2007The Journal of Medical InvestigationOpen access

The effect of G-CSF in a myocardial ischemia reperfusion model rat

Kiyoshi Ieishi, Masahiro Nomura, Tomohito Kawano, Sayuri Fujimoto, Hiroyuki Ikefuji, Yoshiko Noda, Akiyoshi Nishikado, Susumu Ito

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Abstract

PURPOSE: It has been reported that G-CSF administration improves cardiac function by reducing the area of the infarct in a myocardial infarction model rat. In the present study, myocardial infarction model rats, produced by ligation of the left anterior coronary artery, were prepared. The G-CSF effect for treating cardiac muscle cell disorders by ischemia reperfusion was studied. METHODS: Myocardial infarction model rats were produced by ligation of the left anterior descending coronary artery in 12-week-old Wistar rats. G-CSF was administered subcutaneously daily at a dose of 100 microg/kg/day for 5 days to rats with a complete ligation (MI-G group, n=6) and rats in which the ligated coronary artery was reperfused 30 minutes after the ligation (R-G group, n=6). Physiological saline was subcutaneously administered to rats with a complete ligation and reperfusion (MI-C and R-C groups, respectively, n=6 each), as controls. After 4 weeks, the infarct area ratio (%), cardiac function on echocardiography (left ventricular ejection fraction), and a myocardial histopathological diagnosis were carried out and the results compared among the groups. RESULTS: No significant differences were found in the proportion of the residual heart muscle in the infarct lesion, myocardial wall thickness, or left ventricular ejection fraction between the MI-G and MI-C groups. In contrast, the infarct area, myocardial wall thickness, and left ventricular ejection fraction were significantly improved in the R-G group compared to the R-C group (p<0.05). CONCLUSIONS: Any inhibitory effect of G-CSF on the infarct lesion was found in the myocardial infarction reperfusion model rat, but only a small effect was found in rats with a complete ligation-induced myocardial infarction. The findings in the present study, therefore, suggest that G-CSF is effective for treating cardiac muscle cell disorders by ischemia reperfusion.

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PURPOSE: It has been reported that G-CSF administration improves cardiac function by reducing the area of the infarct in a myocardial infarction model rat. In the present study, myocardial infarction model rats, produced by ligation of the left anterior coronary artery, were prepared. The G-CSF effect for treating cardiac muscle cell disorders by ischemia reperfusion was studied. METHODS: Myocardial infarction model rats were produced by ligation of the left anterior descending coronary artery in 12-week-old Wistar rats. G-CSF was administered subcutaneously daily at a dose of 100 microg/kg/day for 5 days to rats with a complete ligation (MI-G group, n=6) and rats in which the ligated coronary artery was reperfused 30 minutes after the ligation (R-G group, n=6). Physiological saline was subcutaneously administered to rats with a complete ligation and reperfusion (MI-C and R-C groups, respectively, n=6 each), as controls. After 4 weeks, the infarct area ratio (%), cardiac function on echocardiography (left ventricular ejection fraction), and a myocardial histopathological diagnosis were carried out and the results compared among the groups. RESULTS: No significant differences were found in the proportion of the residual heart muscle in the infarct lesion, myocardial wall thickness, or left ventricular ejection fraction between the MI-G and MI-C groups. In contrast, the infarct area, myocardial wall thickness, and left ventricular ejection fraction were significantly improved in the R-G group compared to the R-C group (p<0.05). CONCLUSIONS: Any inhibitory effect of G-CSF on the infarct lesion was found in the myocardial infarction reperfusion model rat, but only a small effect was found in rats with a complete ligation-induced myocardial infarction. The findings in the present study, therefore, suggest that G-CSF is effective for treating cardiac muscle cell disorders by ischemia reperfusion.

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Available abstract

PURPOSE: It has been reported that G-CSF administration improves cardiac function by reducing the area of the infarct in a myocardial infarction model rat. In the present study, myocardial infarction model rats, produced by ligation of the left anterior coronary artery, were prepared. The G-CSF effect for treating cardiac muscle cell disorders by ischemia reperfusion was studied. METHODS: Myocardial infarction model rats were produced by ligation of the left anterior descending coronary artery in 12-week-old Wistar rats. G-CSF was administered subcutaneously daily at a dose of 100 microg/kg/day for 5 days to rats with a complete ligation (MI-G group, n=6) and rats in which the ligated coronary artery was reperfused 30 minutes after the ligation (R-G group, n=6). Physiological saline was subcutaneously administered to rats with a complete ligation and reperfusion (MI-C and R-C groups, respectively, n=6 each), as controls. After 4 weeks, the infarct area ratio (%), cardiac function on echocardiography (left ventricular ejection fraction), and a myocardial histopathological diagnosis were carried out and the results compared among the groups. RESULTS: No significant differences were found in the proportion of the residual heart muscle in the infarct lesion, myocardial wall thickness, or left ventricular ejection fraction between the MI-G and MI-C groups. In contrast, the infarct area, myocardial wall thickness, and left ventricular ejection fraction were significantly improved in the R-G group compared to the R-C group (p<0.05). CONCLUSIONS: Any inhibitory effect of G-CSF on the infarct lesion was found in the myocardial infarction reperfusion model rat, but only a small effect was found in rats with a complete ligation-induced myocardial infarction. The findings in the present study, therefore, suggest that G-CSF is effective for treating cardiac muscle cell disorders by ischemia reperfusion.

Key concepts: Medicine, Ligation, Ejection fraction, Myocardial infarction, Internal medicine, Cardiology, Cardiac function curve, Left coronary artery

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