Terrier de La Chaise A, Brembilla-Perrot B, Clozel J P, Cherrier F, Faivre G
Arch Mal Coeur Vaiss. 1985 Aug;78(8):1156-62.
The electrophysiological effects of prostacyclin (PGI2) at increasing doses (2.5, 5 and 10 ng/kg/min) were assessed in 16 patients during classical investigations of sinus node function and atrioventricular conduction and during programmed atrial and right ventricular under basal conditions and during prostacyclin perfusion. Ten patients had normal sinus node function and atrioventricular conduction under basal conditions. Stastistically significant changes were observed during PGI2 perfusion: shortening of the sinus cycle length (p 0.01), decreased intraatrial conduction time (p less than 0.05), reduced atrial functional refractory period (p less than 0.01) and reduced effective and functional refractory periods of the AV node (p less than 0.05), increased anterograde (p less than 0.01) and retrograde (p less than 0.05) Wenckebach point. The changes were dose dependent. No significant changes were observed in sinus node recovery periods of the His Purkinje system. Similar changes were recorded on 4 other patients with various conduction defects. Paired atrial stimulation induced manifestations of hyperexcitability in 5 patients. In 2 patients with normal responses under basal conditions it was possible to induce non-sustained atrial tachycardia during PGI2 administration. In 3 patients with inducible atrial tachycardia under basal conditions, it was still possible to induce the tachycardia after PGI2 but this disappeared in all but one patient with the sick sinus syndrome after the addition of propranolol. The changes in ventricular excitability were studied by a specific protocol in 16 patients. Of the 13 patients without inducible ventricular tachycardia under basal conditions, 4 developed inducible non-sustained ventricular tachycardia after PGI2. Three patients had inducible VT under basal conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
在16例患者中，于基础状态及前列环素（PGI2）灌注期间，在进行窦房结功能及房室传导的经典检查以及程控心房和右心室刺激时，评估了递增剂量（2.5、5和10 ng/kg/min）的PGI2的电生理效应。10例患者在基础状态下窦房结功能及房室传导正常。在PGI2灌注期间观察到具有统计学意义的变化：窦房结周期长度缩短（p<0.01），心房内传导时间缩短（p<0.05），心房功能不应期缩短（p<0.01），房室结有效和功能不应期缩短（p<0.05），文氏点的前向（p<0.01）和逆向（p<0.05）传导增加。这些变化呈剂量依赖性。希氏-浦肯野系统的窦房结恢复时间未观察到显著变化。在另外4例有各种传导缺陷的患者中也记录到了类似变化。成对心房刺激在5例患者中诱发了兴奋性增高的表现。在2例基础状态下反应正常的患者中，在PGI2给药期间可诱发非持续性房性心动过速。在3例基础状态下可诱发房性心动过速的患者中，PGI2给药后仍可诱发心动过速，但除1例病态窦房结综合征患者外，在加用普萘洛尔后所有患者的心动过速均消失。通过特定方案对16例患者的心室兴奋性变化进行了研究。在13例基础状态下不能诱发室性心动过速的患者中，4例在PGI2给药后出现可诱发的非持续性室性心动过速。3例患者在基础状态下可诱发室性心动过速。（摘要截取自250字）
