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川崎病患者多巴酚丁胺负荷诱导的无症状心肌缺血期间内皮源性血管调节因子的变化

Changes in endothelium-derived vascular regulatory factors during dobutamine-stress-induced silent myocardial ischemia in patients with Kawasaki disease.

作者信息

Hino Y, Ohkubo T, Katsube Y, Ogawa S

机构信息

Department of Pediatrics, Nippon Medical School Hospital, Tokyo, Japan.

出版信息

Jpn Circ J. 1999 Jul;63(7):503-8. doi: 10.1253/jcj.63.503.

Abstract

The changes in endothelium-derived vascular regulatory factors during dobutamine (DOB)-induced myocardial ischemia (MI) were investigated in 21 patients with Kawasaki disease aged from 11 months to 18 years. They were classified into an ischemia group (8 patients) and a non-ischemia group (13 patients) based on the results of 99mTc myocardial scintigraphy and DOB stress 99mTc myocardial scintigraphy. In the ischemia group, MI was relatively mild, because there were ischemic changes on the electrocardiogram and no significant symptoms during DOB stress. Catheters were positioned near the orifice of the coronary artery (Ao) and at the coronary sinus (CS). Hemodynamics and the blood concentrations of lactic acid and endothelin-1, as well as NO3-, 6-keto-prostaglandin F1alpha, and thromboxane B2, (which are inactive metabolites of nitric oxide, prostaglandin I2 and thromboxane A2, respectively), were measured at rest and after DOB stress (maximum dose: 30 microg x kg(-1) x min(-1)). The CS/Ao ratio was determined for all parameters. The rate-pressure product, an index of work load, and the cardiac index were significantly increased by DOB stress in both groups. Coronary angiography showed no vasospasm of the epicardial coronary arteries before or after DOB stress in either group. The plasma concentrations of endothelin-1 and 6-keto-prostaglandin F1alpha were significantly increased after DOB stress in the ischemia group, but the serum concentration of NO did not increase. The lack of an increase in NO production during DOB stress may have contributed to the worsening of MI in patients with Kawasaki disease.

摘要

在21例年龄从11个月至18岁的川崎病患者中,研究了多巴酚丁胺(DOB)诱发心肌缺血(MI)期间内皮源性血管调节因子的变化。根据99mTc心肌闪烁显像和多巴酚丁胺负荷99mTc心肌闪烁显像的结果,将他们分为缺血组(8例)和非缺血组(13例)。在缺血组中,心肌缺血相对较轻,因为心电图上有缺血性改变,且在多巴酚丁胺负荷期间无明显症状。将导管置于冠状动脉口(Ao)附近和冠状窦(CS)处。在静息状态和多巴酚丁胺负荷后(最大剂量:30μg·kg-1·min-1)测量血流动力学、乳酸和内皮素-1的血浓度,以及NO3-、6-酮-前列腺素F1α和血栓素B2(分别是一氧化氮、前列腺素I2和血栓素A2的无活性代谢产物)。对所有参数测定CS/Ao比值。两组中,多巴酚丁胺负荷均使作为工作量指标的心率-血压乘积和心脏指数显著增加。冠状动脉造影显示,两组在多巴酚丁胺负荷前后均未出现心外膜冠状动脉痉挛。缺血组在多巴酚丁胺负荷后内皮素-1和6-酮-前列腺素F1α的血浆浓度显著升高,但血清NO浓度未增加。多巴酚丁胺负荷期间NO生成未增加可能导致了川崎病患者心肌缺血的恶化。

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