2006Zhonghua laonian yixue zazhiRequires access

Effects of telmisartan on cardiac fibroblast after acute myocardial infarction in rats

Lianglong Chen

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Abstract

Objective To evaluate the changes of the activation and proliferation of rat cardiac fibroblasts in infarcted and non-infarcted regions.Methods The model of myocardial infarction (AMI)was developed through the ligation of anterior descending branch of left coronary artery.After 24 hours,the survived 114 rats were randomly assigned to the following 2 groups:(1)AMI group (n=57);(2)telmisartan treatment group(n=57).And a sham-operated group(n=32)was used asa control.All groups were terminated at day 4,7,14,28,respectively(n=10,12,15,20).At the end of the study,heart rate(HR),blood pressure (BP),ventricle relative weight (ventricle weight/body weight,VW/BW) and survival rate were measured,and the activation and proliferation of fibroblast and collagen volume fraction (CVF) were assessed.Results (1)The 28 day accumulated survival rate for treatment group was lower than that for AMI group (P0.05),so were the ratios of VW/BW for treatment group on day 14,28 (all P0.05).(2)In AMI and treatment groups,many myofibroblast with positive α-smooth muscle actin(α-SMA)and vimentin VA phenotype appeared on day 4.The amount of myofibroblast was gradually decreased after day 7.On day 28,the percentages of VA and proliferating cell nuclear antigen(PCNA)positive cells were significantly lower in treatment group than in AMI group (all P0.05).In non-infarcted myocardium,there were no significant differences in α-SMA and PCNA positive rates among the three groups.(3)The CVF was reduced on day 28 in treatment group when compared with AMI group (P0.05).But in non-infarcted myocardium,CVF decreased markedly with telmisartan treatment on day 14,28 when compared with AMI group(all P0.01).Conclusions Telmisartan can improve cardiac remodeling after AMI in rats,decrease the mortality of AMI rats and may have therapeutic benefits in patients after AMI.

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Objective To evaluate the changes of the activation and proliferation of rat cardiac fibroblasts in infarcted and non-infarcted regions.Methods The model of myocardial infarction (AMI)was developed through the ligation of anterior descending branch of left coronary artery.After 24 hours,the survived 114 rats were randomly assigned to the following 2 groups:(1)AMI group (n=57);(2)telmisartan treatment group(n=57).And a sham-operated group(n=32)was used asa control.All groups were terminated at day 4,7,14,28,respectively(n=10,12,15,20).At the end of the study,heart rate(HR),blood pressure (BP),ventricle relative weight (ventricle weight/body weight,VW/BW) and survival rate were measured,and the activation and proliferation of fibroblast and collagen volume fraction (CVF) were assessed.Results (1)The 28 day accumulated survival rate for treatment group was lower than that for AMI group (P0.05),so were the ratios of VW/BW for treatment group on day 14,28 (all P0.05).(2)In AMI and treatment groups,many myofibroblast with positive α-smooth muscle actin(α-SMA)and vimentin VA phenotype appeared on day 4.The amount of myofibroblast was gradually decreased after day 7.On day 28,the percentages of VA and proliferating cell nuclear antigen(PCNA)positive cells were significantly lower in treatment group than in AMI group (all P0.05).In non-infarcted myocardium,there were no significant differences in α-SMA and PCNA positive rates among the three groups.(3)The CVF was reduced on day 28 in treatment group when compared with AMI group (P0.05).But in non-infarcted myocardium,CVF decreased markedly with telmisartan treatment on day 14,28 when compared with AMI group(all P0.01).Conclusions Telmisartan can improve cardiac remodeling after AMI in rats,decrease the mortality of AMI rats and may have therapeutic benefits in patients after AMI.

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Available abstract

Objective To evaluate the changes of the activation and proliferation of rat cardiac fibroblasts in infarcted and non-infarcted regions.Methods The model of myocardial infarction (AMI)was developed through the ligation of anterior descending branch of left coronary artery.After 24 hours,the survived 114 rats were randomly assigned to the following 2 groups:(1)AMI group (n=57);(2)telmisartan treatment group(n=57).And a sham-operated group(n=32)was used asa control.All groups were terminated at day 4,7,14,28,respectively(n=10,12,15,20).At the end of the study,heart rate(HR),blood pressure (BP),ventricle relative weight (ventricle weight/body weight,VW/BW) and survival rate were measured,and the activation and proliferation of fibroblast and collagen volume fraction (CVF) were assessed.Results (1)The 28 day accumulated survival rate for treatment group was lower than that for AMI group (P0.05),so were the ratios of VW/BW for treatment group on day 14,28 (all P0.05).(2)In AMI and treatment groups,many myofibroblast with positive α-smooth muscle actin(α-SMA)and vimentin VA phenotype appeared on day 4.The amount of myofibroblast was gradually decreased after day 7.On day 28,the percentages of VA and proliferating cell nuclear antigen(PCNA)positive cells were significantly lower in treatment group than in AMI group (all P0.05).In non-infarcted myocardium,there were no significant differences in α-SMA and PCNA positive rates among the three groups.(3)The CVF was reduced on day 28 in treatment group when compared with AMI group (P0.05).But in non-infarcted myocardium,CVF decreased markedly with telmisartan treatment on day 14,28 when compared with AMI group(all P0.01).Conclusions Telmisartan can improve cardiac remodeling after AMI in rats,decrease the mortality of AMI rats and may have therapeutic benefits in patients after AMI.

Key concepts: Medicine, Ventricle, Myocardial infarction, Myofibroblast, Ligation, Internal medicine, Proliferating cell nuclear antigen, Cardiology

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