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J M deTarnowsky

Publications and source records attributed to J M deTarnowsky.

11 recordsLinked to original sources
PubMed1988

Integration of heart rate and sympathetic neural effects on AV conduction.

Sympathetic activation increases heart rate (HR) and reduces atrioventricular interval (AVI), whereas atrial pacing alone increases AVI. We sought to differentiate the direct effects of sympathetic activation on atrioventricular (AV) conduction time from the indirect changes associated with concurrent alterations in HR. We recorded electrocardiograms, blood pressure (BP), and intracardiac electrograms from chloralose-anesthetized autonomically decentralized dogs. Beat-by-beat HR and AVI data were collected continuously. Sympathetic stimulation (0.25-2.5 Hz; mean 0.81 Hz) resulted in a HR change of +60 beats/min after 60 s. This tachycardia was associated with a mean decrease in AVI of 22 ms. Computer-driven atrial pacing to reproduce the HR associated with control sympathetic stimulation caused a mean AVI increase of 10 ms. Propranolol (200 micrograms) was then administered via the sinoatrial node artery and sympathetic stimulation repeated. Although HR remained constant, AVI decreased by 14.8 ms. The AVIs associated with an identical HR achieved by two different mechanisms (sympathetic stimulation and atrial pacing) were significantly different. Although removal of the contribution of sympathetically induced HR changes on AV conduction might be expected to result in potentiation of neural effects at the AV node, none was evident. Thus sympathetic activity restricted to the AV node is less effective in influencing AV conduction than the response that occurs when HR changes occur concurrently. Therefore, the opposing actions of HR and sympathetic tone on AV conduction may not be predicted by a simple linear relationship.

Animals↗
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

Effect of perfusion rate of cholinergic agonist on sinus node automaticity.

Recent evidence supports a complex relationship between pressure in the sinus node artery and heart rate. In addition, it has been suggested that acetylcholine effects vary depending upon the pressure at which the drug is injected. We examined the cardiac chronotropic responses to acetylcholine, delivered via the sinus node artery using a constant flow perfusion technique. Dogs were anesthetized with chloralose and prepared to record ECG, arterial pressure and bipolar electrograms from the sinus node, sulcus terminalis, right atrium, right ventricle and His bundle. The sinus node artery was catheterized, distribution verified and autologously perfused via the femoral artery. Both vagi and both stellate ganglia were transected. Analog data were processed by computer for each cycle length during perfusion with normal Tyrode solution or Tyrode solution containing acetylcholine. Perfusion of normal Tyrode solution (1-4ml/min) resulted in prolongation in cycle length which was greater at higher flow rates but rapidly dissipated at all flow rates. Beyond mechanically-induced bradycardia, acetylcholine initially prolonged cycle length but cycle length prolongation faded with time. Delivery of acetylcholine at higher flow rates resulted in significantly greater prolongation of cycle length. Cycle length always returned back toward control although perfusion of acetylcholine continued. Thus, responses to acetylcholine are influenced not only by drug concentration but also by the flow rate at which the drug is delivered. This suggests a coupling of mechanical and pharmacologic components of chronotropic influences at the sinus node.

Acetylcholine↗
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

Acetylcholine-calcium interactions in the canine atrium and sinus node.

Although the enhancement of acetylcholine release by extracellular calcium is well recognized, the potential arrhythmogenicity of vagal-calcium interactions has not been studied. We used anesthetized mongrel dogs and recorded: ECG, arterial pressure, and electrograms from the sinus node, sulcus terminalis, right atrium, right ventricle, and His bundle. All animals were autonomically decentralized. The sinus node artery was catheterized, its distribution was verified, and it was autologously perfused via the femoral artery. Vagal stimulation was carried out during autologous blood perfusion of the sinus node artery and again during perfusion with oxygenated Tyrode solution, with calcium concentrations ranging from 1.8 to 16.2 mmol. Vagal slowing of rate was accentuated in the presence of calcium concentrations as low as 2.7 mmol. Further increments in calcium concentration resulted in vagally-induced atrial fibrillation. Fibrillation was characterized by rapid, regular repetitive activity which was superceded by chaotic atrial rhythm at about 10 seconds and blocked by atropine. Elevations in calcium alone (5.4 to 16.2 mmol) resulted in atrial fibrillation which was chaotic in appearance and not blocked by atropine. We conclude that increases in calcium concentration within the distribution of the sinus node artery are arrhythmogenic alone, and also enhance vagally-induced changes in atrial rhythmicity.

Acetylcholine↗
PubMed1984

Postvagal potentiation of the chronotropic effect of norepinephrine.

Following termination of vagal stimulation, heart rate increases above control (postvagal tachycardia). This phenomenon has been attributed to vagally mediated release of norepinephrine in the sinus node region, although other contributory factors may be important. The possibility that, during the postvagal period, the chronotropic efficacy of norepinephrine is enhanced was investigated. Mongrel dogs (N = 6) were pretreated with reserpine in order to minimize postvagal tachycardia and hence allow reliable detection of enhanced responsiveness to norepinephrine. The dogs were then anesthetized with chloralose, autonomically decentralized, and instrumented to record electrocardiogram, aortic blood pressure, and electrograms from right atrium and right ventricle. Thirty-, forty-, or sixty-second infusions of norepinephrine were administered via the sinus node artery. The mean cycle length decrease produced by norepinephrine alone was 95 msec (which corresponds to a heart rate increase of + 19.6 bpm). After a 30-sec period of vagal stimulation, norepinephrine infusions produced a cycle length decrease of 139 msec (+32.5 bpm). These results are significant at the P less than 0.05 level. It is concluded that norepinephrine infusions produce a significantly greater magnitude of tachycardia when administered postvagally. It is proposed that this postvagal potentiation of the chronotropic effect of norepinephrine may contribute to postvagal tachycardia. Indeed, there may be a synergistic relationship between this phenomenon and vagally mediated release of norepinephrine in the mediation of postvagal tachycardia.

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↗