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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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 2000-05, Vol.278 (5), p.H1577-H1584
Hauptverfasser: Okada, Toshiki, Watanabe, Yukinaga, Brusilow, Saul W, Traystman, Richard J, Koehler, Raymond C
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container_end_page H1584
container_issue 5
container_start_page H1577
container_title American journal of physiology. Heart and circulatory physiology
container_volume 278
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
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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. 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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. 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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 &gt;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>
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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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