The effect of G-CSF in a myocardial ischemia reperfusion model rat.
OBJECTIVE
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.
Ieishi
Kiyoshi
K
Division of Cardiology, Kagawa Prefectural Shirotori Hospital, Kagawa, Japan.
Nomura
Masahiro
M
Kawano
Tomohito
T
Fujimoto
Sayuri
S
Ikefuji
Hiroyuki
H
Noda
Yoshiko
Y
Nishikado
Akiyoshi
A
Ito
Susumu
S
D000818:Animals; D004195:Disease Models, Animal; D004452:Echocardiography; D016179:Granulocyte Colony-Stimulating Factor / Q000627:therapeutic use*; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000473:pathology; D009206:Myocardium / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D016277:Ventricular Function, Left
D016179:Granulocyte Colony-Stimulating Factor