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首页> 外文期刊>American Journal of Physiology >Myocardial vascular and metabolic adaptations in chronically anemic fetal sheep.
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Myocardial vascular and metabolic adaptations in chronically anemic fetal sheep.

机译：慢性贫血胎羊的心肌血管和代谢适应。

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Little is known about the vascular and metabolic adaptations that take place in the fetal heart to maintain cardiac function in response to increased load. Chronic fetal anemia has previously been shown to result in increased ventricular mass, increased myocardial vascularization, and increased myocardial expression of hypoxia-inducible factor-1 (HIF-1) and vascular endothelial growth factor (VEGF). We therefore sought to determine whether chronic fetal anemia induces expression of HIF-1-regulated angiogenic factors and glycolytic enzymes in the fetal myocardium. Anemia was produced in chronically instrumented fetal sheep by daily isovolemic hemorrhage (80-100 ml) for either 3 (n = 4) or 7 days (n 11) beginning at 134 days of gestation (term 145 days). Catheterized, nonbled twins served as controls. Isovolemic hemorrhage over 7 days resulted in decreased fetal hematocrit (37 +/- 1 to 20 +/- 1%) and arterial oxygen content (6.5 +/- 0.4 to 2.8 +/- 0.2 ml O2/dl). Myocardial blood flow and vascularization were significantly increased after 7 days of anemia. Myocardial HIF-1 protein expression and VEGF (left ventricular), VEGF receptor-1 (right ventricular), and VEGF receptor-2 (right ventricular, left ventricular) mRNA levels were elevated (P < 0.05) in 7-day anemic compared with control animals. Myocardial expressions of the glycolytic enzymes aldolase, lactate dehydrogenase A, phosphofructokinase (liver), and phosphoglycerol kinase were also significantly elevated after 7 days of anemia. Despite the absence of a significant increase in myocardial HIF-1alpha protein in 3-day anemic fetuses, expressions of VEGF, VEGF receptor-1, and the glycolytic enzymes were greater in 3-day compared with 7-day anemic animals. These data suggest that HIF-1 likely participates in the fetal myocardial response to anemia by coordinating an increase in gene expressions that promote capillary growth and anaerobic metabolism. However, factors other than HIF-1 also appear important in the regulation of these genes. We speculate that the return of mRNA levels of angiogenic and glycolytic enzymes toward control levels in the 7-day anemic fetus is explained by a significantly increased resting myocardial blood flow, resulting from coronary vascular growth and increased coronary conductance, and a return to a state of adequate oxygen and nutrient delivery, obviating the need for enhanced transcription of genes encoding angiogenic and glycolytic enzymes.
机译：人们对胎儿心脏中发生的血管和代谢适应机制知之甚少，以适应负荷增加而维持心脏功能。先前已证明，慢性胎儿贫血会导致心室质量增加，心肌血管生成增加以及缺氧诱导因子1（HIF-1）和血管内皮生长因子（VEGF）的心肌表达增加。因此，我们寻求确定慢性胎儿贫血是否诱导胎儿心肌中HIF-1调节的血管生成因子和糖酵解酶的表达。在妊娠134天（足月145天）开始的每天3次（n = 4）或7天（n 11）的每日等容性出血（80-100 ml），会在慢性仪器化的胎羊中产生贫血。导尿管未出血双胞胎作为对照。 7天的等容性出血导致胎儿血细胞比容降低（37 +/- 1至20 +/- 1％）和动脉血氧含量（6.5 +/- 0.4至2.8 +/- 0.2 ml O2 / dl）。贫血7天后，心肌血流量和血管生成显着增加。与第7天贫血相比，心肌HIF-1蛋白表达和VEGF（左心室），VEGF受体1（右心室）和VEGF受体2（右心室，左心室）mRNA水平升高（P <0.05）。控制动物。贫血7天后，糖酵解酶醛缩酶，乳酸脱氢酶A，磷酸果糖激酶（肝）和磷酸甘油激酶的心肌表达也显着升高。尽管在3天贫血的胎儿中心肌HIF-1α蛋白没有显着增加，但与7天贫血动物相比，在3天中VEGF，VEGF受体-1和糖酵解酶的表达更高。这些数据表明，HIF-1可能通过协调促进毛细血管生长和厌氧代谢的基因表达的增加来参与胎儿对贫血的心肌反应。但是，HIF-1以外的因素在这些基因的调节中也很重要。我们推测在7天贫血胎儿中，血管生成酶和糖酵解酶的mRNA水平向控制水平的返回是由冠状动脉血管生长和冠状动脉电导率增加导致的静息心肌血流量显着增加所解释的足够的氧气和养分输送，因此无需增强编码血管生成和糖酵解酶的基因的转录。

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