Depressed in vivo myocardial reactivity to dobutamine in streptozotocin diabetic rats: influence of exercise training.

Depressed in vivo myocardial reactivity to dobutamine in streptozotocin diabetic rats: influence of exercise training.
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链脲佐菌素糖尿病大鼠体内心肌对多巴酚丁胺的反应性降低:运动训练的影响。

DOI:
10.1093/cvr/22.6.417
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发表时间:
1988
影响因子:
10.8
通讯作者:
Tow,JP
Tow,JP
中科院分区:
医学1区
文献类型:
--
作者:
Heller,BA;Paulson,DJ;Kopp,SJ;Peace,DG;Tow,JP

文献摘要

被引文献

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为了评价慢性糖尿病对在体心肌对β 1肾上腺素能受体刺激的反应性的影响,以及评价运动训练对预防糖尿病所致心脏异常的治疗作用,对4组大鼠进行了研究:安静对照组、训练对照组、安静糖尿病组和训练糖尿病组。训练后大鼠在链脲佐菌素55 mg·kg-1 iv诱导糖尿病模型前进行跑台训练。然后在8周的训练中逐渐增加运动的持续时间、速度和等级,直到大鼠可以以18 m/min的速度跑90 min,5%等级。通过跖肌细胞色素氧化酶活性的增加证实了训练效果。通过心内导管术评估体内心脏收缩性能。在基础状态下和静脉注射多巴酚丁胺10 - 10 ~ 5 × 10 - 7 mol·kg-1体重后,测量心率、左心室内收缩压峰值和正负dP/dt。在基础状态下,四组间左心室内收缩压峰值、正性dP/dt和心率无差异,但负性dP/dt在两组中均较低。与久坐对照组相比,久坐糖尿病组对多巴酚丁胺的反应,反映在所测量的心脏动力学变量中,显著减弱。运动训练倾向于改善心脏功能,使其达到久坐对照组的水平;然而,久坐组和训练过的糖尿病组之间的差异无统计学意义。运动训练也没有显著改变对照组对多巴酚丁胺的反应。这些结果表明,心肌反应性β肾上腺素能刺激受损糖尿病大鼠。运动训练的强度未能显着改善这种情况。
To assess the effects of chronic diabetes on in vivo myocardial reactivity to beta1adrenergic receptor stimulation and to evaluate the therapeutic effect of exercise training in preventing the cardiac abnormalities induced by diabetes four groups of rats were studied: sedentary control, trained control, sedentary diabetic, and trained diabetic. Trained rats were adapted to treadmill running before the induction of diabetes with streptozotocin 55 mg·kg−1iv. The duration, speed, and grade of exercise were then progressively increased during eight weeks of training until the rats could run for 90 min at 18 m/min, 5% grade. A training effect was confirmed by an increase in plantaris muscle cytochrome oxidase activity. In vivo cardiac contractile performance was assessed by intracardiac catheterisation. Heart rate, left intraventricular peak systolic pressure, and positive and negative dP/dt were measured under basal conditions and after the intravenous administration of dobutamine 10−10to 5 × 10−7mol·kg−1body weight. Under basal conditions, there were no differences among the four groups in left intraventricular peak systolic pressure, positive dP/dt, and heart rate, but negative dP/dt was lower in both diabetic groups. The response to dobutamine of the sedentary diabetic group, as reflected in the measured cardiodynamic variables, was significantly attenuated compared with that of the sedentary control group. Exercise training tended to improve cardiac function towards the level detected in the sedentary controls; however, the differences between sedentary and trained diabetic groups were not statistically significant. Exercise training also did not significantly alter the response of the control group to dobutamine. These findings suggest that myocardial reactivity to betai adrenergic stimulation is impaired in diabetic rats. Exercise training at the intensity used failed significantly to improve this condition.