2008South China Journal of Cardiovascular DiseasesRequires access

Effects of cardiotrophin 1 C-terminal peptides on rats following myocardial ischemia reperfusion injury

Xiaofang Zhang

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Abstract

Objectives To observe the effect of cardiotrophin 1 C-terminal polypeptides(CT1C) administered pre-and post-ischemia on myocardial injury and oxidative injury after acute ischemia reperfusion in SD rats.Methods The ischemia reperfusion heart model was established by ligating/ loosening the left posterior decending branch of coronary artery.Methods pairs of rats were treated with CT1 C-terminal polypeptides either before or after myocardial ischemia,and the plasma NO content and the serum CK activity and MDA content were examined.Results The plasma NO content were decreased and the serum CK activity and MDA content were increased significantly in the ischemia reperfusion group(P 0.01),on the contrary,the plasma NO content were increased and the serum CK activity and MDA content were decreased significantly in the and post-ischemia group(P 0.01).Though the serum CK activity and MDA content were more higher in pre-ischemia group than that in the ischemia reperfusion group(P 0.01),the plasma NO were higher than the latter,but lower than that in the post-ischemia group(P 0.01).Conclusions The results suggested that the CT1C can exert myocardial protection and antioxidative ability administered after myocardial ischemia,but impair the endurance of cardioamyocytes against ischemia reperfusion injury when CT1C was used long time.

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Objectives To observe the effect of cardiotrophin 1 C-terminal polypeptides(CT1C) administered pre-and post-ischemia on myocardial injury and oxidative injury after acute ischemia reperfusion in SD rats.Methods The ischemia reperfusion heart model was established by ligating/ loosening the left posterior decending branch of coronary artery.Methods pairs of rats were treated with CT1 C-terminal polypeptides either before or after myocardial ischemia,and the plasma NO content and the serum CK activity and MDA content were examined.Results The plasma NO content were decreased and the serum CK activity and MDA content were increased significantly in the ischemia reperfusion group(P 0.01),on the contrary,the plasma NO content were increased and the serum CK activity and MDA content were decreased significantly in the and post-ischemia group(P 0.01).Though the serum CK activity and MDA content were more higher in pre-ischemia group than that in the ischemia reperfusion group(P 0.01),the plasma NO were higher than the latter,but lower than that in the post-ischemia group(P 0.01).Conclusions The results suggested that the CT1C can exert myocardial protection and antioxidative ability administered after myocardial ischemia,but impair the endurance of cardioamyocytes against ischemia reperfusion injury when CT1C was used long time.

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Available abstract

Objectives To observe the effect of cardiotrophin 1 C-terminal polypeptides(CT1C) administered pre-and post-ischemia on myocardial injury and oxidative injury after acute ischemia reperfusion in SD rats.Methods The ischemia reperfusion heart model was established by ligating/ loosening the left posterior decending branch of coronary artery.Methods pairs of rats were treated with CT1 C-terminal polypeptides either before or after myocardial ischemia,and the plasma NO content and the serum CK activity and MDA content were examined.Results The plasma NO content were decreased and the serum CK activity and MDA content were increased significantly in the ischemia reperfusion group(P 0.01),on the contrary,the plasma NO content were increased and the serum CK activity and MDA content were decreased significantly in the and post-ischemia group(P 0.01).Though the serum CK activity and MDA content were more higher in pre-ischemia group than that in the ischemia reperfusion group(P 0.01),the plasma NO were higher than the latter,but lower than that in the post-ischemia group(P 0.01).Conclusions The results suggested that the CT1C can exert myocardial protection and antioxidative ability administered after myocardial ischemia,but impair the endurance of cardioamyocytes against ischemia reperfusion injury when CT1C was used long time.

Key concepts: Medicine, Ischemia, Reperfusion injury, Internal medicine, Myocardial ischemia, Anesthesia, Cardiology

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