Effects of Insulin on Altered Mechanical and Electrical Papillary Muscle Activities of Diabetic Rats

Abstract

Since insulin compounds can restore some metabolic parameters and lipid profile alterations of the diabetic rat heart, we investigated whether these beneficial effects extend to diabetic rat cardiac dysfunctions. Twenty-four male Wistar albino rats, 6 months of age with an average body weight of 250-320 g, were divided randomly into three groups, each consisting of eight rats: control-group (C) rats were fed with standard rat nutrient and water; diabetic-group (D) rats were treated with a single intramuscular injection of streptozotocin (STZ, 45 mg/kg), dissolved in 0.01 M sodium citrate, pH adjusted to 4.5; and insulin-treated diabetic group (D + INS) rats were treated with subcutaneous injections of 1 IU/l insulin (INS) twice a day after a single intramuscular injection of STZ (45 mg/kg). Treatment of D rats with INS caused a time-dependent decrease in blood glucose. We found that the lipid profile and HbA(1c) levels in the D + INS group reached the values of control rats at the end of the treatment period. Contraction force in group D was compared with values from groups C and D + INS (p < 0.05). Values were obtained at a muscle contraction and relaxation time of milliseconds, with contraction time in D compared to C and D compared to D + INS and C (p < 0.05). Rate-dependent changes in action potential configuration in left ventricular papillary muscle obtained from 8-week control, STZ-treated D and D + INS rats showed significant membrane potential changes between C and STZ-treated D animals. Action potential amplitude showed significant changes between matched D + INS and STZ-treated D animals. Depolarization time showed significant changes between C and STZ-treated D animals and between the D + INS and D groups. Half-repolarization time showed significant changes between D + INS and STZ-treated D animals and compared to the D and C groups. Our data suggest that the beneficial effects of insulin treatment on the mechanical and electrical activities of the diabetic rat heart appear to be due to restoration of the diminished K+ currents, partially related to the restoration of hyperglycemia.