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<creators>
<creator>
<creatorName>Cobeţ, V.A.</creatorName>
<affiliation>Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu“, Moldova, Republica</affiliation>
</creator>
<creator>
<creatorName>Tacu, L.</creatorName>
<affiliation>Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu“, Moldova, Republica</affiliation>
</creator>
<creator>
<creatorName>Cobet, E.</creatorName>
<affiliation>Universitatea de Stat din Moldova, Moldova, Republica</affiliation>
</creator>
<creator>
<creatorName>Rotaru, V.F.</creatorName>
<affiliation>Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu“, Moldova, Republica</affiliation>
</creator>
<creator>
<creatorName>Ciobanu, L.M.</creatorName>
<affiliation>IMSP Institutul de Cardiologie, Moldova, Republica</affiliation>
</creator>
<creator>
<creatorName>Rotaru, A.</creatorName>
<affiliation>Harvard Medical School, Boston, Statele Unite ale Americii</affiliation>
</creator>
</creators>
<titles>
<title xml:lang='en'>Angiotensin 1-7 blunts in vitro induced acute heart failure</title>
</titles>
<publisher>Instrumentul Bibliometric National</publisher>
<publicationYear>2017</publicationYear>
<relatedIdentifier relatedIdentifierType='ISSN' relationType='IsPartOf'>1388-9842</relatedIdentifier>
<dates>
<date dateType='Issued'>2017-04-01</date>
</dates>
<resourceType resourceTypeGeneral='Text'>Journal article</resourceType>
<descriptions>
<description xml:lang='en' descriptionType='Abstract'><p>Background: Angiotensin 1-7 (Ang 1-7) comprises consistent evidences regarding cardiovascular regulatory benefits due to Ang II receptor AT1 modulation via mass receptor. Aim: Evaluation of the Ang 1-7 cardiac effects in the in vitro induced acute heart failure. Material and methods: Acute heart failure (AHF) was induced using the model of isolated rat pumping heart perfused by Krebs solution without glucose during 20 min according to Neely-Rovetto model (glucose is a single energetic substrate in this model) &ndash; control series. In another series heart has been perfused without glucose, but Ang 1-7 was added till final c oncentration o f 1 0-7 M&ndash; medicated series. Left ventricle (LV) functional parameters were assayed during inotropic stimulation by norepinephrine (NE) and endothelin 1 (ET-1) in concentration of 10-6 M, or ischemia-reperfusion impact (15 min of total ischemia followed by 20 min of reperfusion) reproduced in Langendorff isovolumic isolated heart. Results: Cardiac output (CO) significantly decreased after 20 min perfusion of isolate heart without glucose by 25,9% (29,4 &plusmn; 1,3 vs 39,7 &plusmn; 2,1 ml/min). Action of Ang 1-7 led to a less decline of CO compared to control (34,8 &plusmn; 1,6 vs 29,4 &plusmn; 1,3 ml/min, p &lt; 0,05). NE stimulation induced an increase of control CO by 10,7% associated by LV end-diastolic pressure (LVEDP) elevation of 30,3% while in medicated series response was better: CO increased by 14,4% and LVEDP boosted only by 17,6% ((19,3 &plusmn; 1,6 (Ang 1-7) vs 27,4 &plusmn; 1,7 (control) mm Hg, p &lt; 0,05). Stimulated by ET-1 control isolated heart responded by a negative inotropic effect, and both systolic LV pressure and CO fallen respectively by 13,2% and 9,6%. Ang 1-7 insured a positive inotropic response during ET-1 action leading to CO and LV systolic pressure increase respectively by 10,5% and 11,7%. Ang 1-7 also improved the dynamics of LVEDP during ischemia-reperfusion. Thus, LVEDP was in medicated series significantly less than control index at finish of both ischemia (41,3 &plusmn; 3,2 vs 55,4 &plusmn; 4,4 mm Hg) and reperfusion (17,2 &plusmn; 1,4 vs 28,7 &plusmn; 2,2 mm Hg) periods. Conclusion: Angiotensin 1-7 is a component of renin-angiotensin-aldosterone system which has a benefic action on acutely developing heart failure due to energy privation, manifested by improvement of inotropic response of NE and reinstated positive inotropic of ET-1 action as well as significant diminution of LVEDP during ischemia-reperfusion syndrome.</p></description>
</descriptions>
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