Welcome to Chinese Journal of Clinical Pharmacology and Therapeutics,Today is Chinese

Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2004, Vol. 9 ›› Issue (9): 1037-1040.

Previous Articles     Next Articles

Influnce of aminoguanidine on myocardial function and ultrastractue in diabetic rats

FU Li-Juan, WANG Hong-Xin, PANG Dong-Bo1, LI Yan-Qin2   

  1. Department of Parmacology,1The First Affiliated Hospital,2Department of Electron Microscope, Jinzhou Medical College, Jinzhou 121001, Liaoning, China
  • Received:2004-07-09 Revised:2004-08-10 Online:2004-09-26 Published:2020-11-23

Abstract: AIM: To explore the protective effects of the nonenzymation glycosylation inhibitor-aminoguanidine (AG)on the cardiac function and ultrastructure in diabetes-induced rats.METHODS: Sprague-Dawley rats were randomly divided into control group, sreptozotocin(STZ)-induced diabetic group and aminoguanidine treated diabetic group (150 mg·kg-1·d-1 water given after diabetes induced).The serum fructosamine content levels and the cardiac mass index and some related parameters were determined at 12 weeks.RESULTS: The serum fructosamine content levels and the cardiac mass were higher than that in the control group. The value of±dp/dtmax tite was decreased in diabetic group at 12 weeks compared with the control group. Electron microscopic morphometry of heart samples revealed typical diabetic alterations consisting in a focal loss, disorganization of myofibril, mitochondril swelling, and lysis of cistae. In AG treated group, The serum fructosamine content levels and the cardiac mass decreased, the value of±dp/dtmax was increased markedly compared with diabetic rats. Microvascular membrane, proliferation of the collegen in the extracellular matrix and nyocardial ultrastructure were better than diabetes.CONCLUSION: There are changes of myocardial function, ultrastractue abnormalities and ventricular hypertropfhy in diabetic rats. AG can inhibit the progress of diabetic cardiomyopathy.

Key words: aminoguanidine, nonenzymation glycosylation, diabetic rat, cardiomyopathy

CLC Number: