剧烈运动训练对恢复链脲佐菌素诱导糖尿病大鼠主动脉内皮 NO 依赖性舒张作用无效。

Intense exercise training is not effective to restore the endothelial NO-dependent relaxation in STZ-diabetic rat aorta.

机构信息

Laboratory Movement Sport and Health Sciences, UFR APS University of Rennes 2, Avenue Charles Tillon, Rennes cedex, France.

出版信息

Cardiovasc Diabetol. 2013 Feb 11;12:32. doi: 10.1186/1475-2840-12-32.

BACKGROUND

The aim of this study was to examine the effects of intense physical training on vascular function in streptozotocin-diabetic rats. We focused on the endothelium-dependent relaxation (EDR) induced by acetylcholine (ACh) and stable ADP adenosine-5'- O - (2-thiodiphosphate) (ADPβS).

METHODS

Control or diabetic male Wistar rats (n=44) were randomly assigned to sedentary or trained groups. The training program consisted in a regular period of running on a treadmill during 8 weeks (10° incline and up to 25 m/min, 60 min/day). The reactivity of isolated thoracic aorta rings of healthy, diabetic and/or trained has been tested.

RESULTS

ACh and ADPβS-induced EDR were observed in phenylephrine (PE) pre-contracted vessels. As compared to sedentary control group, diabetic rats showed an increase in PE-induced contraction and a decrease in ACh and ADPβS-induced EDR (p<0.05). Moreover, there were no increase in ACh and ADPβS-induced EDR in diabetic rats. N-Nitro-L-Arginine Methyl Ester inhibited the nitric oxide synthase in diabetic and control rats, thereby resulting in a strong inhibition of the EDR induced by ACh and ADPβS (10-6 M).

CONCLUSION

Diabetes induced an endothelium dysfunction. Nevertheless, our intense physical training was not effective to restore the aorta endothelial function.

背景

本研究旨在探讨剧烈体育训练对链脲佐菌素诱导糖尿病大鼠血管功能的影响。我们重点关注乙酰胆碱（ACh）诱导的内皮依赖性舒张（EDR）和稳定的 ADP 腺苷-5'- O -（2-硫代二磷酸）（ADPβS）。

方法

将雄性 Wistar 糖尿病大鼠（n=44）随机分为安静组或训练组。训练方案包括 8 周的跑步机常规跑步（10°倾斜度和最高 25 m/min，每天 60 分钟）。测试了健康、糖尿病和/或训练大鼠的离体胸主动脉环的反应性。

结果

在苯肾上腺素（PE）预收缩的血管中观察到 ACh 和 ADPβS 诱导的 EDR。与安静对照组相比，糖尿病大鼠的 PE 诱导收缩增加，ACh 和 ADPβS 诱导的 EDR 减少（p<0.05）。此外，糖尿病大鼠的 ACh 和 ADPβS 诱导的 EDR 没有增加。N-硝基-L-精氨酸甲酯抑制糖尿病和对照组大鼠的一氧化氮合酶，从而强烈抑制 ACh 和 ADPβS（10-6 M）诱导的 EDR。