实验性急性心脏容量过载后组织学改变的早期可逆性。

IF 1.3
American journal of cardiovascular disease Pub Date : 2022-08-15 eCollection Date: 2022-01-01
Christa Huuskonen, Mari Hämäläinen, Nooa Kivikangas, Timo Paavonen, Eeva Moilanen, Ari A Mennander
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引用次数: 0

摘要

卸载心脏可能有助于急性心脏容量过载(AVO)后的恢复。我们通过实验研究了异位心脏移植对AVO术后心肌预后的组织学影响。32只同基因Fisher 344大鼠腹腔动静脉瘘手术诱导AVO。7颗心脏在AVO术后1天异位移植,模拟左心室非工作状态(AVO+Tx)。另外,6只未做AVO或手术的大鼠(Normal)和5只做假手术的大鼠(sham)作为对照。采用组织学和定量反转录聚合酶链反应(qRT-PCR)分析缺氧诱导因子1α (HIF1α)、诱导型一氧化氮合酶(iNOS)、e-选择素、房利钠肽(ANP)、脑利钠肽(BNP)、血管内皮生长因子α (VEGFα)、基质金属蛋白酶9 (MMP9)、几丁质酶3样蛋白(YKL-40)和转化生长因子β (TGFβ)。与AVO组相比,AVO+Tx组右心室和心间隔动脉相对缺血减少(分别为0.04±0.01比0.09±0.02,PSU, P=0.040和0.04±0.01比0.16±0.02,PSU, P=0.008)。定量RT-PCR结果显示,与AVO组相比,AVO+Tx组iNOS、YKL-40和VEGFα表达增加(5.78±1.23比2.46±0.81,P=0.039; 22.39±5.22比10.79±1.70,P=0.039; 1.15±0.22比0.60±0.08,P=0.030; 1.32±0.16比2.85±0.70,P=0.039)。异位移植卸载心脏可诱导AVO术后心肌内动脉早期缺血恢复。非工作状态可逆转AVO后急性缺血性心肌损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Early reversibility of histological changes after experimental acute cardiac volume-overload.

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.

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来源期刊
American journal of cardiovascular disease
American journal of cardiovascular disease CARDIAC & CARDIOVASCULAR SYSTEMS-
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