Acute effects of mildly intoxicating levels of alcohol on left ventricular function in conscious dogs.
Acute effects of mildly intoxicating levels of alcohol on left ventricular function in conscious dogs.
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轻度醉酒水平对清醒狗左心室功能的急性影响。
DOI：
10.1172/jci114646
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Little,WC
中科院分区：
文献类型：
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作者：
Cheng,CP;Shihabi,Z;Little,WC
我们评估了自主神经阻滞前后酒精对清醒狗左心室（LV）性能的影响。对 10 只动物进行仪器仪表，根据超声左心室内部尺寸确定左心室体积，并用微压计测量左心室压力。从手术中完全恢复后，在清醒状态下对动物进行研究。饮酒前检测不到血液酒精，饮酒后 20 分钟血液酒精浓度为 67 +/- 14 mg/dl（平均值 +/- SD）。对酒精的反应是，左心室收缩压轻微降低，左心室舒张末压轻微升高。左心室压力 (dP/dtmax) 和每搏输出量的最大时间导数降低。收缩末期容积（VES）以及有效动脉弹性显着增加。心率没有显着变化。在静脉输注酒精（0.2 g/kg）之前、立即和之后 20 分钟，通过急性腔静脉闭塞产生可变负载的压力-容积环。左心室性能的三个测量指标是从这些可变负载的压力-容积环中得出的：收缩末期压力-容积关系；每搏功-舒张末期容积关系；和最大 dP/dt-VED 关系。所有三个关系的斜率都因酒精反应而显着下降，并且所有三个关系都向右移动，表明左心室收缩性能下降。自主神经阻滞后，观察到酒精对左心室性能的类似但更大的抑制。通过注入多巴酚丁胺恢复左心室功能。我们得出的结论是，轻度中毒水平的酒精（血液浓度低于 100 mg/dl）能够在有意识的动物中产生左心室收缩抑制，这在自主神经阻断后更为明显。这表明左心室功能受损的患者即使少量也应避免饮酒。
We assessed the effect of alcohol, before and after autonomic blockade, on left ventricular (LV) performance in conscious dogs. 10 animals were instrumented to determine LV volume from ultrasonic LV internal dimensions and measure LV pressure with a micromanometer. The animals were studied in the conscious state after full recovery from the operation. Blood alcohol was undetectable before and 67 +/- 14 mg/dl (mean +/- SD) at 20 min after alcohol administration. In response to alcohol, the LV systolic pressure was reduced slightly, the left ventricular end-diastolic pressure increased slightly. The maximum time derivative of LV pressure (dP/dtmax) and stroke volume were decreased. The end-systolic volume (VES), as well as effective arterial elastance, were significantly increased. There was no significant change in heart rate. Variably loaded pressure-volume loops were generated by acute caval occlusion before, immediately, and 20 min after the intravenous infusion of alcohol (0.2 g/kg). Three measures of LV performance were derived from these variably loaded pressure-volume loops: the end-systolic pressure-volume relation; the stroke work-end-diastolic volume relation; and maximum dP/dt-VED relation. The slopes of all three relations were significantly decreased in response to alcohol, and all three relations were shifted toward the right, indicating a depression of LV contractile performance. Similar, but greater depressions of LV performance with alcohol were observed following autonomic blockade. LV performance was restored by infusing dobutamine. We conclude that mildly intoxicating levels of alcohol (blood concentration less than 100 mg/dl) are capable of producing LV contractile depression in conscious animals, which is more marked after autonomic blockade. This suggests that patients with impaired LV function should avoid even small amounts of alcohol.