Direct effects of dobutamine on the coronary microcirculation: Comparison with adenosine using myocardial contrast echocardiography

Direct effects of dobutamine on the coronary microcirculation: Comparison with adenosine using myocardial contrast echocardiography
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多巴酚丁胺对冠状动脉微循环的直接影响:使用心肌造影超声心动图与腺苷进行比较

DOI:
10.1067/s0894-7317(03)00423-1
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发表时间:
2003-08-01
影响因子:
6.5
通讯作者:
Kaul, S
Kaul, S
中科院分区:
医学2区
文献类型:
--
作者:
Bin, JP;Le, E;Kaul, S

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多巴酚丁胺对毛细血管血容量(VOL)和血流速度(VEL)的直接影响尚不清楚。我们假设这些与腺苷更相似,因为它对冠状循环中的[32]受体有影响。对总共9只开胸麻醉的狗,在静息状态下放置2个非临界狭窄后,以及分别在冠状动脉内给予5 μ g/kg(-1)/min(-1)腺苷和2 μ g/kg(-1)/min(-1)多巴酚丁胺期间进行了研究。采用心肌声学造影测量VOL和VEL,二维超声心动图测量室壁增厚,放射性标记微球测量心肌血流量(MBF)。多巴酚丁胺显著增加心率-血压乘积,而腺苷对心率-血压乘积没有影响。在正常心肌中,腺苷对VOL没有影响,MBF的增加都是VEL增加的结果。多巴酚丁胺也主要引起VEL增加,而VOL仅增加30%,表明毛细血管募集适度。在狭窄的床中,两种药物以相同的量衰减MBF的增加,这与VEL增加的衰减相关,VEL增加继发于毛细血管阻力增加15%,因为毛细血管去募集。两种药物的MBF-室壁增厚关系用相同的函数描述:y = 1 - exp(x),对于每种MBF水平,多巴酚丁胺的室壁增厚显著高于腺苷。我们的结论是,MBF的增加,在正常心肌与冠脉内多巴酚丁胺发生主要是从VEL的增加,而不是从增加的体积。在床与非临界狭窄,MBF和VEL的增加是相似的两种药物。与冠状动脉内注射腺苷相似,冠状动脉内注射多巴酚丁胺也会导致非严重冠状动脉狭窄远端的毛细血管去募集。
The direct effects of dobutamine on capillary blood volume (VOL) and blood flow velocity (VEL) are not known. We hypothesized that these would be more similar to that of adenosine because of its effects on the [32 receptors on the coronary circulation. A total of 9 open-chest anesthetized dogs were studied after placement of 2 noncritical stenoses at rest and during separate intracoronary administrations of 5 mug/kg(-1)/min(-1) of adenosine and 2 mug/kg(-1)/min(-1) of dobutamine. VOL and VEL were measured using myocardial contrast echocardiography, wall thickening with 2-dimensional echocardiography, and myocardial blood flow (MBF) with radiolabeled microspheres. Dobutamine increased the rate-pressure product significantly, whereas adenosine had no effect on the rate-pressure product. In the normal myocardium, adenosine had no effect on VOL and increases in MBF were all a result of increases in VEL. Dobutamine also caused mostly an increase in VEL and only a 30% increase in VOL indicating modest capillary recruitment. In the bed with stenosis both drugs attenuated increase in MBF by the same amount, which was associated with an attenuation in the increase in VEL secondary to a 15% increase in capillary resistance because of capillary derecruitment. The MBF-wall thickening relation was described for both drugs by the same function: y = 1 - exp(x) with wall thickening being significantly higher for dobutamine compared with adenosine for each level of MBF. We conclude that the increase in MBF in the normal myocardium with intracoronary dobutamine occurs mostly from an increase in VEL rather than from an increase in VOL. In the bed with a noncritical stenosis, the increases in MBF and VEL are similar for both drugs. Similar to intracoronary adenosine, intracoronary dobutamine also caused capillary derecruitment distal to a noncritical coronary stenosis.