超声心动图评价正常受试者口服葡萄糖负荷时心肌收缩反应。

M L Souza, C A Leme, J R Cavicchio, M J Saad, J A Gontijo
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引用次数: 0

摘要

胰岛素对心肌功能改变的实际机制缺乏实验数据。在本研究中,我们使用超声心动图研究了心肌收缩对口服葡萄糖负荷的反应。15名健康志愿者在禁食过夜和口服75克葡萄糖150分钟后进行了研究。口服葡萄糖负荷导致血浆葡萄糖和胰岛素水平升高,并伴有左心室缩短显著增加(葡萄糖负荷后30和60分钟分别从基线时的35.2 +/- 0.7%增加到38.5 +/- 0.6%和39 +/- 0.9%,与基线相比P < 0.05);射血分数由0.73% +/- 0.01升高至0.77% +/- 0.01 (P < 0.05);葡萄糖后60分钟和90分钟心率分别从68.3 +/- 1.9增加到74 +/- 1.6和75.3 +/- 1.5次/ min (P < 0.008),血压产物从7.29 +/- 0.2增加到8.31 +/- 0.3 mmHg x beats / min (P < 0.007)。同时,与基础值相比,平均动脉压显著降低(10 +/- 1.5%,P < 0.018)。这些结果表明,心肌收缩反应对口服葡萄糖负荷有显著变化,可能与压力感受器反射反应有关,也可能被胰岛素的有效血管扩张作用所覆盖。然而,我们不能排除对心脏的影响也可能是由于胰岛素诱导的交感神经激活或直接的心肌效应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Myocardial contractile response to an oral glucose load in normal subjects evaluated by echocardiography.

There is a paucity of experimental data on the actual mechanism of insulin-induced changes on the myocardial function. In the present study we investigated the myocardial contractile, response to an oral glucose load using echocardiography. Fifteen healthy volunteers were studied after overnight fast and 150 minutes after the oral load of 75 g glucose. Oral glucose load caused an increase in plasma glucose and insulin levels, which was accompanied by a significant increase in left ventricular shortening (from 35.2 +/- 0.7% at baseline, to 38.5 +/- 0.6% and 39 +/- 0.9% at 30 and 60 minutes post glucose load, respectively [P < 0.05 vs baseline]; ejection fraction rose from 0.73% +/- 0.01 to 0.77% +/- 0.01 (P < 0.05); pressure rate product increased from 7.29 +/- 0.2 to 8.31 +/- 0.3 mmHg x beats per min (P < 0.007) and heart rate enhanced from 68.3 +/- 1.9 to 74 +/- 1.6 (P < 0.034) and 75.3 +/- 1.5 beats per min (P < 0.008) at 60 and 90 minutes after glucose, respectively. Meanwhile, mean arterial pressure decreased significantly (10 +/- 1.5%, P < 0.018) when compared to basal values. These results indicate a significant change in the myocardial contractile response to an oral glucose load, probably related to baroreceptor reflex response as well as an overridden by a potent vasodilator action of insulin. Nevertheless, we could not rule out that the cardiac effects may also be due an insulin-induced sympathetic activation or a direct myocardial effect.

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