Biochemical and physiological responses of the diabetic rat heart to induced myocardial ischemia.
The purpose of this investigation was to compare the biochemical responses of normal and streptozotocin (STZ) diabetic rat hearts to myocardial ischemia. As expected, left ventricular peak systolic pressure (LVPSP) declined with the onset of ischemia. The time required to reach 75% (LVPSP75) and 50% (LVPSP50) of baseline LVPSP100 was significantly (p less than 0.05) more rapid in diabetic and iodoacetate-treated hearts when compared to control animals. Diabetic rats experienced a significant (p less than 0.05) reduction in myocardial glycogen levels with ischemia. Despite enhanced glycogenolysis in diabetic rat hearts, cardiac lactate failed to accumulate in significant amounts. Overall, myocardial ATP and CP levels declined, but the reduction appears not to be associated with the fall in LVPSP. The results confirm that ventricular pressure development decreases rapidly following iodoacetate treatment. Similar declines in function were observed in the diabetic heart suggesting that glycolytic pathway inhibition and/or diminished glycolytic flux is responsible for the reduction in left ventricular pressure during myocardial ischemia.
D000818:Animals; D001794:Blood Pressure; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D006003:Glycogen / Q000378:metabolism; D006352:Heart Ventricles / Q000503:physiopathology; D007773:Lactates / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013311:Streptozocin
D007773:Lactates; D013311:Streptozocin; D006003:Glycogen