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X综合征患者的心肌β-肾上腺素能受体密度与血浆儿茶酚胺

Myocardial beta-adrenoceptor density and plasma catecholamines in syndrome X.

作者信息

Rosen S D, Boyd H, Rhodes C G, Kaski J C, Camici P G

机构信息

MRC Clinical Sciences Centre, Hammersmith Hospital, London, United Kingdom.

出版信息

Am J Cardiol. 1996 Jul 1;78(1):37-42. doi: 10.1016/s0002-9149(96)00223-8.

DOI:10.1016/s0002-9149(96)00223-8
PMID:8712115
Abstract

Recent research has cast doubt on the ischemic hypothesis of etiology of syndrome X (anginal pain, ischemic-like changes in the stress electrocardiogram, but normal coronary arteriogram). Abnormalities of pain perception have been shown and abnormal sympathetic nervous system activation has also been implicated. The aim of this study was to test the hypothesis that downregulation of myocardial beta adrenoceptors is demonstrable in patients with syndrome X. Such downregulation would be consistent with raised myocardial catecholamine concentrations. We performed positron emission tomography with (11)C-CGP-12177 to measure beta-adrenoceptor density. Plasma catecholamines were sampled simultaneously and assayed using high-performance liquid chromatography. Twenty syndrome X patients (11 female, age 57 +/- 9 SD years, range 33 to 69) and 18 matched controls (9 women, age 50 +/- 13 years, range 25 to 65; p = NS vs patients) were studied. Myocardial beta-adrenoceptor density did not differ between syndrome X patients and controls: 8.0 (1.9) pmol/g for patients versus 8.3 (2.1) pmol/g for controls; p = 0.62. No differences were found between patients and controls for plasma norepinephrine (2.82 [1.07] and 2.76 [1.18] nM, respectively; p = 0.89) or for epinephrine (0.29 [0.14] and 0.30 [0.20] nM, respectively; p = 0.84). In patients with syndrome X, beta-adrenoceptor density is normal and, by inference, myocardial catecholamines would also be normal. This weakens the case for a generalized enhancement of sympathetic activation in this disorder, although increased sympathetic reactivity during actual episodes of chest pain remains a possibility.

摘要

近期研究对X综合征(心绞痛、运动心电图出现类似缺血性改变,但冠状动脉造影正常)病因的缺血假说提出了质疑。研究显示了痛觉感知异常,并且交感神经系统异常激活也与之相关。本研究的目的是检验X综合征患者心肌β肾上腺素能受体下调这一假说。这种下调与心肌儿茶酚胺浓度升高相一致。我们使用(11)C-CGP-12177进行正电子发射断层扫描以测量β肾上腺素能受体密度。同时采集血浆儿茶酚胺样本,并使用高效液相色谱法进行测定。研究了20例X综合征患者(11例女性,年龄57±9标准差岁,范围33至69岁)和18例匹配的对照组(9例女性,年龄50±13岁,范围25至65岁;与患者相比p=无显著性差异)。X综合征患者和对照组之间的心肌β肾上腺素能受体密度无差异:患者为8.0(1.9)pmol/g,对照组为8.3(2.1)pmol/g;p=0.62。患者和对照组之间的血浆去甲肾上腺素(分别为2.82[1.07]和2.76[1.18]nM;p=0.89)或肾上腺素(分别为0.29[0.14]和0.30[0.20]nM;p=0.84)也无差异。在X综合征患者中,β肾上腺素能受体密度正常,由此推断,心肌儿茶酚胺也正常。这削弱了该疾病中交感神经激活普遍增强的观点,尽管在实际胸痛发作期间交感反应性增加仍有可能。

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