Krishnan S, Levy M N
Department of Investigative Medicine, Mount Sinai Medical Center, Cleveland, Ohio 44106.
J Am Coll Cardiol. 1994 May;23(6):1484-90. doi: 10.1016/0735-1097(94)90396-4.
We evaluated the effects of alpha 1- and beta-adrenergic receptor blockade on the changes in idioventricular rate induced by occlusion and reperfusion of the left anterior descending coronary artery in anesthetized dogs.
Because sinus rate usually exceeds idioventricular rate, the experimental induction of complete atrioventricular (AV) block may improve the definition of the effects of coronary occlusion and reperfusion on idioventricular pacemaker mechanisms.
We injected formaldehyde into the AV node to induce complete AV block in 35 chloralose-anesthetized dogs. Animals were assigned to untreated (n = 22), prazosin-treated (n = 6) and propranolol-treated (n = 7) groups. We paced the hearts at 120 beats/min during a 20- to 60-min period of complete coronary occlusion, but we did not pace the heart during reperfusion.
In the untreated group, the idioventricular rate did not change significantly during coronary artery occlusions of 20 or 40 min, but it did increase significantly during the last 20 min of a 60-min occlusion. Prazosin and propranolol each attenuated but did not abolish this rate increase. The idioventricular rate increased markedly but transiently soon after reperfusion in all untreated animals. This tachycardia was virtually abolished by either prazosin or propranolol.
The increase in idioventricular rate that develops during the last 20 min of a 60-min coronary occlusion is modulated but probably not mediated by adrenergic mechanisms. The pronounced ventricular tachycardia after reperfusion is virtually abolished by either alpha 1- or beta-adrenergic antagonists. Hence, this tachycardia requires the simultaneous activation of alpha 1- and beta-adrenergic mechanisms in dogs.
我们评估了α1和β肾上腺素能受体阻滞剂对麻醉犬左前降支冠状动脉闭塞和再灌注诱导的心室自主节律变化的影响。
由于窦性心律通常超过心室自主节律,实验性诱导完全性房室传导阻滞可能有助于更清晰地界定冠状动脉闭塞和再灌注对心室自主起搏机制的影响。
我们向35只氯醛糖麻醉的犬的房室结注射甲醛以诱导完全性房室传导阻滞。将动物分为未治疗组(n = 22)、哌唑嗪治疗组(n = 6)和普萘洛尔治疗组(n = 7)。在完全冠状动脉闭塞的20至60分钟期间,我们以每分钟120次的频率起搏心脏,但在再灌注期间未起搏心脏。
在未治疗组中,在20分钟或40分钟冠状动脉闭塞期间心室自主节律没有显著变化,但在60分钟闭塞的最后20分钟期间显著增加。哌唑嗪和普萘洛尔均减轻但未消除这种心率增加。在所有未治疗的动物中,再灌注后心室自主节律立即显著但短暂地增加。这种心动过速几乎被哌唑嗪或普萘洛尔消除。
在60分钟冠状动脉闭塞的最后20分钟期间出现的心室自主节律增加受到调节,但可能不是由肾上腺素能机制介导的。再灌注后明显的室性心动过速几乎被α1或β肾上腺素能拮抗剂消除。因此,这种心动过速需要犬体内α1和β肾上腺素能机制同时被激活。