7i56Rqk5S-gV00I5c</recordid><startdate>20000501</startdate><enddate>20000501</enddate><creator>Okada, Toshiki</creator><creator>Watanabe, Yukinaga</creator><creator>Brusilow, Saul W</creator><creator>Traystman, Richard J</creator><creator>Koehler, Raymond C</creator><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>20000501</creationdate><title>Interaction of glutamine and arginine on cerebrovascular reactivity to hypercapnia</title><author>Okada, Toshiki ; Watanabe, Yukinaga ; Brusilow, Saul W ; Traystman, Richard J ; Koehler, Raymond C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-9ba7e89640b5f7d6d3303e6d44557eaa4128924f0167c895109daf27966997eb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Acetates - administration & dosage</topic><topic>Ammonia - blood</topic><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Arginine - administration & dosage</topic><topic>Arginine - metabolism</topic><topic>Arterioles - drug effects</topic><topic>Blood Pressure - drug effects</topic><topic>Carbon Dioxide - metabolism</topic><topic>Cerebrovascular Circulation - drug effects</topic><topic>Cerebrovascular Circulation - physiology</topic><topic>Drug Synergism</topic><topic>Glutamic Acid - blood</topic><topic>Glutamic Acid - cerebrospinal fluid</topic><topic>Glutamine - administration & dosage</topic><topic>Glutamine - blood</topic><topic>Glutamine - cerebrospinal fluid</topic><topic>Glutamine - metabolism</topic><topic>Hypercapnia - blood</topic><topic>Hypercapnia - metabolism</topic><topic>Infusions, Intravenous</topic><topic>Male</topic><topic>Pia Mater - blood supply</topic><topic>Pia Mater - drug effects</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Sodium Acetate - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Okada, Toshiki</creatorcontrib><creatorcontrib>Watanabe, Yukinaga</creatorcontrib><creatorcontrib>Brusilow, Saul W</creatorcontrib><creatorcontrib>Traystman, Richard J</creatorcontrib><creatorcontrib>Koehler, Raymond C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Okada, Toshiki</au><au>Watanabe, Yukinaga</au><au>Brusilow, Saul W</au><au>Traystman, Richard J</au><au>Koehler, Raymond C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interaction of glutamine and arginine on cerebrovascular reactivity to hypercapnia</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2000-05-01</date><risdate>2000</risdate><volume>278</volume><issue>5</issue><spage>H1577</spage><epage>H1584</epage><pages>H1577-H1584</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>Department of Anesthesiology and Critical Care Medicine and
Department of Pediatrics, Johns Hopkins Medical Institutions,
Baltimore, Maryland 21205
Glutamine is
purported to inhibit recycling of citrulline to arginine and to limit
nitric oxide release in vitro. However, vasoactive effects of glutamine
have not been clearly demonstrated in vivo. During hyperammonemia,
impaired cerebrovascular reactivity to CO 2 is related to
glutamine accumulation. We tested the hypotheses that 1 )
glutamine infusion in the absence of hyperammonemia impairs cerebrovascular CO 2 reactivity and 2 ) arginine
infusion preserves CO 2 reactivity during glutamine infusion
and during hyperammonemia. Pentobarbital sodium-anesthetized rats were
equipped with a closed cranial window for measuring pial arteriolar
diameter. Intravenous infusion of 3 mmol · kg 1 · h 1
of L -glutamine for 6 h produced threefold increases in
plasma and cerebrospinal fluid concentrations. Dilation to hypercapnia was reduced by 45% compared with that of a time control group at 6 h
but not at 3 h of glutamine infusion. Coinfusion of 2 mmol · kg 1 · h 1
of L -arginine with glutamine maintained the hypercapnic
vasodilation at the control value. Infusion of ammonium acetate at a
rate known to produce threefold increases in cortical tissue glutamine
concentration resulted in no significant hypercapnic vasodilation.
Coinfusion of arginine with ammonium acetate maintained hypercapnic
vasodilation at 60% of the control value. Arginine infusion did not
augment hypercapnic vasodilation in a control group. We conclude that glutamine modulates cerebrovascular CO 2 reactivity in vivo.
Glutamine probably acts by limiting arginine availability because the
vascular inhibitory effect required >3 h to develop and because
arginine infusion counteracted the vascular effect of both endogenously and exogenously produced increases in glutamine.
ammonia; carbon dioxide; cerebral blood vessels; nitric oxide; rat</abstract><cop>United States</cop><pmid>10775136</pmid><doi>10.1152/ajpheart.2000.278.5.h1577</doi></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0363-6135 |
ispartof | American journal of physiology. Heart and circulatory physiology, 2000-05, Vol.278 (5), p.H1577-H1584 |
issn | 0363-6135 1522-1539 |
language | eng |
recordid | cdi_pubmed_primary_10775136 |
source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
subjects | Acetates - administration & dosage Ammonia - blood Analysis of Variance Animals Arginine - administration & dosage Arginine - metabolism Arterioles - drug effects Blood Pressure - drug effects Carbon Dioxide - metabolism Cerebrovascular Circulation - drug effects Cerebrovascular Circulation - physiology Drug Synergism Glutamic Acid - blood Glutamic Acid - cerebrospinal fluid Glutamine - administration & dosage Glutamine - blood Glutamine - cerebrospinal fluid Glutamine - metabolism Hypercapnia - blood Hypercapnia - metabolism Infusions, Intravenous Male Pia Mater - blood supply Pia Mater - drug effects Rats Rats, Wistar Sodium Acetate - administration & dosage |
title | Interaction of glutamine and arginine on cerebrovascular reactivity to hypercapnia |
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