Sylvén C, Beermann B, Edlund A, Lewander R, Jonzon B, Mogensen L
Department of Internal Medicine, Huddinge Hospital, Sweden.
Eur Heart J. 1988 Dec;9 Suppl N:6-10. doi: 10.1093/eurheartj/9.suppl_n.6.
Chest pain provoked by intravenous injection of adenosine was compared with natural angina pectoris in five patients with ischaemic heart disease. In seven healthy subjects a possible myocardial site for provocation of the chest pain was evaluated by analysis of time delays from injection to symptoms. The healthy volunteers were given the maximum tolerable dose of adenosine intravenously, together with 99Technetium-diethylentriaminpentaacetate (99Tcm-DTPA). Chest pain started after 4.1 +/- 2.4 s and reached its maximum 8.4 +/- 4.1 s after maximum left ventricular radioactivity. The patients with a history of typical angina pectoris were given similar doses of intravenous adenosine and the provoked chest pain did not differ in quality from the patients' habitual angina pectoris. The patients did not develop electrocardiographic signs suggesting myocardial ischaemia. Heart rate and blood pressure did not indicate increased myocardial work. In conclusion, the results concur with the hypothesis that adenosine elicits angina pectoris by stimulation of intracardiac adenosine receptors.
对5例缺血性心脏病患者静脉注射腺苷诱发的胸痛与自然心绞痛进行了比较。在7名健康受试者中，通过分析从注射到出现症状的时间延迟，评估了胸痛诱发的可能心肌部位。给健康志愿者静脉注射最大耐受剂量的腺苷，同时注射99锝-二乙三胺五乙酸（99Tcm-DTPA）。胸痛在4.1±2.4秒后开始，在左心室放射性达到最大值后8.4±4.1秒达到峰值。有典型心绞痛病史的患者接受了类似剂量的静脉注射腺苷，诱发的胸痛在性质上与患者习惯性心绞痛无异。患者未出现提示心肌缺血的心电图征象。心率和血压未显示心肌做功增加。总之，结果与腺苷通过刺激心内腺苷受体诱发心绞痛的假说相符。
