Biomedical subjects

C C Whitson

Publications and source records attributed to C C Whitson.

5 recordsLinked to original sources

PubMed1987

Atrioventricular nodal accommodation: rate- and time-dependent effects.

To characterize intrinsic rate- and time-dependent properties of the atrioventricular (AV) node, we examined whether AV interval (AVI) would be comparable at identical heart rates (HR) reached using different types of stimulation paradigms. We compared changes in AVI during five consecutive 30-s, 20 beat/min increases in HR from control with AVI changes induced by 30-s single-step protocols to each of the same levels. In addition, HR was maintained at each level for 30, 60, 90, 120, and 150 s to control for the influences of time. Chloralose-anesthetized dogs (n = 16) were autonomically decentralized and instrumented to record electrocardiogram, blood pressure, and multiple intracardiac electrograms. Computer-generated HR steps were begun 20 beats/min above control, while continuously recording AVI. The beat-by-beat changes in AVI within each step were quantitated for all protocols. Differences between AVI during single- and multiple-step protocols were most pronounced during the first 15 s of atrial pacing. Accommodation in AVI (change in AV conduction time associated with an increased but constant heart rate) was evident during both protocols. The degree of accommodation during multiple-step protocols was modulated by the cumulative effects of earlier HR; however, a similar degree of accommodation occurred at higher HR irrespective of protocol used. Finally, the time to onset of loss of 1:1 AV conduction was significantly shorter when HR was increased using a multiple-step protocol. Thus the intrinsic response of the AV node to HR change is dependent on absolute level of HR, duration of rate change, and the potential cumulative effects of any earlier HR steps.

Animals↗

PubMed1987

Postpacing tachycardia: autonomic involvement.

The cessation of pacing from the sinus node region is followed by a transient sinus tachycardia or postpacing tachycardia (PPT). We sought to characterize autonomic involvement in PPT. We used alpha-chloralose-anesthetized dogs and recorded electrocardiograms, blood pressure, and electrograms from the sinus node, right atrium, right ventricle, and His bundle. Both vagi and both stellate ganglia were transected. PPT developed immediately after either linear or stepped heart rate changes. PPT followed pacing from the rostral but not the caudal region of the sulcus terminalis. Independent manipulation of absolute level of heart rate (+33, +66, and +100 beats/min above control) and duration of atrial pacing (10, 20, and 30 s) revealed that PPT is dependent predominantly on the duration of pacing and less on level of heart rate. During pacing in the control state, a 1:1 atrial capture was maintained. After atropine administration (0.2 mg/kg iv), PPT increased significantly in magnitude, time to peak PPT was shortened significantly, and loss of 1:1 atrial capture during pacing was evident at pacing rates of from 10 to 60 beats above control. In contrast, propranolol significantly attenuated PPT. We conclude that acetylcholine, released during pacing from the sinus node region, suppresses inherent sinus node acceleration induced by the concurrent release of intramural catecholamines. During pacing, acetylcholine release is essential for the maintenance of 1:1 atrial capture and significantly modulates both the latency and magnitude of PPT.

Animals↗

PubMed1986

Beat-by-beat modulation of AV conduction. II. Autonomic neural mechanisms.

We examined the mechanism by which autonomic neural activity associated with respiration and blood pressure modulates atrioventricular (AV) conduction in conscious dogs. Mongrel dogs were anesthetized and instrumented under sterile conditions to record atrial and ventricular electrograms and blood pressure. In the conscious state, electrocardiogram (ECG), respiration, blood pressure, and electrograms were recorded continuously, and heart rate and AV interval were plotted graphically as a function of time. To delineate the role(s) of sympathetic and parasympathetic activity, AV conduction was studied during abrupt and linear changes in heart rate after administration of atropine, propranolol, or both. In the basal state and after propranolol, AV interval oscillated with respiration both in the absence of atrial pacing and at pacing rates 10-100 beats/min above control. Following atropine, oscillations in AV interval associated with respiration were abolished; however, linear and abrupt heart rate increases resulted in AV conduction changes that were associated with fluctuations in blood pressure. In contrast, after both atropine and propranolol, alterations in blood pressure or respiration did not influence AV conduction and rate-dependent prolongation of AV conduction occurred. We conclude that in the basal state, AV conduction is influenced predominately by changes in parasympathetic activity which is the major determinant of respiratory-related AV interval oscillations; after atropine, sympathetic activity produces fluctuations in both AV conduction and blood pressure; and intrinsic rate-dependent properties of the AV node are modulated continually by both divisions of the autonomic nervous system.

Animals↗

PubMed1985

Dynamic interactions between heart rate and atrioventricular conduction.

We examined the beat-by-beat alterations in atrioventricular (AV) conduction time that accompany both linear and abrupt changes in heart rate (HR). We used alpha-chloralose-anesthetized and autonomically decentralized dogs (n = 10) and recorded electrocardiogram (ECG), arterial pressure, and electrograms from sinus node, right ventricle, and His bundle. Abrupt or linear HR changes of known slope were generated by computer and displayed graphically with AV interval as a function of time. HR was increased linearly from 10 to 110 beats/min above control over 15, 30, and 60 s and then decreased in a linear fashion. AV interval was dependent on direction of HR change with marked asymmetry between increases and decreases in HR. Similar data were apparent irrespective of whether the decrease followed the increase or vice versa. To study determinants of 1:1 conduction, HR was increased linearly by 200 beats/min above control over 15, 30, and 60 s. As rate of change of HR increased, 1:1 conduction continued to a higher HR; however, the last conducted AV interval was negatively correlated with rate of change of HR. Abrupt sustained increases in HR of 25, 50, 75, and 100% above control resulted in marked accommodation of AV interval only at higher levels of HR. Thus in the absence of autonomic neural tone, 1) cardiac cycle length is not associated with a fixed AV interval but is dependent on magnitude and direction of HR change; and 2) the HR at which 1:1 AV conduction fails is significantly altered by the rate of change of HR.

Animals↗

PubMed1984

Autoregulation of cardiac cycle length: role of catecholamines.

The mechanism of autoregulation of cardiac cycle length during phasic alterations in perfusion via the sinus node artery is unclear. Inasmuch as transient catecholamine release has been documented during sinus node artery injections, we sought to determine whether autoregulation of cycle length might be related to a beta receptor-mediated process. We used chloralose-anesthetized mongrel dogs. A right thoracotomy was performed, the vagi and sympathetic inputs to the heart were cut and electrograms were recorded from the sinoatrial (SA) node, right atrium, right ventricle and His bundle. The SA node artery was catheterized and distribution verified. Perfusion of normal Tyrode's solution via the SA node artery at 3 ml/min resulted in significant cycle length slowing which was maximal immediately after onset of perfusion. Plots of the derivative of cycle length with respect to time indicated either a monophasic or biphasic pattern of response. Administration of propranolol (2 mg/kg i.v.) resulted in a significant prolongation of control cycle length. Perfusion of normal Tyrode's solution after propranolol resulted in significantly greater degrees of cycle length prolongation (as judged by integration of area under cycle length curves) as well as only monophasic response patterns. These results suggest that infusions of normal Tyrode's solution, via the SA node artery, at physiologic flow rates are accompanied by concurrent catecholamine release throughout the infusion. This catecholamine release may contribute to the homeostatic regulation of cardiac cycle length.

Animals↗