Maczewski Michał, Mackiewicz Urszula
Department of Clinical Physiology, Medical Center of Postgraduate Education, Marymoncka 99, 01-813 Warsaw, Poland.
Cardiovasc Pathol. 2007 Mar-Apr;16(2):79-84. doi: 10.1016/j.carpath.2006.11.003. Epub 2006 Dec 18.
Brain natriuretic peptide is a marker of the severity of congestive heart failure. However, the relation between its concentration and ventricular remodeling after myocardial infarction remains unknown. Thus, we studied plasma brain natriuretic peptide over 6 months after myocardial infarction in the rat and correlated it with parameters of left ventricular remodeling.
Myocardial infarction was induced in 152 male Wistar rats by left coronary artery ligation. Rats were followed up for 1 week, 1 month, 3 months, or 6 months after myocardial infarction. Then left ventricular end-diastolic volume and maximal systolic pressure were assessed in the isolated heart, heart and lung weights were obtained, wall stress was calculated, cardiomyocyte size was measured, and plasma brain natriuretic peptide was assessed with enzyme-linked immunosorbent assay.
Large (> or =40%) but not small/intermediate infarcts were accompanied by progressive ventricular dilation and increase in wall stress, left ventricular weight, and lung weight, while systolic pressure, which was already depressed 1 week after myocardial infarction, did not show progression over time. Plasma brain natriuretic peptide reached its peak on Day 3 after myocardial infarction and did not progress any further; it correlated with infarct size and the extent of left ventricular dilation.
Thus, after a large myocardial infarction in the rat, despite progressive left ventricular dilation and increase in wall stress, plasma brain natriuretic peptide did not progress over time. This indicates that, although plasma brain natriuretic peptide is a good indicator of infarct size and left ventricular dilation, it cannot be used to trace progressive ventricular remodeling in the rat heart after myocardial infarction.
脑钠肽是充血性心力衰竭严重程度的标志物。然而，其浓度与心肌梗死后心室重构之间的关系尚不清楚。因此，我们研究了大鼠心肌梗死后6个月内血浆脑钠肽水平，并将其与左心室重构参数进行关联。
通过结扎左冠状动脉，在152只雄性Wistar大鼠中诱导心肌梗死。在心肌梗死后1周、1个月、3个月或6个月对大鼠进行随访。然后在离体心脏中评估左心室舒张末期容积和最大收缩压，获取心脏和肺脏重量，计算壁应力，测量心肌细胞大小，并采用酶联免疫吸附测定法评估血浆脑钠肽水平。
大面积（≥40%）而非小面积/中等面积梗死伴随着心室逐渐扩张以及壁应力、左心室重量和肺脏重量增加，而心肌梗死后1周就已降低的收缩压并未随时间进展。血浆脑钠肽在心肌梗死后第3天达到峰值，之后未进一步升高；它与梗死面积和左心室扩张程度相关。
因此，在大鼠发生大面积心肌梗死后，尽管左心室逐渐扩张且壁应力增加，但血浆脑钠肽并未随时间进展。这表明，尽管血浆脑钠肽是梗死面积和左心室扩张的良好指标，但它不能用于追踪大鼠心肌梗死后心脏的进行性心室重构。
