【摘要】 目的　探讨静脉应用血管内皮生长因子 (VEGF)是否对急性心肌梗死大鼠有利。方法　 33只成年雄性SD大鼠 ,结扎左冠状动脉后 2 4h随机接受VEGF 肝素 (治疗组 )或肝素 生理盐水 (对照组 )治疗。VEGF(2 μg/ml)加肝素 (5 0U)或肝素 生理盐水 (5 0U/ml)每天经尾静脉注射 ,共用 7d(治疗组n =8;对照组n =10 )和 14d(治疗组n =7;对照组n =8)。于结扎后 9d和 16d分别测定血流动力学参数、心肌梗死面积和侧支微血管的变化。结果　结扎后 9d与对照组比较 ,治疗组有显著高的左室最大收缩 (+ )或舒张 (- )速率 (±dp/dtmax)和微血管计数 ,显著低的左室舒张末压 (LVEDP)和梗死面积。心肌梗死后 16d ,治疗组显著增高平均动脉压 (MAP)、左室收缩压 (LVSP)、±dp/dtmax和微血管计数 ,显著降低LVEDP和梗死面积。VEGF治疗对心率、心脏重量、体重以及心脏重量 /体重比值无显著影响。结论　本研究显示 ,静脉应用VEGF 14d能够明显改善急性心肌梗死大鼠的血流动力学、缩小梗死面积和促进心肌内新血管的形成。更多还原

【Abstract】 Objective To determine whether intravenous administration of vascular endothelial growth factor (VEGF) is beneficial to a rat model of acute myocardial infarction. Methods Thirty-three male Sprague-Dawley rats weighing approximately 290 g were subjected to left coronary artery ligation. Twenty-four hours after surgery, the rats were randomized to receive VEGF 165 -heparin (treated group) or heparin-saline (control group). VEGF 165 (2 μg/ml)with heparin (50 U) or heparin-saline (50 U/ml) was administered daily via the tail vein for 7 days (treated group, n =8;control group, n =10) and 14 days (treated group, n= 7; control group, n= 8). Hemodynamic parameters, infarct size and collateral microvessels were measured at 9 or 16 days after coronary ligation. Results As compared with control animals at 9 days after ligation, VEGF treated rats had a significantly higher maximum rate of left ventricular pressure rise (+dp/dt max ) or fall (±dp/dt max ) and microvessel counts, and lower left ventricular end-diastolic pressure (LVEDP) and infarct size. At 16 days after myocardial infarction, the VEGF treatment apparently increased mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), ±dp/dt max and microvessel counts, and decreased LVEDP and infarct size. VEGF treatment did not affect the heart rate, heart weight, body weight or the ratio of heart weight to body weight. Conclusion The current investigation shows that intravenous administration of VEGF for 14 days is capable of significantly improving hemodynamics, reducing infarct size and promoting myocardial neovascularization in a rat model of acute myocardial infarction.更多还原