The effects of multiple increases in sinus cycle length on sinus node recovery time (SNRT) were examined in 5 dogs. Pacing was performed from the left atrial appendage for 30 and 60 seconds using at least 4 different pacing cycle lengths selected between 230 and 620 msec. Each dog received propranolol (1 mg/kg, IV) prior to any measurements. The effects of increases in sinus cycle length on SNRT were first assessed during 2 levels (4 and 8 Hz) of continuous vagal stimulation. From a control cycle length of 439 +/- 28 msec (mean +/- SE), the vagal stimulations lengthened the sinus cycle lengths to 604 +/- 10 msec and 758 +/- 16 msec respectively. Sinus cycle length was then prolonged by combined muscarinic and beta-receptor blockade resulting in a sinus cycle length of 549 +/- 9 msec. Autonomic blockade plus verapamil (3-10 mg IV) resulted in sinus cycle lengths of 612 +/- 14 and 721 +/- 18 msec respectively, which were not significantly different from those obtained with vagal stimulation. Data relating SNRT to the sinus cycle length, pacing cycle length, duration of pacing and the negative chronotropic interventions used to achieve the changes in the sinus cycle length were analyzed via covariance analysis. The results demonstrate that the single most important determinant of SNRT is the sinus cycle length. Furthermore, equivalent increases in sinus cycle length whether obtained by vagal stimulation, autonomic blockade or intravenous verapamil results in SNRTs that are not significantly different. Therefore, in the sinus node, changes in the rate of pacemaker activity, regardless of how they are achieved, will largely determine the changes in SNRT.

Adrenergic beta-Antagonists↗

PubMedDate not supplied

Differential effects of sympathetic activity on AV junctional automaticity and AV conduction.

Rapid ventricular response during episodes of supraventricular tachycardia are often followed, on abrupt cessation of the tachycardia, by prolonged pauses terminated by a sluggish and sometimes erratic escape of a supraventricular pacemaker. Such chronotropic-dromotropic paradoxes are readily reproduced in the animal laboratory following elimination of the sinus node and bilateral decentralization of the stellate ganglia and vagi. This study examined whether left stellate stimulation (0.5, 1, 2, 4, 8 and 16 Hz) or lack thereof differentially affected AV junctional automaticity and AV conduction. In the absence of any sympathetic neural activity (maximal sympathetic deficit), the AV junctional rate averaged a mere 22 +/- 2 percent of its peak performance, whereas under the same conditions, anterograde AV conduction averaged 73 +/- 5 percent and retrograde VA conduction 56 +/- 13 percent of their respective peak performances. On comparing the response curve (normalized responses) for AV junctional automaticity with that obtained for anterograde AV conduction the differences were significant at all frequencies between 0 and 4 Hz. Retrograde VA conduction (as assessed by the fastest ventricular pacing rate still conducted 1:1 to the atria) was always significantly less than anterograde AV conduction (as assessed by the fastest atrial pacing still conducted 1:1 to the ventricles). These results indicate that AV junctional automaticity is considerably more affected by sympathetic deficit than are either anterograde or retrograde AV conduction. In other words, AV junctional automaticity is far more dependent upon sympathetic input than AV conduction. While sympathetic influence is critical to the escape and maintenance of AV junctional automaticity both anterograde and retrograde AV conduction are remarkably resilient even under conditions of severe sympathetic deficit.

Animals↗

PubMedDate not supplied

Post-excitatory depression in thoracic sympathetic efferent neural traffic during a cardiogenic hypertensive chemoreflex.

Serotonin injected in the left atrium activates a cardiogenic hypertensive chemoreflex in dogs. To elucidate patterns of the neural traffic, records were obtained from thoracic sympathetic efferent nerves (either the anterior ansa of the left stellate ganglion or the T4 input to the left stellate) in 8 anesthetized dogs with chest open. Serotonin (200 micrograms, left atrium) caused a massive sympathetic discharge during the hypertension and bracardia characteristic of the chemoreflex. Following the initial sympathetic discharge, there was a consistent post-excitatory depression of neural traffic, to a level significantly less than control discharge (two-tailed p less than .05). This post-excitatory depression began 11 +/- 5.4 (S.D.) seconds after injection of serotonin and 6.6 +/- 5.3 seconds after the peak neural discharge. It lasted 140 +/- 94 seconds, being maximal initially with gradual recovery. Complete block of the hypertension by the combined administration of phentolamine, propranolol, and nitroglycerin failed to abolish the efferent neural events, including post-excitatory depression, in all but one dog. We conclude that post-excitatory depression in thoracic sympathetic efferent neural traffic cannot be mediated exclusively through the secondary engagement of a baroreceptor mechanism and that it most likely is an integral part of the cardiogenic hypertensive chemoreflex.

Animals↗

PubMedDate not supplied

Clonidine attenuation of a cardiogenic hypertensive chemoreflex.

Clonidine is an antihypertensive agent with a primary action mediated by alpha adrenergic stimulation in the central nervous system, thus inhibiting sympathetic efferent activity. Serotonin activates a cardiogenic hypertensive chemoreflex which induces discharges of sympathetic efferent neurons. The purpose of this study was to determine the effects of intravenous clonidine upon the thoracic sympathetic efferent discharges in chloralose-anesthetized dogs, their peripheral autonomic receptors being blocked with atropine, propranolol, and phentolamine. Efferent nerve traffic was quantified using a Schmitt trigger and Digital PDP8/e computer. Control spontaneous activity (tone) following autonomic blockade was normalized at 100%. Serotonin (100 microgram/ml, 2 ml, left atrium) caused an increase in the reflex efferent sympathetic activity to 192% +/- 16% of control (p less than 0.001). Following clonidine, the tone was decreased to 63% +/- 6% of control, and the reflex sympathetic discharge elicited by serotonin was significantly (p less than 0.001) reduced from 192% to 116% +/- 9% of control tone (before clonidine). The attenuation of the reflexly elicited discharge was significantly (p less than 0.05) greater than the attenuation of the tone. In four dogs that did not receive atropine, the vago-vagal reflex sinus bradycardia induced by serotonin was not affected by clonidine.

Animals↗

PubMedDate not supplied

Fine structure of the conduction system and working myocardium in the little brown bat, Myotis lucifugus.

In the little brown bat, Myotis lucifugus, topography and ultrastructure of the sinus node and the atrioventricular (AV) node resemble those in large mammalian hearts, except that the P cells in the sinus node are smaller than those in the bat AV node or those in the sinus node of slower hearts (e.g., dog, man). Despite rich innervation in the bat nodes, true neuromuscular synapses are rarely formed. Bat working cardiocytes have a well developed sarcoplasmic reticulum, but otherwise resemble working myocytes of larger mammals.

Animals↗