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[α-肾上腺素能受体阻断对冷加压试验诱导的外周血管收缩的影响。充血性心力衰竭患者中α1和α2肾上腺素能受体功能完整性的证据]

[Effect of alpha-adrenergic receptor blockade on peripheral vasoconstriction induced by the cold pressor test. Evidence for functional integrity of alpha 1 and alpha 2 adrenergic receptors in patients with congestive heart failure].

作者信息

Maione A, Rapacciuolo A, Esposito G, Di Lorenzo E, Ceravolo R, Indolfi C, Chiariello M

机构信息

Cattedra di Cardiologia, II Facoltà di Medicina e Chirurgia, Università degli Studi Federico II, Napoli.

出版信息

Cardiologia. 1992 Dec;37(12):839-45.

PMID:1363884
Abstract

Central sympathetic stimulation results in direct vascular vasoconstriction mediated by activation of alpha-adrenergic receptors. However, it is unknown whether this vasoconstriction is mediated by alpha 1 or alpha 2-adrenoceptor subtypes. In patients with congestive heart failure (CHF), both circulating and neuronally released catecholamines produces vasoconstriction via alpha-adrenergic stimulation. This vasoconstriction produces detrimental hemodynamic effect in CHF patients since it increases right and left ventricular filling pressures and pulmonary and systemic vascular resistances. While the myocardial alpha 1-adrenoceptors seems not to be down-regulated in heart failure, the functional integrity of vascular alpha 1 and alpha 2-adrenoceptors in CHF remains to be elucidated. Accordingly, the present study was designed to assess whether the limb vascular response to alpha 1 or alpha 2-adrenoceptor stimulation is impaired in patients with CHF. We studied 25 control subjects and 19 patients with CHF due to primary dilated cardiomyopathy. Forearm blood flow was measured by venous occlusion plethysmography. Sympathetic stimulation was produced by cold. The intraarterial pump-infusions of BHT 933 (a selective alpha 2-adrenoceptors agonist agent, 0.1, 1, 10 micrograms/kg/min for 5 min) produced the same peripheral vasoconstriction in CHF and in control subjects: 32 +/- 23.9%, 47.3 +/- 20% and 55 +/- 26.1% respectively at I, II, and III dose in CHF and 28.7 +/- 38.6%, 36 +/- 14.5%, and 57 +/- 13.8% respectively at I, II, and III dose in control subjects. The dose response to BHT 933 was not different in the 2 groups.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

中枢交感神经刺激通过激活α-肾上腺素能受体导致直接的血管收缩。然而,这种血管收缩是由α1还是α2肾上腺素能受体亚型介导尚不清楚。在充血性心力衰竭(CHF)患者中,循环和神经释放的儿茶酚胺均通过α-肾上腺素能刺激产生血管收缩。这种血管收缩在CHF患者中产生有害的血流动力学效应,因为它会增加左右心室充盈压以及肺血管和体循环血管阻力。虽然心力衰竭时心肌α1-肾上腺素能受体似乎未下调,但CHF中血管α1和α2-肾上腺素能受体的功能完整性仍有待阐明。因此,本研究旨在评估CHF患者对α1或α2肾上腺素能受体刺激的肢体血管反应是否受损。我们研究了25名对照受试者和19名因原发性扩张型心肌病导致CHF的患者。通过静脉阻塞体积描记法测量前臂血流量。通过冷刺激产生交感神经刺激。动脉内泵注BHT 933(一种选择性α2-肾上腺素能受体激动剂,0.1、1、10微克/千克/分钟,持续5分钟)在CHF患者和对照受试者中产生相同的外周血管收缩:CHF患者在I、II和III剂量时分别为32±23.9%、47.3±20%和55±26.1%,对照受试者在I、II和III剂量时分别为28.7±38.6%、36±14.5%和57±13.8%。两组对BHT 933的剂量反应无差异。(摘要截断于250字)

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