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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0007818,
umls-concept:C0028128,
umls-concept:C0068821,
umls-concept:C0332206,
umls-concept:C0373440,
umls-concept:C0392747,
umls-concept:C0428714,
umls-concept:C0443172,
umls-concept:C0596253,
umls-concept:C0871261,
umls-concept:C1280500,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2911692
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pubmed:issue |
6
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pubmed:dateCreated |
1992-11-25
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pubmed:abstractText |
The importance of nitric oxide (NO) for CBF variations associated with arterial carbon dioxide changes was investigated in halothane-anesthetized rats by using an inhibitor of nitric oxide synthase, NG-nitro-L-arginine (NOLAG). CBF was measured by intracarotid injection of 133Xe. In normocapnia, intracarotid infusion of 1.5, or 7.5, or 30 mg/kg NOLAG induced a dose-dependent increase of arterial blood pressure and a decrease of normocapnic CBF from 85 +/- 10 to 78 +/- 6, 64 +/- 5, and 52 +/- 5 ml 100 g-1 min-1, respectively. This effect lasted for at least 2 h. Raising PaCO2 from a control level of 40 to 68 mm Hg increased CBF to 230 +/- 27 ml 100 g-1 min-1, corresponding to a percentage CBF response (CO2 reactivity) of 3.7 +/- 0.6%/mm Hg PaCO2 in saline-treated rats. NOLAG attenuated this reactivity by 32, 49, and 51% at the three-dose levels. Hypercapnia combined with angiotensin to raise blood pressure to the same level as the highest dose of NOLAG did not affect the CBF response to hypercapnia. L-Arginine significantly prevented the effect of NOLAG on normocapnic CBF as well as blood pressure and also abolished its inhibitory effect on hypercapnic CBF. D-Arginine had no such effect. Decreasing PaCO2 to 20 mm Hg reduced control CBF to 46 +/- 3 ml 100 g-1 min-1 with no further reduction after NOLAG. Furthermore, NOLAG did not change the percentage CBF response to an extracellular acidosis induced by acetazolamide (50 mg/kg).(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0271-678X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
947-53
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1400648-Animals,
pubmed-meshheading:1400648-Arginine,
pubmed-meshheading:1400648-Blood Pressure,
pubmed-meshheading:1400648-Blood-Brain Barrier,
pubmed-meshheading:1400648-Carbon Dioxide,
pubmed-meshheading:1400648-Cerebrovascular Circulation,
pubmed-meshheading:1400648-Dose-Response Relationship, Drug,
pubmed-meshheading:1400648-Hypercapnia,
pubmed-meshheading:1400648-Hypocapnia,
pubmed-meshheading:1400648-Male,
pubmed-meshheading:1400648-Nitric Oxide,
pubmed-meshheading:1400648-Nitroarginine,
pubmed-meshheading:1400648-Rats,
pubmed-meshheading:1400648-Rats, Wistar
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pubmed:year |
1992
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pubmed:articleTitle |
Effect of nitric oxide blockade by NG-nitro-L-arginine on cerebral blood flow response to changes in carbon dioxide tension.
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pubmed:affiliation |
Department of Clinical Physiology/Nuclear Medicine, Bispebjerg Hospital, Copenhagen, Denmark.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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