Supraventricular pacemaker underdrive in the absence of sinus nodal influences in the conscious dog.

Abstract

The ability to reduce and maintain heart rate by electrical stimulation (underdrive) was tested in three groups of chronically instrumented dogs: sinoatrial node intact, ectopic atrial pacemaker produced by injection of rapidly hardening latex into the sinoatrial nodal artery, and idioventricular pacemaker produced by injection of formalin into the atrioventricular node. In the conscious unsedated state, underdrive of sinoatrial or idioventricular pacemakers resulted in competition between driven and intrinsic foci. However, the cycle length of ectopic atrial pacemakers could be increased by 148.4 +/- 30.7 msec (P less than 0.001) and maintained at that value. Cessation of underdrive resulted in a period of pacemaker suppression similar to that produced following overdrive. Single premature stimuli produced marked cycle length prolongations in dogs with ectopic atrial foci. Total autonomic blockade had no significant effect on the production of underdrive. Thus, the results of the present experiments provide evidence for maintained capture of cardiac pacemakers at rates significantly below intrinsic control and indicate that underdrive varies as a function of pacemaker site. Underdrive may explain the failure of junctional escape in the presence of slower atrial rhythms.

Decreased intercellular coupling improves the function of cardiac pacemakers derived from mouse embryonic stem cells

“…Underdrive of cardiac preparations was reported to have a low rate of success [35, 36] and it is not fully understood how it is established electrophysiologically. It is not the aim of this paper to solve this conundrum, but it is known that a pacemaker cycle can be disrupted by premature stimuli.…”

Transmural myocardial infarction in the dog produces sympathectomy in noninfarcted myocardium.

“…Then, the ligature at the origin of the diagonal branch was tied and retracted, the distal ligature positioned in such a manner as to prevent bleeding due to retrograde flow, and the diagonal branch cannulated with PE-50 catheter. The cannula was secured in the artery, and 0.3-0.5 ml of vinyl latex solution (Carolina Biological Supply) was rapidly injected into the artery through the cannula to embolize the vasculature.6 7 The cannula was removed, the proximal ligature left in place, and the distal ligature tied tightly around the embolized artery. Preliminary experiments had demonstrated that after embolization, 60-90 minutes were required for the preparation to stabilize before reproducible ERP determinations could be made.…”

Electrophysiology of coronary reperfusion. A mechanism for reperfusion arrhythmias.

“…Indeed, the similar finding of a rapid improvement in conduction after 35 minutes of coronary occlusion was taken as strong evidence against a reentrant mechanism in the feline model of reperfusion arrhythmias (9). However, although conduction improves with reperfusion, in those areas of the heart rendered unresponsive by ischemia, the conduction improvement Ventricular automaticity was assessed in five dogs during reperfusion after complete atrioventricular (AV) block was produced by injecting formalin into the AV node according to the method described bv Loeb et a 1 ( 71). The heart was exposed via a right thoracotomy using standard surgical techniques.…”