Unloading the heart may aid recovery after acute cardiac volume-overload (AVO). We experimentally investigated whether unloading the heart after AVO by heterotopic transplantation histologically impacts myocardial outcome. Thirty-two syngeneic Fisher 344 rats underwent surgery for abdominal arterial-venous fistula to induce AVO. Seven hearts were heterotopically transplanted one day after AVO to simulate a non-working state of the left ventricle (AVO+Tx). In addition, six rats without AVO or surgery (Normal) and five rats with sham surgery (Sham) served as controls. Myocardial outcome was studied using histology and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) analysis for hypoxia inducible factor 1alpha (HIF1α), inducible nitric oxide synthase (iNOS), E-selectin, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), vascular endothelial growth factor alpha (VEGFα), matrix metalloprotease 9 (MMP9), chitinase-3-like protein (YKL-40) and transforming growth factor beta (TGFβ). Relative ischemia of the right ventricle and septal intramyocardial arteries was decreased in AVO+Tx as compared with AVO (0.04±0.01 vs. 0.09±0.02, PSU, P=0.040 and 0.04±0.01 vs. 0.16±0.02, PSU, P=0.008, respectively). Quantitative RT-PCR showed an increase in the expression of iNOS, YKL-40 and VEGFα, and decrease in ANP in AVO+Tx as compared with AVO (5.78±1.23 vs. 2.46±0.81, P=0.039, 22.39±5.22 vs. 10.79±1.70, P=0.039 and 1.15±0.22 vs. 0.60±0.08, P=0.030, and 1.32±0.16 vs. 2.85±0.70, P=0.039, respectively). Unloading the heart by heterotopic transplantation induces early ischemic recovery of intramyocardial arteries after AVO. A non-working state reverses acute ischemic myocardial injury after AVO.
Keywords: Acute volume-overload (AVO); heterotopic rat cardiac transplantation; intramyocardial artery; ischemia.
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