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心房利钠肽输注对变异型心绞痛患者过度通气诱发发作的抑制作用。

Suppression of hyperventilation-induced attacks with infusion of atrial natriuretic peptide in patients with variant angina pectoris.

作者信息

Tanaka H, Yasue H, Yoshimura M, Morita E, Jougasaki M, Kato H, Miyao Y, Nakao K

机构信息

Division of Cardiology, Kumamoto University School of Medicine, Japan.

出版信息

Am J Cardiol. 1993 Jul 15;72(2):128-33. doi: 10.1016/0002-9149(93)90147-5.

Abstract

Atrial natriuretic peptide (ANP) is reported to dilate a major coronary artery in both experimental animals and humans. Spasm of a major coronary artery is the cause of variant angina pectoris and can be induced by hyperventilation. The effect of the ANP infusion on anginal attack induced by hyperventilation was studied in patients with variant angina pectoris. The study was performed in the early morning on 3 consecutive days in 11 patients with variant angina pectoris in whom the attacks were reproducibly induced by hyperventilation. On days 1 and 3 (saline solution infusion), and day 2 (ANP infusion), hyperventilation was started 14 minutes after beginning infusion of ANP (0.1 microgram/kg/min) or saline solution for 6 minutes. The attacks were induced in all 11 patients by hyperventilation on days 1 and 3. However, the attacks were not induced in any patient on day 2 of the ANP infusion. The plasma ANP level increased from 33 +/- 7 pg/ml to the peak level of 2,973 +/- 479 pg/ml (p < 0.01) at the end of the ANP infusion, and the plasma level of cyclic guanosine monophosphate (cGMP) increased from 5 +/- 1 pmol/ml to the peak level of 58 +/- 6 pmol/ml (p < 0.01) 5 minutes after the ANP infusion. The plasma levels of ANP and cGMP did not change after hyperventilation on days 1 and 3. It is concluded that the ANP infusion suppresses the attacks induced by hyperventilation in patients with variant angina pectoris, and cGMP is related to the mechanisms of suppression of the attacks.

摘要

据报道,在实验动物和人类中,心钠素(ANP)可扩张一条主要冠状动脉。主要冠状动脉痉挛是变异型心绞痛的病因,且可由过度通气诱发。本研究探讨了ANP输注对变异型心绞痛患者过度通气诱发的心绞痛发作的影响。该研究于清晨连续3天对11例变异型心绞痛患者进行,这些患者的发作可通过过度通气反复诱发。在第1天和第3天(输注生理盐水)以及第2天(输注ANP),在开始输注ANP(0.1微克/千克/分钟)或生理盐水6分钟后14分钟开始过度通气,持续6分钟。在第1天和第3天,所有11例患者均因过度通气诱发发作。然而,在输注ANP的第2天,没有任何患者诱发发作。输注ANP结束时,血浆ANP水平从33±7皮克/毫升升至峰值水平2973±479皮克/毫升(p<0.01),输注ANP 5分钟后,血浆环磷酸鸟苷(cGMP)水平从5±1皮摩尔/毫升升至峰值水平58±6皮摩尔/毫升(p<0.01)。在第1天和第3天过度通气后,血浆ANP和cGMP水平未发生变化。结论是,输注ANP可抑制变异型心绞痛患者过度通气诱发的发作,且cGMP与发作抑制机制有关。

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