Nobe S, Aomine M, Arita M, Ito S, Takaki R
Department of Physiology, Medical College of Oita, Japan.
Cardiovasc Res. 1990 May;24(5):381-9. doi: 10.1093/cvr/24.5.381.
The aim of the study was to investigate the effects of chronic diabetes mellitus on electromechanical properties of ventricular papillary muscles.
Conventional glass microelectrodes and tension recording techniques were used in isolated hearts of rats made diabetic for 30-40 weeks by single intravenous injections of streptozotocin.
Experimental animals were male Wistar rats of 200-250 g. Diabetic rats (n = 14) were given streptozotocin 65 mg.kg-1; controls (n = 15) were given vehicle only.
(1) The maximum upstroke velocity of the action potential duration of diabetic muscles was decreased compared to control, with no difference in the resting potential. (2) At all stimulation frequencies (0.2, 1 and 5 Hz), and particularly the lower ones, the action potential duration of diabetic muscles was longer than control. (3) In diabetic muscles, frequency dependent shortening of the late phase of action potential duration (APD75, APD90) was more pronounced, and frequency dependent lengthening of the early phase (APD25, APD50) was less pronounced. (4) A blocker of transient outward current, 4-aminopyridine, lengthened the early phase of action potential durations by the same amount in diabetic and control muscles. (5) A Ca2+ channel blocker, CoCl2, dramatically shortened all levels of action potential duration, with much greater effect on diabetic muscles. (6) Ryanodine lengthened the early phase of action potential duration and shortened the late phase in both diabetic and control muscles. It enhanced the difference between the groups in the early phase. (7) Developed tension in the presence of ryanodine (ryanodine resistant tension component) was greater in diabetic muscles than in control.
The findings suggest that altered Ca2+ current, but not altered Na(+)-Ca2+ exchange current or altered transient outward current, significantly prolongs action potential duration in diabetic rat ventricular muscles.
本研究旨在探讨慢性糖尿病对心室乳头肌电机械特性的影响。
采用传统玻璃微电极和张力记录技术，对通过单次静脉注射链脲佐菌素制成糖尿病模型30 - 40周的大鼠离体心脏进行研究。
实验动物为体重200 - 250克的雄性Wistar大鼠。糖尿病大鼠（n = 14）给予链脲佐菌素65毫克/千克；对照组（n = 15）仅给予溶剂。
（1）糖尿病肌肉动作电位持续时间的最大上升速度与对照组相比降低，静息电位无差异。（2）在所有刺激频率（0.2、1和5赫兹）下，尤其是较低频率时，糖尿病肌肉的动作电位持续时间比对照组更长。（3）在糖尿病肌肉中，动作电位持续时间后期（APD75、APD90）的频率依赖性缩短更明显，而早期（APD25、APD50）的频率依赖性延长则不明显。（4）瞬时外向电流阻滞剂4 - 氨基吡啶使糖尿病肌肉和对照肌肉动作电位持续时间的早期延长相同幅度。（5）Ca2 +通道阻滞剂CoCl2显著缩短了所有水平的动作电位持续时间，对糖尿病肌肉的作用更大。（6）兰尼碱使糖尿病肌肉和对照肌肉动作电位持续时间的早期延长，后期缩短。它增强了两组在早期的差异。（7）在存在兰尼碱的情况下（兰尼碱抗性张力成分），糖尿病肌肉产生的张力大于对照肌肉。
研究结果表明，Ca2 +电流改变而非Na(+) - Ca2 +交换电流或瞬时外向电流改变，显著延长了糖尿病大鼠心室肌肉的动作电位持续时间。
