Normalisation of diabetic heart pump function at decreased functional load.

V. Lakomkin, A. Abramov, E. Lukoshkova, I. Studneva, A. V. Prosvirin, V. Kapelko
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Abstract

Aim      To study left ventricular (LV) hemodynamics in presence of decreased blood inflow to the heart as well as changes in myocardial content of energy metabolites in diabetic rats.Material and methods  Diabetic cardiomyopathy is characterized by impaired heart contractility and by transition of cardiomyocyte energy metabolism fatty acids exclusively as a source of energy. This reduces the efficiency of energy utilization and increases the heart vulnerability to hypoxia. This study was performed on rats with type 1 diabetes mellitus induced by administration of streptozotocin (60 mg/kg). The LV pump function was studied with a catheter that allows simultaneous measurement of LV pressure and volume in each cardiac cycle.Results Blood glucose was approximately sixfold increased at 2 weeks. Heart failure was detected with decreases in ejection fraction by 27%, minute volume by 39%, and stroke work by 41%. Systolic dysfunction was based on a decrease in LV peak ejection velocity by more than 50%. Furthermore, the LV developed pressure and contractility index were within the normal range, while 1.5 times increased arterial stiffness was the factor that hampered ejection. The sum of adenine nucleotides was decreased by 21%, the ATP content was decreased by 29%, and also creatine phosphate formation was reduced in the myocardium of diabetic rats. Lactate content in the diabetic myocardium was increased almost threefold, which indicated mobilization of aerobic glycolysis. With the reduced preload, equal diastolic volume (0.3 ml), and equal blood pressure (60 mm Hg), the diabetic heart pump function did not differ from the control.Conclusion      In type 1 diabetes mellitus, decreases in functional load and oxygen consumption normalize the myocardial pump function with disturbed energy metabolism.
降低功能负荷时糖尿病心脏泵功能的正常化。
目的研究糖尿病大鼠左心室血流动力学及心肌能量代谢物含量的变化。材料和方法糖尿病性心肌病的特点是心脏收缩能力受损,心肌细胞能量代谢脂肪酸的过渡完全作为能量来源。这降低了能量利用的效率,增加了心脏对缺氧的脆弱性。本研究采用链脲佐菌素(60 mg/kg)诱导的1型糖尿病大鼠。使用导管研究左室泵功能,该导管可同时测量每个心动周期的左室压力和容积。结果2周时血糖升高约6倍。射血分数下降27%,分钟容量下降39%,卒中功下降41%,从而检测出心力衰竭。收缩功能障碍是基于左室峰值射血速度下降超过50%。左室发展压力和收缩指数在正常范围内,动脉僵硬度升高1.5倍是阻碍射血的因素。糖尿病大鼠心肌腺嘌呤核苷酸总数减少21%,ATP含量减少29%,磷酸肌酸生成减少。糖尿病心肌乳酸含量几乎增加了三倍,这表明有氧糖酵解的动员。在预负荷降低、舒张容积相等(0.3 ml)、血压相等(60 mm Hg)的情况下,糖尿病患者的心脏泵功能与对照组没有差异。结论1型糖尿病患者功能负荷和耗氧量的降低使心肌泵功能恢复正常,能量代谢紊乱。
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来源期刊
CiteScore
0.10
自引率
0.00%
发文量
40
审稿时长
12 weeks
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