Primary Bradycardia Research Articles

Preliminary processes in O-R elicitation

A tentative theory of preliminary processes in orienting response (OR) elicitation is presented, based upon the observed fractionation of phasic responses in the OR context. Three hypothetical preliminary processes, which are considered to involve stimulus registration and the encoding of stimulus novelty and magnitude, interact to produce what is conceptualized as Sokolov's functional OR. The initial process of stimulus registration may have its physiological basis in primary bradycardia, and the other processes are somewhat analogous to those in dual-process theory. Such coding of stimulus parameters appears compatible with the neuronal model used by Sokolov as the basis for OR formation. The entire process of OR elicitation is considered to be steered by cortical set in the Pavlovian tradition of the dominant focus. Each hypothetical preliminary process is associated in the theory with specific physiological response measures, leading to the distinction between such components of the OR and indices of the OR (most obviously, the GSR) which generally follow the functional relationships claimed by Sokolov to characterize the OR. The present theory is compatible with a different interpretation of Sokolov's unitary OR theory than that previously current in Western psychology.

The location of chronotropic cardioinhibitory vagal motoneurons in the medulla of the rabbit

Vagal preganglionic motoneurons originating in nucleus ambiguus (NA) and dorsal vagal nucleus (DVN) were identified via retrograde labeling with horseradish peroxidase (HRP). DVN and NA were then explored for cardiovascular responsive sites using microstimulation. Stimulation within DVN from slightly caudal to obex to 3.00 mm rostral to obex produced a primary bradycardia (n = 15, X = −123 bpm). Stimulation within NA from slightly rostral to obex to 1.5 mm caudal to obex produced a similar primary bradycardia (n = 15, X = −127 bpm). Extracellular recordings were made from 7 cells in DVN and 10 cells in NA in regions producing maximal bradycardia to electrical stimulation. These cells were antidromically activated by cervical vagus nerve (VN) stimulation, increased their firing rates to systemic injection of phenylephrine (PE), revealed an expiratory rhythm, showed an increase in firing rate coinciding with spontaneous and elicited decreases in heart rate, had conduction velocities in the A-delta and B-fiber range, and produced bradycardia upon stimulation through the recording electrode with thresholds as low as 4 μA. The data indicate that in rabbits, chronotropic cardioinhibitory vagal motoneurons are discretely localized on the lateral, caudal portions of DVN and NA between 0.5 mm caudal and 1.5 mm rostral to obex.

Primary bradycardia and the evoked cardiac response in the OR context

This study sought evidence for linkages between the deceleratory evoked cardiac response (ECR) commonly observed in the OR context and the primary bradycardia of the Laceys. Individual HR protocols from a parametric study of the unitary OR were examined for both cardiac effects. Because of the small amount of data, a procedure of time-series analysis was initially used to remove respiratory sinus arrhythmia noise from the individual protocols. Previous criticism of the uncritical use of this procedure in situations with systematic respiratory changes led to statistical adjustment for this variable by covariance analysis. Evidence was obtained for a brief deceleratory ECR which failed to show the effects of stimulus novelty or intensity that were apparent in the GSR. This slowing of the heart rate began in the cardiac cycle containing the stimulus onset, as expected of primary bradycardia. The magnitude of this immediate slowing showed the dependence upon cardiac phase associated with primary bradycardia, and was also unaffected by stimulus novelty or intensity. These results support a view of the ECR as a cumulative primary bradycardia reflecting stimulus registration, a preliminary process in OR elicitation.

Parabrachial area as mediator of bradycardia in rabbits

This study examined the role of the parabrachial nucleus (PBN) in the mediation of bradycardia and in the reception of barosensory information. The 82 rabbits in the investigation were anesthetized with ethyl carbamate. Train stimulation of medial or lateral PBN produced primary bradycardia (mean peak change: −74 beats/min) associated with a pressor response (average peak mean change: +10 mm Hg) of longer latency. Section of the cervical vagus nerves indicated that the bradycardia was mediated primarily by the parasympathetic nervous system. Heart rate and blood pressure responses to train stimulation did not vary systematically as a function of respiratory pattern; paralyzing animals with decamethonium hydrochloride and artificially ventilating them also did not influence the cardiovascular responses to stimulation. Single-pulse stimulation of PBN in conjunction with extracellular single neuron recording established that neurons originating in or projecting through PBN project to the commissural region of nucleus tractus solitarius (NTS) where synapse is made with neurons receiving barosensory input. In addition to establishing the existence of descending functional projections passing from PBN to NTS, injections of HRP into PBN revealed direct descending anatomical projections to PBN from regions of the forebrain previously implicated in the mediation of bradycardia. These included central nucleus of amygdala, lateral preoptic region, medial forebrain bundle, bed nucleus of stria terminals, anterior and lateral hypothalamus. and zona incerta. The present investigation also indicated that PBN receives barosensory information. Single-pulse electrical stimulation of the aortic nerve (AN) activated neurons in NTS at an average latency of 7.5 ms and in PBN at a mean latency of 12.1 ms. Mean latency of 9 neurons in NTS activated antidromically by PBN stimulation was 3.4 ms. Conduction velocity of the monosynaptic fibers projecting from NTS to PBN was approximately 3.5. m/s, which would be characteristic of finely myelinated fibers. Injection of HRP into PBN confirmed the existence of direct ascending projections to PBN from regions of NTS (e.g. lateral commissural area) previously shown to receive primary barosensory input. However, the finding that only 1 of 9 NTS neurons antidromically activated by PBN stimulation also received barosensory stimulation, indicates that additional study is needed of the mono- and oligosynaptic functional projections from NTS to PBN. The present study did provide evidence that PBN both receives barosensory information at short latency over a direct route, and serves as a relay for descending projections mediating bradycardia.

Presidential address, 1979. Cognitive modulation of time-dependent primary bradycardia.

ABSTRACTIn one experiment, 60 male college students counted silently the number of rarely presented tones embedded in a sequence of “standard” tones. The tones differed by 50 Hz. Both rare and standard tones produced a primary bradycardia which exhibited time‐dependency: Stimuli which happened to fall relatively early in the cardiac cycle prolonged the duration of that very cycle more than late‐occurring stimuli. The latter slowed the subsequent cardiac cycle. These effects are identical qualitatively with those found in acute animal experiments upon direct electrical stimulation of the vagus, and they verified and extended results from previous experiments with human subjects in response to other sensorimotor events. The effects of expectancy, evaluated by serial positional effects on the magnitude and slope of time‐dependent cardiac slowing, were different for standard and for rare tones. Comparisons with P300, the late positive component of the average evoked potential, suggest that while P300 is most strongly associated with poststimulus decisional processes, primary bradycardia and its time‐dependent aspects reflect both early stimulus registration and later decision making. The results suggest limbic and neocortical modulation of primary bradycardia. In a second experiment with 20 male college students, in which tones were presented at experimentally controlled times within the cardiac cycle, the basic effects obtained with post hoc separation of tones into relative cycle time of occurrence were verified.

Reversal of hypoxic bradycardia by halothane or midcollicular decerebration

Previous work suggests a primary vagal bradycardia during hypoxic excitation of the arterial chemoreceptors. In this study we examined whether tachycardia, resulting from withdrawal of vagal inhibition of the cardiac pacemaker, may also occur during hypoxia. Cats with cervical spinal section were ventilated with hypoxic gas mixtures or allowed to remain apneic in expiration while heart rate was continually monitored. During recovery from halothane anesthesia or following electrolytic midcollicular decerebration, the bradycardic response to hypoxic or asphyxic stimulation was reduced or was reversed to tachycardia. The extent of reduction or reversal of the bradycardia was positively correlated with the level of the arterial pressure which was adjusted by either hemorrhage or infusion of phenylephrine. These findings indicate a tachycardic component of the vagal response to hypoxia, integrated in the pontomedullary region of the brainstem and resulting from interaction between the chemoreceptor and baroreceptor reflexes.

On the mechanism for bradycardia induced by acute systemic anoxia in the dog.

The effects of acute systemic anoxia on heart rate were investigated in 46 anaesthetized, artificially ventilated and spontaneously breathing dogs. Severe anoxia produced by inhalation of 100 per cent nitrogen over a period of 1 to 3 min elicited in both groups of animals a biphasic response consisting of a primary tachycardia and secondary bradycardia. Whereas primary tachycardia was usually moderate, secondary bradycardia was very pronounced and amounted to a 45.8 per cent reduction of heart rate in artificially ventilated dogs, and to 67.2 per cent in dogs breathing spontaneously. Bilateral cervical vagotomy, atropinization and ganglionic blockade caused consistently a considerable reduction or abolition of anoxic bracycardia. On the contrary, elimination of the sympatho-adrenal system by means of spinal cord destruction and bilateral adrenalectomy was conducive to an evident enhancement of bradycardia. The intensity of bradycardia was not reduced following denervation of carotid and aortic baro- and chemoreceptors. On the contrary, denervation invariably resulted in a considerable increase of bradycardia. It is concluded that secondary anoxic bradycardia is mainly due to the increased tone of the vagal cardioinhibitory center, the local depressant action of anoxia on the heart itself being of minor importance. Increased vagal tone is opposed by the concomitant stimulation of the sympatho-adrenal system. Anoxic bradycardia cannot be regarded as resulting from stimulation of carotid and aortic receptors. It is, therefore, inferred that some other mechanism, reflex or central, is activated during acute systemic anoxia giving rise to the increased vagal discharge to the heart.