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 SM ISO690:2012KOBETS, Valery, TACU, Lilia, COBET, E., ROTARU, Victor, CIOBANU, Lucia, ROTARU, Adrian. Angiotensin 1-7 blunts in vitro induced acute heart failure. In: European Journal of Heart Failure, 2017, vol. 19, supl. nr. 1, p. 597. ISSN 1388-9842. |
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  European Journal of Heart Failure |
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| Volumul 19, Supliment nr. 1 / 2017 / ISSN 1388-9842 /ISSNe 1879-0844 | ||||||
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| Pag. 597-597 | ||||||
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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) – 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– 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 ± 1,3 vs 39,7 ± 2,1 ml/min). Action of Ang 1-7 led to a less decline of CO compared to control (34,8 ± 1,6 vs 29,4 ± 1,3 ml/min, p < 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 ± 1,6 (Ang 1-7) vs 27,4 ± 1,7 (control) mm Hg, p < 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 ± 3,2 vs 55,4 ± 4,4 mm Hg) and reperfusion (17,2 ± 1,4 vs 28,7 ± 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. |
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Cerif XML Export
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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) – 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– 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 ± 1,3 vs 39,7 ± 2,1 ml/min). Action of Ang 1-7 led to a less decline of CO compared to control (34,8 ± 1,6 vs 29,4 ± 1,3 ml/min, p < 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 ± 1,6 (Ang 1-7) vs 27,4 ± 1,7 (control) mm Hg, p < 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 ± 3,2 vs 55,4 ± 4,4 mm Hg) and reperfusion (17,2 ± 1,4 vs 28,7 ± 2,2 mm Hg) periods. 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