Der Einfluss des Zytokins Monozyten-Chemoattraktives Protein-1 (MCP-1) auf Gefäßneubildung im chronischen Myokardinfarktmodell der Ratte

Background: Monocyte Chemotactic Protein-1 (MCP-1) stimulates the invasion of monocytes into ischemic tissue and their adhesion to endothelial cells. It has been shown to be involved in the mediation/stimulation of arteriogenesis in experimental models of limb ischemia. So far, effects of MCP-1 have not been tested in the ischemic/infarcted myocardium. Methods: Ten female Sprague-Dawley rats underwent myocardial infarction by ligation of the left anterior descending coronary artery. After six weeks, saline (group 1) or MCP-1 (group 2) was injected as a single dose directly into the myocardium following thoracotomy. Left ventricular dimensions and fractional shortening (FS) were assessed by transthoracic echocardiography prior to and 6 weeks after infarction, and 4 weeks after injection. For histological analysis of neo-angiogenesis, tissue was stained by Elastica-van-Gieson and von Willebrand-factor. Results: FS reduced from 58.4 ± 2.06 (x +/- SEM) to 26.3 ± 4.3 in group 1 and from 60.4 ± 2.85 to 24.8 ± 5.01 in group 2 six weeks after myocardial infarction. After another four weeks, there was no difference in FS between the saline and MCP-1 treated group (group 1: FS = 25 ± 5.18, group 2: FS = 26.3 ± 2.7, p0.005). There was no difference in the number of arteriolar structures between the two groups (group 1: 16.4 ± 0.68; group 2: 19 ± 1.52, p<0.05). Conclusion: A single intramyocardial injection of MCP-1 results in an increased number of capillaries compared to saline injection. In contrast, the number of arteriolar structures was not increased compared to controls. There was no improvement of left ventricular function by MCP-1-injection. Thus, a single injection of MCP-1 induces angiogenesis but not arteriogenesis in the infarcted rat heart, which does not contribute to cardiac function

Der Einfluss des Zytokins Monozyten-Chemoattraktives Protein-1 (MCP-1) auf Gefäßneubildung im chronischen Myokardinfarktmodell der Ratte

Background: Monocyte Chemotactic Protein-1 (MCP-1) stimulates the invasion of monocytes into ischemic tissue and their adhesion to endothelial cells. It has been shown to be involved in the mediation/stimulation of arteriogenesis in experimental models of limb ischemia. So far, effects of MCP-1 have not been tested in the ischemic/infarcted myocardium. Methods: Ten female Sprague-Dawley rats underwent myocardial infarction by ligation of the left anterior descending coronary artery. After six weeks, saline (group 1) or MCP-1 (group 2) was injected as a single dose directly into the myocardium following thoracotomy. Left ventricular dimensions and fractional shortening (FS) were assessed by transthoracic echocardiography prior to and 6 weeks after infarction, and 4 weeks after injection. For histological analysis of neo-angiogenesis, tissue was stained by Elastica-van-Gieson and von Willebrand-factor. Results: FS reduced from 58.4 ± 2.06 (x +/- SEM) to 26.3 ± 4.3 in group 1 and from 60.4 ± 2.85 to 24.8 ± 5.01 in group 2 six weeks after myocardial infarction. After another four weeks, there was no difference in FS between the saline and MCP-1 treated group (group 1: FS = 25 ± 5.18, group 2: FS = 26.3 ± 2.7, p0.005). There was no difference in the number of arteriolar structures between the two groups (group 1: 16.4 ± 0.68; group 2: 19 ± 1.52, p<0.05). Conclusion: A single intramyocardial injection of MCP-1 results in an increased number of capillaries compared to saline injection. In contrast, the number of arteriolar structures was not increased compared to controls. There was no improvement of left ventricular function by MCP-1-injection. Thus, a single injection of MCP-1 induces angiogenesis but not arteriogenesis in the infarcted rat heart, which does not contribute to cardiac function