Laboratory of Nutrition and Metabolic Regulation, Institute of Nutrition and Food Technology (INTA), University of Chile, El Líbano, Casilla, Macul, Santiago, Chile.
Cardiovasc Toxicol. 2012 Mar;12(1):64-72. doi: 10.1007/s12012-011-9139-6.
It has been suggested that prenatal exposure to cadmium may alter the cardiovascular function during adulthood. Using the left coronary artery ligation model of acute myocardial infarction, we studied the cardiac function of female adult offspring rats exposed to cadmium (30 ppm) during gestation. The cardiac ischemic zone in the control and cadmium-exposed groups was measured 72 h post-ligation using the TPT staining technique. Offspring from cadmium-treated dams showed a significantly smaller infarcted area compared with the control group (7.1 ± 1.5 vs. 19.6 ± 2.8%, P ≤ 0.05). We also performed echocardiographic and biochemical studies, which positively correlated with the differences observed previously. To evaluate whether the effects were associated to pre-infarct tissue damage and/or angiogenic molecules, we performed histological studies and measured the expression of vascular endothelial growth factor (VEGF), and platelet endothelial cellular adhesion molecule-1 (PECAM-1). Results revealed a higher heart vascularization in the exposed offspring that was associated with an increase in PECAM and a decrease in VEGF expression. We conclude that prenatal exposure to cadmium induces fetal adaptive responses involving changes in the expression of some cardiac angiogenic molecules resulting in long-term resistance to infarction.
有人提出，产前接触镉可能会改变成年后的心血管功能。我们使用左冠状动脉结扎法建立急性心肌梗死模型，研究了妊娠期暴露于镉（30ppm）的雌性成年后代大鼠的心脏功能。结扎后 72 小时，用 TPT 染色技术测量对照组和镉暴露组的心脏缺血区。与对照组相比，来自镉处理母鼠的后代的梗死面积明显较小（7.1±1.5%比 19.6±2.8%，P≤0.05）。我们还进行了超声心动图和生化研究，这些研究与之前观察到的差异呈正相关。为了评估这些影响是否与梗死前组织损伤和/或血管生成分子有关，我们进行了组织学研究，并测量了血管内皮生长因子（VEGF）和血小板内皮细胞黏附分子-1（PECAM-1）的表达。结果表明，暴露组的心脏血管化程度更高，这与 PECAM 的增加和 VEGF 表达的减少有关。我们的结论是，产前接触镉会诱导胎儿产生适应性反应，涉及一些心脏血管生成分子的表达变化，从而导致长期对梗死的抵抗。
