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<resource xmlns:xsi='http://www.w3.org/2001/XMLSchema-instance' xmlns='http://datacite.org/schema/kernel-3' xsi:schemaLocation='http://datacite.org/schema/kernel-3 http://schema.datacite.org/meta/kernel-3/metadata.xsd'>
<creators>
<creator>
<creatorName>Ambros, A.G.</creatorName>
<affiliation>Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu“, Moldova, Republica</affiliation>
</creator>
<creator>
<creatorName>Lîsîi, L.T.</creatorName>
<affiliation>Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu“, Moldova, Republica</affiliation>
</creator>
<creator>
<creatorName>Cebotari, I.</creatorName>
<affiliation>Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu“, Moldova, Republica</affiliation>
</creator>
<creator>
<creatorName>Rusu (Teodoru), D.</creatorName>
</creator>
<creator>
<creatorName>Luţcan, C.</creatorName>
</creator>
</creators>
<titles>
<title xml:lang='ro'>Monoxidul de carbon – messager gazos în circulaţia cerebrovasculară
</title>
</titles>
<publisher>Instrumentul Bibliometric National</publisher>
<publicationYear>2010</publicationYear>
<relatedIdentifier relatedIdentifierType='ISSN' relationType='IsPartOf'>1857-1719</relatedIdentifier>
<dates>
<date dateType='Issued'>2010-10-01</date>
</dates>
<resourceType resourceTypeGeneral='Text'>Journal article</resourceType>
<descriptions>
<description xml:lang='en' descriptionType='Abstract'>Carbon monoxide as a gaseous messenger in the cerebrovacular circulation
The primary objectives of this article are to review the potential role of carbon monoxide
(CO) as an endogenous mediator in cerebrovascular circulation. It is produced from heme by a constitutively expressed enzyme (heme oxygenase (HO)-2) expressed highly in the brain and by an inducible enzyme (HO-1). CO production is regulated by controlling substrate availability, HO-2 catalytic activity, and HO-1 expression. CO dilates arterioles by binding to heme that is linked to large conductance Ca2  activated K  channels (BKCa channels), which elevates channel Ca2  sensitivity, increases coupling of Ca2  sparks to BKCa channel openings and, thereby, hyperpolarizes the vascular smooth muscle. In addition to dilating blood vessels, CO can either inhibit or accentuate vascular cell proliferation and apoptosis, depending on conditions.</description>
<description xml:lang='ro' descriptionType='Abstract'>Rolul monoxidului de carbon (CO) ca mediator endogen în circulaţia cerebrovasculară
reprezintă conţinutul acestui articol. Este produs de hem la acţiunea unei enzime constitutive
(hemoxigenaza (HO)-2) expresată intens în creier şi a unei enzime inductibile (hemoxigenaza
(HO)-1). Sinteza CO este reglată prin controlul cantităţii de substrat disponibil, activitatea
catalitică a HO-2 şi expresia HO-1. CO induce dilatarea arteriolelor prin cuplarea cu proteina
hem şi ataşarea acestui complex la canalele BKCa, mărind astfel afinitatea canalelor faţă de ionii de Ca2 . Ulterior are loc cuplarea ionilor la canal şi activarea lor, ceea ce duce la hiperpolarizarea membranei prin transportul ionilor de K  in exteriorul celulei. În afară de acţiunea vasodilatatoare, CO poate inhiba sau induce atît proliferarea, cît şi apoptoza celulelor vasculare, în dependenţă de condiţii.</description>
</descriptions>
<formats>
<format>application/pdf</format>
</formats>
</resource>