Objective        To investigate the effect of macrophages on extracellular matrix repair and ventricular remodeling after acute myocardial infarction (AMI) in rats induced by ischemia/reperfusion (I/R).       Methods        T

he peritoneal macrophages of Wistar rats were adherently cultured. The survival animals induced by I/R were randomly divided into a sham operation group (n=12)

an AMI group (n=23) and a macrophage transplantation group (MΦ group

n=20). At the 7th and 28th day after the induction of I/R

the histopathology of left ventricular myocardial tissues including index of expansion

infarct size

cardiomyocyte cross-sectional area (CSA) in non-infarct region

proportion of mature collagen fibers in infarct region and collagen volume fraction (CVF) in infarct region and non-infarct region were examined.       Results       Compared with the AMI group

the index of expansion and the CSA in non-infarct region at the 7th day (0.27±0.13 vs  0.41±0.19

P0.05; 330.65±57.30 vs  408.00±99.98 μm

2

P0.01) and the 28th day (0.30±0.11 vs  0.48±0.12

P0.01; 335.80±92.52 vs  515.41±93.13 μm

2

P0.01) all decreased in the MΦ group. The CVF in infarct region at the 7th day [(53.51±5.82)% vs  (45.05±3.66)%

P0.01

]

and the 28th day [(79.17±5.58)% vs  (73.17±5.94)%

P0.01

]

of the MΦ group were greater than those of the AMI group

while the CVF in non-infarct region at the 7th day [(2.37±0.65)% vs  (4.84±1.81)%

P0.01

]

and the 28th day [(2.64±0.63)% vs  (6.01±1.34)%

P0.01

]

of the MΦ group were less than those of the AMI group. Compared with the AMI group

the proportion of mature collagen fibers in infarct region increased in the MΦ group at the 7th day (0.566±0.009 vs  0.509±0.011

P0.01) and the 28th day (2.162±0.047 vs  1.454±0.020

P0.01).        Conclusion        Macrophage intra-myocardial transplantation can promote collagen deposition and maturation

reduce infarct size

and alleviate fibrosis and myocardial hypertrophy in non-infarct region

so as to improve left ventricular remodeling after AMI.